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Contarini, Gabriella (2019) Addressing the maturation of higher-order cognitive functions relevant to psychiatric disorders in mice. [Ph.D. thesis]

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Abstract (italian or english)

Psychiatric disorders are a large class of debilitating mental illnesses that affect everyday life of patients and people around them. In fact, they result in alteration of thinking, moods, behavior and increased risk of disability, pain, death, or loss of freedom. Nevertheless, the exact mechanisms behind these diseases are still unknown. Over the last few years, researchers focused on the study of abnormalities in brain neurodevelopment genetic mutations, impact of traumatic events and the interaction between these factors. In particular, both genetic and environmental factors may influence brain developmental process throughout childhood, adolescence and adulthood. Previous studies investigated how genetic and environmental risk factors act during sensitive brain developmental periods whereby altering adult behavior and possibly causing vulnerability to neuropsychiatric disorders. Different brain systems have been involved in the development of psychiatric disorders. However, for disorders such as attentional deficit hyperactivity disorder (ADHD), schizophrenia, and post-traumatic stress disorder (PTSD) there are consistent evidence of a major implication of the dopaminergic and endocannabinoid systems.
Dopamine (DA) plays an important role acting as a trophic factor, in the development of neuronal cyto-architecture and also modulating neurodevelopmental processes during the embryonic and postnatal period. In particular, dopaminergic alterations within the prefrontal cortex (PFC) or Striatum, two brain area involved in cognition, learning and emotion, have been previously correlated to the etiology of neuropsychiatric disorders like schizophrenia, autism and ADHD. On the other hand, several studies have related dysfunctions of endocannabinoid system to psychiatric disorders. In fact, the relationship between cannabis consumption, especially during critical period of brain development, and schizophrenia onset has been demonstrated.


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EPrint type:Ph.D. thesis
Tutor:Giusti , Pietro
Supervisor:Papaleo, Francesco
Ph.D. course:Ciclo 31 > Corsi 31 > SCIENZE FARMACOLOGICHE
Data di deposito della tesi:23 May 2019
Anno di Pubblicazione:11 March 2019
Key Words:emotion
Settori scientifico-disciplinari MIUR:Area 05 - Scienze biologiche > BIO/14 Farmacologia
Struttura di riferimento:Dipartimenti > Dipartimento di Scienze del Farmaco
Codice ID:11951
Depositato il:08 Nov 2019 12:26
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Bibliography Cerca con Google

Chapter 1 Cerca con Google

[1] American Psychiatric Association, Diagnostic and statistical manual of mental disorders (5th ed.). . Cerca con Google

[2] D. Hoops and C. Flores, “Making Dopamine Connections in Adolescence,” Trends Neurosci., vol. 40, no. 12, pp. 709–719, Dec. 2017. Cerca con Google

[3] C. Regehr and V. R. Leblanc, “PTSD, Acute Stress, Performance and Decision-Making in Emergency Service Workers,” 2017. Cerca con Google

[4] D. Scheggia et al., “Remote memories are enhanced by COMT activity through dysregulation of the endocannabinoid system in the prefrontal cortex,” Mol. Psychiatry, vol. 23, no. 4, 2018. Cerca con Google

[5] T. Halldorsdottir and E. B. Binder, “Gene × Environment Interactions: From Molecular Mechanisms to Behavior,” Annu. Rev. Psychol., vol. 68, no. 1, pp. 215–241, Jan. 2017. Cerca con Google

[6] R. H. Wozniak, N. B. Leezenbaum, J. B. Northrup, K. L. West, and J. M. Iverson, “The development of autism spectrum disorders: variability and causal complexity,” Wiley Interdiscip. Rev. Cogn. Sci., vol. 8, no. 1–2, p. e1426, Jan. 2017. Cerca con Google

[7] P. Moran et al., “Gene × Environment Interactions in Schizophrenia : Evidence from Genetic Mouse Models,” vol. 2016, 2016. Cerca con Google

[8] Q. Yu et al., “Dopamine and serotonin signaling during two sensitive developmental periods differentially impact adult aggressive and affective behaviors in mice,” Mol. Psychiatry, vol. 19, no. 6, pp. 688–698, 2014. Cerca con Google

[9] A. Carlsson, “Antipsychotic drugs, neurotransmitters, and schizophrenia,” Am. J. Psychiatry, vol. 135, no. 2, pp. 165–173, Feb. 1978. Cerca con Google

[10] F. Papaleo et al., “Genetic Dissection of the Role of Catechol- O - Methyltransferase in Cognition and Stress Reactivity in Mice,” vol. 28, no. 35, pp. 8709–8723, 2008. Cerca con Google

[11] M. Mereu et al., “Dopamine transporter (DAT) genetic hypofunction in mice produces alterations consistent with ADHD but not schizophrenia or bipolar disorder,” Neuropharmacology, vol. 121, pp. 179–194, 2017. Cerca con Google

[12] M. E. Sloan, C. W. Grant, J. L. Gowin, V. A. Ramchandani, and B. Le Foll, “Endocannabinoid signaling in psychiatric disorders: a review of positron emission tomography studies,” Acta Pharmacol. Sin., p. 1, Aug. 2018. Cerca con Google

[13] I. Ibarra-Lecue et al., “The endocannabinoid system in mental disorders: Evidence from human brain studies,” 2018. Cerca con Google

[14] E. Puighermanal, A. Busquets-Garcia, R. Maldonado, and A. Ozaita, “Cellular and intracellular mechanisms involved in the cognitive impairment of cannabinoids,” Philos. Trans. R. Soc. B Biol. Sci., vol. 367, no. 1607, pp. 3254–3263, 2012. Cerca con Google

[15] E. H. Simpson, C. Kellendonk, and E. Kandel, “A Possible Role for the Striatum in the Pathogenesis of the Cognitive Symptoms of Schizophrenia,” Neuron, vol. 65, no. 5, pp. 585–596, 2010. Cerca con Google

[16] D. Parolaro, N. Realini, D. Vigano, C. Guidali, and T. Rubino, “The endocannabinoid system and psychiatric disorders,” Exp. Neurol., vol. 224, no. 1, pp. 3–14, 2010. Cerca con Google

[17] A. Caspi et al., “Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: Longitudinal evidence of a gene X environment interaction,” Biol. Psychiatry, vol. 57, no. 10, pp. 1117–1127, 2005. Cerca con Google

[18] J. Mcgrath, S. Saha, D. Chant, and J. Welham, “Schizophrenia : A Concise Overview of Incidence , Prevalence , and Mortality,” vol. 30, pp. 67–76, 2008. Cerca con Google

[19] L. H. Shen, M. H. Liao, and Y. C. Tseng, “Recent advances in imaging of dopaminergic neurons for evaluation of neuropsychiatric disorders,” J. Biomed. Biotechnol., vol. 2012, 2012. Cerca con Google

[20] H. Takahashi, “PET neuroimaging of extrastriatal dopamine receptors and prefrontal cortex functions,” J. Physiol. Paris, vol. 107, no. 6, pp. 503–509, 2013. Cerca con Google

[21] R. Brisch et al., “A morphometric analysis of the septal nuclei in schizophrenia and affective disorders: Reduced neuronal density in the lateral septal nucleus in bipolar disorder,” Eur. Arch. Psychiatry Clin. Neurosci., vol. 261, no. 1, pp. 47–58, 2011. Cerca con Google

[22] “Giros et al., 1996.pdf.” . Cerca con Google

[23] M. Matsumoto et al., “Catechol O-methyltransferase mRNA expression in human and rat brain: evidence for a role in cortical neuronal function.,” Neuroscience, vol. 116, no. 1, pp. 127–137, 2003. Cerca con Google

[24] B. S. Mcewen and N. York, “Catechol- O -methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior,” vol. 95, no. August, pp. 9991–9996, 1998. Cerca con Google

[25] J. A. Gogos et al., “Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior,” Proc. Natl. Acad. Sci., vol. 95, no. 17, pp. 9991–9996, 1998. Cerca con Google

[26] S. R. Sesack, V. A. Hawrylak, C. Matus, M. A. Guido, and A. I. Levey, “Dopamine axon varicosities in the prelimbic division of the rat prefrontal cortex exhibit sparse immunoreactivity for the dopamine transporter.,” J. Neurosci., vol. 18, no. 7, pp. 2697–708, 1998. Cerca con Google

[27] A. Busquets-Garcia et al., “Pregnenolone blocks cannabinoid-induced acute psychotic-like states in mice,” Mol. Psychiatry, vol. 22, no. 11, pp. 1594–1603, 2017. Cerca con Google

[28] T. T. Y. Lee, M. N. Hill, and F. S. Lee, “Developmental regulation of fear learning and anxiety behavior by endocannabinoids,” Genes, Brain Behav., vol. 15, no. 1, pp. 108–124, 2016. Cerca con Google

[29] M. Qin, Z. Zeidler, K. Moulton, L. Krych, Z. Xia, and C. B. Smith, “Endocannabinoid-mediated improvement on a test of aversive memory in a mouse model of fragile X syndrome,” Behav. Brain Res., vol. 291, pp. 164–171, 2015. Cerca con Google

[30] I. G. Æ. J. P. Æ, T. Aguado, and Æ. M. Guzma, “The endocannabinoid system and the regulation of neural development : potential implications in psychiatric disorders,” pp. 371–382, 2009. Cerca con Google

[31] P. Campolongo and V. Trezza, “The endocannabinoid system: a key modulator of emotions and cognition.,” Front. Behav. Neurosci., vol. 6, no. November, p. 73, 2012. Cerca con Google

[32] R. Tanasescu and C. S. Constantinescu, “Cannabinoids and the immune system: An overview,” Immunobiology, vol. 215, no. 8, pp. 588–597, 2010. Cerca con Google

[33] A. Ameri, “The effects of cannabinoids on the brain,” Prog. Neurobiol., vol. 58, no. 4, pp. 315–348, 1999. Cerca con Google

[34] T. Ohno-Shosaku, T. Maejima, and M. Kano, “Endogenous cannabinoids mediate retrograde signals from depolarized postsynaptic neurons to presynaptic terminals,” Neuron, vol. 29, no. 3, pp. 729–738, 2001. Cerca con Google

[35] F. A. Pamplona and R. N. Takahashi, “Psychopharmacology of the endocannabinoids: far beyond anandamide,” J. Psychopharmacol., vol. 26, no. 1, pp. 7–22, Jun. 2011. Cerca con Google

[36] E. Puighermanal, A. Busquets-garcia, and R. Maldonado, “Cellular and intracellular mechanisms involved in the cognitive impairment of cannabinoids,” pp. 3254–3263, 2012. Cerca con Google

[37] C. R. Lupica and A. C. Riegel, “Endocannabinoid release from midbrain dopamine neurons: A potential substrate for cannabinoid receptor antagonist treatment of addiction,” Neuropharmacology, vol. 48, no. 8 SPEC. ISS., pp. 1105–1116, 2005. Cerca con Google

[38] J. F. Oliveira da Cruz, L. M. Robin, F. Drago, G. Marsicano, and M. Metna-Laurent, “Astroglial type-1 cannabinoid receptor (CB1): A new player in the tripartite synapse,” Neuroscience, vol. 323, pp. 35–42, 2016. Cerca con Google

[39] M. Metna-Laurent and G. Marsicano, “Rising stars: Modulation of brain functions by astroglial type-1 cannabinoid receptors,” Glia, vol. 63, no. 3, pp. 353–364, 2015. Cerca con Google

[40] V. Di Marzo et al., “Formation and inactivation of endogenous cannabinoid anandamide in central neurons,” Nature, vol. 372, p. 686, Dec. 1994. Cerca con Google

[41] G. Marsicano and B. Lutz, “Expression of the cannabinoid receptor CB1 in distinct neuronal subpopulations in the adult mouse forebrain,” Eur. J. Neurosci., vol. 11, no. 12, pp. 4213–4225, 1999. Cerca con Google

[42] D. Piomelli, “The molecular logic of endocannabinoid signalling,” Nat. Rev. Neurosci., vol. 4, no. 11, pp. 873–884, 2003. Cerca con Google

[43] R. I. Wilson, G. Kunos, and R. A. Nicoll, “Presynaptic specificity of endocannabinoid signaling in the hippocampus,” Neuron, vol. 31, no. 3, pp. 453–462, 2001. Cerca con Google

[44] J. P. Leite and L. S. Bueno-junior, “Cannabinoids and Vanilloids in Schizophrenia : Neurophysiological Evidence and Directions for Basic Research,” vol. 8, no. June, pp. 1–27, 2017. Cerca con Google

[45] A. Giuffrida et al., “Cerebrospinal Anandamide Levels are Elevated in Acute Schizophrenia and are Inversely Correlated with Psychotic Symptoms,” pp. 2108–2114, 2004. Cerca con Google

[46] F. M. Leweke et al., “Anandamide levels in cerebrospinal fluid of first-episode schizophrenic patients: Impact of cannabis use,” Schizophr. Res., vol. 94, no. 1–3, pp. 29–36, 2007. Cerca con Google

[47] M. Hellmich and D. Koethe, “Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia,” no. January, 2012. Cerca con Google

[48] R. M. Murray et al., “Cannabis-associated psychosis: Neural substrate and clinical impact,” Neuropharmacology, vol. 124, pp. 89–104, 2017. Cerca con Google

[49] C. Henquet et al., “An Experimental Study of Catechol-O-Methyltransferase Val158Met Moderation of Δ-9-Tetrahydrocannabinol-Induced Effects on Psychosis and Cognition,” Neuropsychopharmacology, vol. 31, no. 12, pp. 2748–2757, 2006. Cerca con Google

[50] C. Henquet et al., “Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people,” Bmj, vol. 330, no. 7481, p. 11, 2005. Cerca con Google

[51] S. Vanheule, R. Meganck, and M. Desmet, “Alexithymia, social detachment and cognitive processing,” Psychiatry Res., vol. 190, no. 1, pp. 49–51, 2011. Cerca con Google

[52] A. Manuscript, “Emotional Images,” vol. 26, no. 10, pp. 1289–1298, 2013. Cerca con Google

[53] M. G. Bossong, H. H. van Hell, G. Jager, R. S. Kahn, N. F. Ramsey, and J. M. Jansma, “The endocannabinoid system and emotional processing: A pharmacological fMRI study with {increment}9-tetrahydrocannabinol,” Eur. Neuropsychopharmacol., vol. 23, no. 12, pp. 1687–1697, 2013. Cerca con Google

[54] B. Platt, S. Kamboj, C. J. A. Morgan, and H. V. Curran, “Processing dynamic facial affect in frequent cannabis-users: Evidence of deficits in the speed of identifying emotional expressions,” Drug Alcohol Depend., vol. 112, no. 1–2, pp. 27–32, 2010. Cerca con Google

[55] C. Hindocha et al., “Acute effects of delta-9-tetrahydrocannabinol, cannabidiol and their combination on facial emotion recognition: A randomised, double-blind, placebo-controlled study in cannabis users,” Eur. Neuropsychopharmacol., vol. 25, no. 3, pp. 325–334, 2015. Cerca con Google

[56] M. Mereu et al., “Dopamine transporter (DAT) genetic hypofunction in mice produces alterations consistent with ADHD but not schizophrenia or bipolar disorder,” Neuropharmacology, vol. 121, 2017. Cerca con Google

[57] M. Ciampoli, G. Contarini, M. Mereu, and F. Papaleo, “Attentional Control in Adolescent Mice Assessed with a Modified Five Choice Serial Reaction Time Task,” Sci. Rep., vol. 7, no. 1, 2017 Cerca con Google

Cerca con Google

Chapter 2 Cerca con Google

[1] P. Fusar-Poli and A. Meyer-Lindenberg, “Striatal presynaptic dopamine in schizophrenia, part i: Meta-analysis of dopamine active transporter (DAT) density,” Schizophr. Bull., vol. 39, no. 1, pp. 22–32, 2013. Cerca con Google

[2] R. Gowrishankar, M. K. Hahn, and R. D. Blakely, “Good riddance to dopamine: Roles for the dopamine transporter in synaptic function and dopamine-associated brain disorders,” Neurochem. Int., vol. 73, no. 1, pp. 42–48, 2014. Cerca con Google

[3] J. K. Pinsonneault et al., “Dopamine Transporter Gene Variant Affecting Expression in Human Brain is Associated with Bipolar Disorder,” Neuropsychopharmacology, vol. 36, no. 8, pp. 1644–1655, 2011. Cerca con Google

[4] J. J. Weinstein, M. O. Chohan, M. Slifstein, L. S. Kegeles, H. Moore, and A. Abi-Dargham, “Pathway-specific dopamine abnormalities in schizophrenia,” Biol. Psychiatry, 2016. Cerca con Google

[5] S. V. Faraone et al., “Molecular genetics of attention-deficit/hyperactivity disorder,” Biological Psychiatry, vol. 57, no. 11. pp. 1313–1323, 2005. Cerca con Google

[6] T. a Greenwood, N. J. Schork, E. Eskin, and J. R. Kelsoe, “Identification of additional variants within the human dopamine transporter gene provides further evidence for an association with bipolar disorder in two independent samples,” Mol Psychiatry, vol. 11, p. 115,125-133, 2006. Cerca con Google

[7] P. M. Moran, C. M. P. O’Tuathaigh, F. Papaleo, and J. L. Waddington, “Dopaminergic function in relation to genes associated with risk for schizophrenia: Translational mutant mouse models,” Prog. Brain Res., vol. 211, pp. 79–112, 2014. Cerca con Google

[8] S. V Faraone, T. J. Spencer, B. K. Madras, Y. Zhang-James, and J. Biederman, “Functional effects of dopamine transporter gene genotypes on in vivo dopamine transporter functioning: a meta-analysis.,” Mol. Psychiatry, vol. 19, no. 8, pp. 880–9, 2014. Cerca con Google

[9] S. R. Jones, R. R. Gainetdinov, M. Jaber, B. Giros, R. M. Wightman, and M. G. Caron, “Profound neuronal plasticity in response to inactivation of the dopamine transporter.,” Proc. Natl. Acad. Sci. U. S. A., vol. 95, no. 7, pp. 4029–34, 1998. Cerca con Google

[10] B. Giros, M. Jaber, S. R. Jones, R. M. Wightman, and M. G. Caron, “Hyperlocomotion and indifference to cocaine and amphetamine in mice lacking the dopamine transporter,” Nature, vol. 379, no. 6566, pp. 606–612, 1996. Cerca con Google

[11] C. Spielewoy, C. Roubert, M. Hamon, M. Nosten-Bertrand, C. Betancur, and B. Giros, “Behavioural disturbances associated with hyperdopaminergia in dopamine-transporter knockout mice.,” Behav. Pharmacol., vol. 11, no. 3–4, pp. 279–290, 2000. Cerca con Google

[12] M. A. Kurian et al., “Clinical and molecular characterisation of hereditary dopamine transporter deficiency syndrome: An observational cohort and experimental study,” Lancet Neurol., vol. 10, no. 1, pp. 54–62, 2011. Cerca con Google

[13] J. Ng et al., “Dopamine transporter deficiency syndrome: Phenotypic spectrum from infancy to adulthood,” Brain, vol. 137, no. 4, pp. 1107–1119, 2014. Cerca con Google

[14] S. Fuke, S. Suo, N. Takahashi, H. Koike, N. Sasagawa, and S. Ishiura, “The VNTR polymorphism of the human dopamine transporter (DAT1) gene affects gene expression,” Pharmacogenomics J., vol. 1, no. 2, pp. 152–156, 2001. Cerca con Google

[15] M. a Mergy et al., “The rare DAT coding variant Val559 perturbs DA neuron function, changes behavior, and alters in vivo responses to psychostimulants.,” Proc. Natl. Acad. Sci. U. S. A., vol. 111, no. 44, pp. E4779-88, 2014. Cerca con Google

[16] E. Chan, J. M. Fogler, and P. G. Hammerness, “Treatment of Attention-Deficit/Hyperactivity Disorder in Adolescents: A Systematic Review.,” JAMA, vol. 315, no. 18, pp. 1997–2008, 2016. Cerca con Google

[17] C. Koehler-Troy, M. Strober, and R. Malenbaum, “Methylphenidate-induced mania in a prepubertal child,” J. Clin. Psychiatry, vol. 47, no. 11, pp. 566–567, 1986. Cerca con Google

[18] M. Toda and A. Abi-Dargham, “Dopamine hypothesis of schizophrenia: Making sense of it all,” Current Psychiatry Reports, vol. 9, no. 4. pp. 329–336, 2007. Cerca con Google

[19] J. Biederman et al., “Influence of gender on attention deficit hyperactivity disorder in children referred to a psychiatric clinic.,” Am. J. Psychiatry, vol. 159, no. 1, pp. 36–42, 2002. Cerca con Google

[20] I. Kawa et al., “Gender differences in bipolar disorder: Age of onset, course, comorbidity, and symptom presentation,” Bipolar Disord., vol. 7, no. 2, pp. 119–125, 2005. Cerca con Google

[21] S. Sannino et al., “COMT Genetic Reduction Produces Sexually Divergent Effects on Cortical Anatomy and Working Memory in Mice and Humans.,” Cereb. cortex, no. September, pp. 2529–2541, 2014. Cerca con Google

[22] J. S. Rao, M. Kellom, E. A. Reese, S. I. Rapoport, and H. W. Kim, “Dysregulated glutamate and dopamine transporters in postmortem frontal cortex from bipolar and schizophrenic patients,” J. Affect. Disord., vol. 136, no. 1–2, pp. 63–71, 2012. Cerca con Google

[23] A. De Bartolomeis, C. Tomasetti, and F. Iasevoli, “Update on the Mechanism of Action of Aripiprazole: Translational Insights into Antipsychotic Strategies beyond Dopamine Receptor Antagonism,” CNS Drugs, vol. 29, no. 9, pp. 773–799, 2015. Cerca con Google

[24] Q. Hong et al., “Homer expression in the hippocampus of an animal model of attention-deficit/hyperactivity disorder,” Mol. Med. Rep., vol. 4, no. 4, pp. 705–712, 2011. Cerca con Google

[25] Q. Hong et al., “Prefrontal cortex Homer expression in an animal model of attention-deficit/hyperactivity disorder,” J. Neurol. Sci., vol. 287, no. 1–2, pp. 205–211, 2009. Cerca con Google

[26] K. D. Lominac et al., “Distinct roles for different Homer1 isoforms in behaviors and associated prefrontal cortex function,” J. Neurosci. Off. J. Soc. Neurosci., vol. 25, no. 50, pp. 11586–11594, 2005. Cerca con Google

[27] F. Managò et al., “Genetic Disruption of Arc/Arg3.1 in Mice Causes Alterations in Dopamine and Neurobehavioral Phenotypes Related to Schizophrenia,” Cell Rep., vol. 16, no. 8, pp. 2116–2128, 2016. Cerca con Google

[28] F. Papaleo, L. Erickson, G. Liu, J. Chen, and D. R. Weinberger, “Effects of sex and COMT genotype on environmentally modulated cognitive control in mice,” pp. 2–7, 2012. Cerca con Google

[29] F. Papaleo et al., “Genetic dissection of the role of catechol-O-methyltransferase in cognition and stress reactivity in mice.,” J. Neurosci., vol. 28, no. 35, pp. 8709–23, 2008. Cerca con Google

[30] H. Huang et al., “Chronic and acute intranasal oxytocin produce divergent social effects in mice.,” Neuropsychopharmacology, vol. 39, no. 5, pp. 1102–14, 2014. Cerca con Google

[31] T. W. Robbins, “The 5-choice serial reaction time task: Behavioural pharmacology and functional neurochemistry,” Psychopharmacology, vol. 163, no. 3–4. pp. 362–380, 2002. Cerca con Google

[32] A. Barbelivien, S. Ruotsalainen, and J. Sirvio, “Metabolic alterations in the prefrontal and cingulate cortices are related to behavioral deficits in a rodent model of attention-deficit hyperactivity disorder,” Cereb Cortex, vol. 11, no. 11, pp. 1056–1063, 2001. Cerca con Google

[33] R. Navarra et al., “Effects of atomoxetine and methylphenidate on attention and impulsivity in the 5-choice serial reaction time test,” Prog. Neuro-Psychopharmacology Biol. Psychiatry, vol. 32, no. 1, pp. 34–41, 2008. Cerca con Google

[34] Y. Chudasama and T. W. Robbins, “Dopaminergic modulation of visual attention and working memory in the rodent prefrontal cortex.,” Neuropsychopharmacology, vol. 29, no. 9, pp. 1628–1636, 2004. Cerca con Google

[35] J. T. Baker et al., “Disruption of cortical association networks in schizophrenia and psychotic bipolar disorder.,” JAMA psychiatry, vol. 71, no. 2, pp. 109–18, 2014. Cerca con Google

[36] H. Huang et al., “A schizophrenia relevant 5-Choice Serial Reaction Time Task for mice assessing broad monitoring, distractibility and impulsivity,” Psychopharmacology (Berl)., vol. 234, no. 13, pp. 2047–2062, 2017. Cerca con Google

[37] D. L. Braff, N. R. Swerdlow, and M. A. Geyer, “Symptom correlates of prepulse inhibition deficits in male schizophrenic patients,” Am. J. Psychiatry, vol. 156, no. 4, pp. 596–602, 1999. Cerca con Google

[38] S. Kohl, K. Heekeren, J. Klosterkötter, and J. Kuhn, “Prepulse inhibition in psychiatric disorders--apart from schizophrenia.,” J. Psychiatr. Res., vol. 47, no. 4, pp. 445–52, 2013. Cerca con Google

[39] W. Perry, A. Minassian, D. Feifel, and D. L. Braff, “Sensorimotor gating deficits in bipolar disorder patients with acute psychotic mania,” Biol. Psychiatry, vol. 50, no. 6, pp. 418–424, 2001. Cerca con Google

[40] D. Feifel, A. Minassian, and W. Perry, “Prepulse inhibition of startle in adults with ADHD,” J. Psychiatr. Res., vol. 43, no. 4, pp. 484–489, 2009. Cerca con Google

[41] R. J. Ralph, M. P. Paulus, F. Fumagalli, M. G. Caron, and M. A. Geyer, “Prepulse inhibition deficits and perseverative motor patterns in dopamine transporter knock-out mice: differential effects of D1 and D2 receptor antagonists.,” J. Neurosci., vol. 21, no. 1, pp. 305–13, 2001. Cerca con Google

[42] P. Wong, C. C. R. Chang, C. E. Marx, M. G. Caron, W. C. Wetsel, and X. Zhang, “Pregnenolone Rescues Schizophrenia-Like Behavior in Dopamine Transporter Knockout Mice,” PLoS One, vol. 7, no. 12, pp. 1–9, 2012. Cerca con Google

[43] G. Masi et al., “Attention-deficit hyperactivity disorder - Bipolar comorbidity in children and adolescents,” Bipolar Disord., vol. 8, no. 4, pp. 373–381, 2006. Cerca con Google

[44] C. Marangoni, L. De Chiara, and G. L. Faedda, “Bipolar Disorder and ADHD: Comorbidity and Diagnostic Distinctions,” Curr. Psychiatry Rep., vol. 17, no. 8, 2015. Cerca con Google

[45] American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders DSM-V. 2013. Cerca con Google

[46] R. Boss?? et al., “Anterior pituitary hypoplasia and dwarfism in mice lacking the dopamine transporter,” Neuron, vol. 19, no. 1, pp. 127–138, 1997. Cerca con Google

[47] R. A. Barkley, “Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD.,” Psychol. Bull., vol. 121, no. 1, pp. 65–94, 1997. Cerca con Google

[48] K. E. Burdick, R. J. Braga, J. F. Goldberg, and A. K. Malhotra, “Cognitive dysfunction in bipolar disorder: Future place of pharmacotherapy,” CNS Drugs, vol. 21, no. 12. pp. 971–981, 2007. Cerca con Google

[49] G. R. I. Barker and E. C. Warburton, “When Is the Hippocampus Involved in Recognition Memory?,” J. Neurosci., vol. 31, no. 29, pp. 10721–10731, 2011. Cerca con Google

[50] A. S. C. França, L. Muratori, G. C. Nascimento, C. M. Pereira, S. Ribeiro, and B. Lobão-Soares, “Object recognition impairment and rescue by a dopamine D2 antagonist in hyperdopaminergic mice,” Behav. Brain Res., vol. 308, pp. 211–216, 2016. Cerca con Google

[51] F. Napolitano et al., “Role of Aberrant Striatal Dopamine D1 Receptor/cAMP/Protein Kinase A/DARPP32 Signaling in the Paradoxical Calming Effect of Amphetamine,” J. Neurosci., vol. 30, no. 33, pp. 11043–11056, 2010. Cerca con Google

[52] P. Wong, Y. Sze, C. C. R. Chang, J. Lee, and X. Zhang, “Pregnenolone sulfate normalizes schizophrenia-like behaviors in dopamine transporter knockout mice through the AKT/GSK3β pathway.,” Transl. Psychiatry, vol. 5, no. 3, p. e528, 2015. Cerca con Google

[53] X. Zhuang et al., “Hyperactivity and impaired response habituation in hyperdopaminergic mice.,” Proc. Natl. Acad. Sci. U. S. A., vol. 98, no. 4, pp. 1982–7, 2001. Cerca con Google

[54] A. Bari, J. W. Dalley, and T. W. Robbins, “The application of the 5-choice serial reaction time task for the assessment of visual attentional processes and impulse control in rats.,” Nat. Protoc., vol. 3, no. 5, pp. 759–767, 2008. Cerca con Google

[55] D. Bottai et al., “Synaptic activity-induced conversion of intronic to exonic sequence in Homer 1 immediate early gene expression,” J Neurosci, vol. 22, no. 1, pp. 167–175, 2002. Cerca con Google

[56] A. de Bartolomeis and F. Iasevoli, “The Homer family and the signal transduction system at glutamatergic postsynaptic density: potential role in behavior and pharmacotherapy.,” Psychopharmacol. Bull., vol. 37, no. 3, pp. 51–83, 2003. Cerca con Google

[57] A. Vazdarjanova, B. L. McNaughton, C. a Barnes, P. F. Worley, and J. F. Guzowski, “Experience-dependent coincident expression of the effector immediate-early genes arc and Homer 1a in hippocampal and neocortical neuronal networks.,” J. Neurosci., vol. 22, no. 23, pp. 10067–10071, 2002. Cerca con Google

[58] L. Yang et al., “The role of Homer 1a in increasing locomotor activity and non-selective attention, and impairing learning and memory abilities,” Brain Res., vol. 1515, pp. 39–47, 2013. Cerca con Google

[59] M. K. Hayashi, H. M. Ames, and Y. Hayashi, “Tetrameric hub structure of postsynaptic scaffolding protein homer,” J. Neurosci. Off. J. Soc. Neurosci., vol. 26, no. 33, pp. 8492–8501, 2006. Cerca con Google

[60] T. M. Hu, C. H. Chen, Y. A. Chuang, S. H. Hsu, and M. C. Cheng, “Resequencing of early growth response 2 (EGR2) gene revealed a recurrent patient-specific mutation in schizophrenia,” Psychiatry Res., vol. 228, no. 3, pp. 958–960, 2015. Cerca con Google

[61] M. J. Huentelman et al., “Association of SNPs in EGR3 and ARC with schizophrenia supports a biological pathway for schizophrenia risk,” PLoS One, vol. 10, no. 10, 2015. Cerca con Google

[62] A. L. Guillozet-Bongaarts et al., “Altered gene expression in the dorsolateral prefrontal cortex of individuals with schizophrenia.,” Mol. Psychiatry, vol. 19, no. 4, pp. 478–85, 2014. Cerca con Google

[63] V. E. Cosgrove, J. R. Kelsoe, and T. Suppes, “Toward a valid animal model of bipolar disorder: How the research domain criteria help bridge the clinical-basic science divide,” Biological Psychiatry, vol. 79, no. 1. pp. 62–70, 2016. Cerca con Google

[64] M. Laruelle and A. Abi-Dargham, “Dopamine as the wind of the psychotic fire: new evidence from brain imaging studies,” J. Psychopharmacol., vol. 13, no. 4, pp. 358–371, 1999. Cerca con Google

[65] C. Gillberg et al., “Long-term stimulant treatment of children with attention-deficit hyperactivity disorder symptoms. A randomized, double-blind, placebo-controlled trial.,” Arch. Gen. Psychiatry, vol. 54, no. 9, pp. 857–864, 1997. Cerca con Google

[66] J. Egeland, “Differentiating attention deficit in adult ADHD and schizophrenia,” Arch. Clin. Neuropsychol., vol. 22, no. 6, pp. 763–771, 2007. Cerca con Google

[67] I. Grande, M. Berk, B. Birmaher, and E. Vieta, “Bipolar disorder.,” Lancet (London, England), vol. 387, no. 10027, pp. 1561–1572, 2015. Cerca con Google

[68] G. Bush, “Attention-Deficit/Hyperactivity Disorder and Attention Networks,” Neuropsychopharmacology, vol. 35, no. 1, pp. 278–300, 2010. Cerca con Google

[69] K. A. Gleason, S. G. Birnbaum, A. Shukla, and S. Ghose, “Susceptibility of the adolescent brain to cannabinoids: long-term hippocampal effects and relevance to schizophrenia.,” Transl. Psychiatry, vol. 2, p. e199, 2012. Cerca con Google

[70] M. Weiss, C. Murray, and G. Weiss, “Adults with attention-deficit/hyperactivity disorder: current concepts.,” J. Psychiatr. Pract., vol. 8, no. 2, pp. 99–111, 2002. Cerca con Google

[71] R. Gallagher and J. Blader, “The diagnosis and neuropsychological assessment of adult attention deficit/hyperactivity disorder. Scientific study and practical guidelines.,” Ann. N. Y. Acad. Sci., pp. 148–171, 2001. Cerca con Google

[72] M. Weiss and C. Murray, “Assessment and management of attention-deficit hyperactivity disorder in adults.,” CMAJ, vol. 168, no. 6, pp. 715–22, 2003. Cerca con Google

[73] J. M. Gold, B. Hahn, G. P. Strauss, and J. A. Waltz, “Turning it upside down: Areas of preserved cognitive function in schizophrenia,” Neuropsychol. Rev., vol. 19, no. 3, pp. 294–311, 2009. Cerca con Google

[74] T. J. Spencer et al., “Effect of psychostimulants on brain structure and function in ADHD: A qualitative literature review of magnetic resonance imaging-based neuroimaging studies,” J. Clin. Psychiatry, vol. 74, no. 9, pp. 902–917, 2013. Cerca con Google

[75] B. Hahn et al., “Visuospatial attention in schizophrenia: Deficits in broad monitoring.,” J. Abnorm. Psychol., vol. 121, no. 1, pp. 119–128, 2012. Cerca con Google

[76] J. T. Nigg, “Response Inhibition and Disruptive Behaviors: Toward a Multiprocess Conception of Etiological Heterogeneity for ADHD Combined Type and Conduct Disorder Early-Onset Type,” in Annals of the New York Academy of Sciences, 2003, vol. 1008, pp. 170–182. Cerca con Google

[77] Y. Chudasama and T. W. Robbins, “Dissociable contributions of the orbitofrontal and infralimbic cortex to pavlovian autoshaping and discrimination reversal learning: further evidence for the functional heterogeneity of the rodent frontal cortex.,” J. Neurosci., vol. 23, no. 25, pp. 8771–8780, 2003. Cerca con Google

[78] M. V Solanto, “Neuropsychopharmacological mechanisms of stimulant drug action in attention-deficit hyperactivity disorder: a review and integration.,” Behav. Brain Res., vol. 94, no. 1, pp. 127–52, 1998. Cerca con Google

[79] F. X. Castellanos, E. J. Fine, D. Kaysen, W. L. Marsh, J. L. Rapoport, and M. Hallett, “Sensorimotor gating in boys with Tourette’s syndrome and ADHD: Preliminary results,” Biol. Psychiatry, vol. 39, no. 1, pp. 33–41, 1996. Cerca con Google

[80] E. M. Ornitz et al., “Prepulse inhibition of startle and the neurobiology of primary nocturnal enuresis,” Biol. Psychiatry, vol. 45, no. 11, pp. 1455–1466, 1999. Cerca con Google

[81] M. C. Hanlon, F. Karayanidis, and U. Schall, “Intact sensorimotor gating in adult attention deficit hyperactivity disorder,” Int. J. Neuropsychopharmacol., vol. 12, no. 5, pp. 701–707, 2009. Cerca con Google

[82] D. L. Braff, M. A. Geyer, and N. R. Swerdlow, “Human studies of prepulse inhibition of startle: Normal subjects, patient groups, and pharmacological studies,” Psychopharmacology, vol. 156, no. 2–3. pp. 234–258, 2001. Cerca con Google

[83] D. L. Braff, C. Grillon, and M. A. Geyer, “Gating and habituation of the startle reflex in schizophrenic patients. Special Issue: : Gating and habituation of the startle reflex in schizophrenic patients,” Arch. Gen. Psychiatry., pp. 206–215, 1992. Cerca con Google

[84] Q. Hong et al., “Increased locomotor activity and non-selective attention and impaired learning ability in SD rats after lentiviral vector-mediated RNA interference of Homer 1a in the brain,” Int. J. Med. Sci., vol. 10, no. 1, pp. 90–102, 2012. Cerca con Google

[85] S. M. Cochran, M. Fujimura, B. J. Morris, and J. A. Pratt, “Acute and delayed effects of phencyclidine upon mRNA levels of markers of glutamatergic and GABAergic neurotransmitter function in the rat brain,” Synapse, vol. 46, no. 3, pp. 206–214, 2002. Cerca con Google

[86] F. Iasevoli, A. Ambesi-Impiombato, G. Fiore, F. Panariello, G. Muscettola, and A. de Bartolomeis, “Pattern of acute induction of Homer1a gene is preserved after chronic treatment with first- and second-generation antipsychotics: effect of short-term drug discontinuation and comparison with Homer1a-interacting genes.,” J. Psychopharmacol., vol. 25, no. 7, pp. 875–87, 2011. Cerca con Google

[87] M. Fromer et al., “De novo mutations in schizophrenia implicate synaptic networks,” Nature, vol. 506, no. 7487, pp. 179–184, 2014. Cerca con Google

[88] S. M. Purcell et al., “A polygenic burden of rare disruptive mutations in schizophrenia,” Nature, vol. 506, no. 7487, pp. 185–190, 2014. Cerca con Google

[89] K. C. Berridge, “The debate over dopamine’s role in reward: The case for incentive salience,” Psychopharmacology, vol. 191, no. 3. pp. 391–431, 2007. Cerca con Google

[90] D. E. Greydanus, M. A. Sloane, and M. D. Rappley, “Psychopharmacology of ADHD in adolescents. [Review] [137 refs],” Adolesc. Med. State Art Rev., vol. 13, no. 3, pp. 599–624, 2002. Cerca con Google

[91] D. S. Segal and R. Kuczenski, “Human methamphetamine pharmacokinetics simulated in the rat: single daily intravenous administration reveals elements of sensitization and tolerance.,” Neuropsychopharmacology, vol. 31, pp. 941–955, 2006. Cerca con Google

[92] T. D. Sotnikova, J. M. Beaulieu, L. S. Barak, W. C. Wetsel, M. G. Caron, and R. R. Gainetdinov, “Dopamine-independent locomotor actions of amphetamines in a novel acute mouse model of parkinson disease,” PLoS Biol., vol. 3, no. 8, 2005. Cerca con Google

[93] T. G. Dinan and J. F. Cryan, “The impact of gut microbiota on brain and behaviour: implications for psychiatry.,” Curr. Opin. Clin. Nutr. Metab. Care, vol. 18, no. 6, pp. 552–8, 2015. Cerca con Google

[94] M. Yamashita et al., “Norepinephrine transporter blockade can normalize the prepulse inhibition deficits found in dopamine transporter knockout mice.,” Neuropsychopharmacology, vol. 31, no. 10, pp. 2132–2139, 2006. Cerca con Google

[95] M. Yamashita et al., “Impaired cliff avoidance reaction in dopamine transporter knockout mice,” Psychopharmacology (Berl)., vol. 227, no. 4, pp. 741–749, 2013. Cerca con Google

[96] L. Gee et al., “The Influence of Bilateral Subthalamic Nucleus Deep Brain Stimulation on Impulsivity and Prepulse Inhibition in Parkinson’s Disease Patients,” Stereotact. Funct. Neurosurg., vol. 93, no. 4, pp. 265–270, 2015. Cerca con Google

[97] A. Conzelmann et al., “Early attentional deficits in an attention-to-prepulse paradigm in ADHD adults.,” J. Abnorm. Psychol., vol. 119, no. 3, pp. 594–603, 2010. Cerca con Google

[98] E. M. Ornitz, G. L. Hanna, and J. de Traversay, “Prestimulation-induced startle modulation in attention-deficit hyperactivity disorder and nocturnal enuresis.,” Psychophysiology, vol. 29, no. 4, pp. 437–451, 1992. Cerca con Google

Cerca con Google

Chapter 3 Cerca con Google

[1] M. Schneider, “Adolescence as a vulnerable period to alter rodent behavior,” Cell Tissue Res., vol. 354, no. 1, pp. 99–106, 2013. Cerca con Google

[2] C. L. Sisk and D. L. Foster, “The neural basis of puberty and adolescence,” Nat. Neurosci., vol. 7, no. 10, pp. 1040–1047, 2004. Cerca con Google

[3] L. Steinberg, “Cognitive and affective development in adolescence,” Trends Cogn. Sci., vol. 9, no. 2, pp. 69–74, 2005. Cerca con Google

[4] D. Yurgelun-Todd, “Emotional and cognitive changes during adolescence,” Curr. Opin. Neurobiol., vol. 17, no. 2, pp. 251–257, 2007. Cerca con Google

[5] R. D. Q. G. Prwlrqdo, R. Ri, and D. Q. G. Grohvfhqfh, “) Urqwdo / Reh ) Xqfwlrqlqj Lq & Klogkrrg.” Cerca con Google

[6] J. M. Gold and G. K. Thaker, “Current progress in schizophrenia research cognitive phenotypes of schizophrenia: Attention,” J. Nerv. Ment. Dis., vol. 190, no. 9, pp. 638–639, 2002. Cerca con Google

[7] M. Zvyagintsev, C. Parisi, N. Chechko, A. R. Nikolaev, and K. Mathiak, “Attention and multisensory integration of emotions in schizophrenia,” Front. Hum. Neurosci., vol. 7, no. October, pp. 1–7, 2013. Cerca con Google

[8] J. M. Gold, B. Hahn, G. P. Strauss, and J. A. Waltz, “Turning it upside down: Areas of preserved cognitive function in schizophrenia,” Neuropsychol. Rev., vol. 19, no. 3, pp. 294–311, 2009. Cerca con Google

[9] S. C. L. Deoni et al., “Mapping Infant Brain Myelination with Magnetic Resonance Imaging,” J. Neurosci., vol. 31, no. 2, pp. 784–791, 2011. Cerca con Google

[10] E. M. Gordon et al., “Strength of default mode resting-state connectivity relates to white matter integrity in children,” Dev. Sci., vol. 14, no. 4, pp. 738–751, 2011. Cerca con Google

[11] A. Manuscript, “<2006 - 4-13 yo - Davidson et al., Neuropsychologia.pdf>,” vol. 44, no. 11, pp. 2037–2078, 2006. Cerca con Google

[12] J. Adamek, H. Herrlich, G. S. Abstract, and C. Catego-, “References 1.,” Form. Asp. Comput., vol. 6, no. 1990, pp. 62–77, 1999. Cerca con Google

[13] M. Ernst, T. Daniele, and K. Frantz, “New perspectives on adolescent motivated behavior: Attention and conditioning,” Dev. Cogn. Neurosci., vol. 1, no. 4, pp. 377–389, 2011. Cerca con Google

[14] T. E. Moffitt et al., “A gradient of childhood self-control predicts health, wealth, and public safety,” Proc. Natl. Acad. Sci., vol. 108, no. 7, pp. 2693–2698, 2011. Cerca con Google

[15] T. Dalgleish et al., “[ No Title ],” J. Exp. Psychol. Gen., vol. 136, no. 1, pp. 23–42, 2007. Cerca con Google

[16] A. B. Clohessy, M. I. Posner, and M. K. Rothbart, “Development of the functional visual field,” Acta Psychol. (Amst)., vol. 106, no. 1–2, pp. 51–68, 2001. Cerca con Google

[17] K. M. Thomas and C. A. Nelson, “Serial Reaction Time Learning in Preschool- and School-Age Children,” J. Exp. Child Psychol., vol. 79, no. 4, pp. 364–387, 2001. Cerca con Google

[18] P. O&apos;Donnell, “Cortical disinhibition in the neonatal ventral hippocampal lesion model of schizophrenia: New vistas on possible therapeutic approaches,” Pharmacol. Ther., vol. 133, no. 1, pp. 19–25, 2012. Cerca con Google

[19] F. Papaleo et al., “Dysbindin-1 modulates prefrontal cortical activity and schizophrenia-like behaviors via dopamine/D2 pathways,” Mol. Psychiatry, vol. 17, no. 1, pp. 85–98, 2012. Cerca con Google

[20] L. Steinberg and A. S. Morris, “Adolescent Devolepmental,” Annu. Rev. Psychol., vol. 52, pp. 83–110, 2001. Cerca con Google

[21] S. L. Andersen, A. T. Thompson, M. Rutstein, J. C. Hostetter, and M. H. Teicher, “Dopamine receptor pruning in prefrontal cortex during the periadolescent period in rats,” Synapse, vol. 37, no. 2, pp. 167–169, 2000. Cerca con Google

[22] “Spear - 2002.pdf.” . Cerca con Google

[23] D. Wahlstrom, T. White, and M. Luciana, “Neurobehavioral evidence for changes in dopamine system activity during adolescence,” Neurosci. Biobehav. Rev., vol. 34, no. 5, pp. 631–648, 2010. Cerca con Google

[24] L. P. Spear, <Spear LP 2000 - Review.pdf>, vol. 24. 2000. Cerca con Google

[25] C. S. Monk et al., “Adolescent immaturity in attention-related brain engagement to emotional facial expressions,” Neuroimage, vol. 20, no. 1, pp. 420–428, 2003. Cerca con Google

[26] K. Rubia et al., “Functional frontalisation with age: Mapping neurodevelopmental trajectories with fMRI,” Neurosci. Biobehav. Rev., vol. 24, no. 1, pp. 13–19, 2000. Cerca con Google

[27] L. Tamm, V. Menon, and A. L. Reiss, “LIHI Certificate #58 - Union Gas | Low Impact Hydropower Institute,” vol. 20, pp. 1231–1238, 2017. Cerca con Google

[28] M. Ernst et al., “Amygdala and nucleus accumbens in responses to receipt and omission of gains in adults and adolescents,” Neuroimage, vol. 25, no. 4, pp. 1279–1291, 2005. Cerca con Google

[29] A. Galvan et al., “Earlier Development of the Accumbens Relative to Orbitofrontal Cortex Might Underlie Risk-Taking Behavior in Adolescents,” J. Neurosci., vol. 26, no. 25, pp. 6885–6892, 2006. Cerca con Google

[30] M. P. Purdue et al., “Erratum: A prospective study of 67 serum immune and inflammation markers and risk of non-Hodgkin lymphoma (Blood (2013) 122:6 (951-957)),” Blood, vol. 123, no. 18, p. 2901, 2014. Cerca con Google

[31] J. McGaughy, J. W. Dalley, C. H. Morrison, B. J. Everitt, and T. W. Robbins, “Selective behavioral and neurochemical effects of cholinergic lesions produced by intrabasalis infusions of 192 IgG-saporin on attentional performance in a five-choice serial reaction time task.,” J. Neurosci., vol. 22, no. 5, pp. 1905–13, 2002. Cerca con Google

[32] J. McGaughy, J. Turchi, and M. Sarter, “Crossmodal divided attention in rats: effects of chlordiazepoxide and scopolamine,” Psychopharmacology (Berl)., vol. 115, no. 1–2, pp. 213–220, 1994. Cerca con Google

[33] F. Papaleo, L. Erickson, G. Liu, J. Chen, and D. R. Weinberger, “Effects of sex and COMT genotype on environmentally modulated cognitive control in mice,” Proc. Natl. Acad. Sci., vol. 109, no. 49, pp. 20160–20165, 2012. Cerca con Google

[34] D. Scheggia, A. Bebensee, D. R. Weinberger, and F. Papaleo, “The ultimate intra-/extra-dimensional attentional set-shifting task for mice,” Biol. Psychiatry, vol. 75, no. 8, pp. 660–670, 2014. Cerca con Google

[35] A. Bari, J. W. Dalley, and T. W. Robbins, “The application of the 5-choice serial reaction time task for the assessment of visual attentional processes and impulse control in rats.,” Nat. Protoc., vol. 3, no. 5, pp. 759–767, 2008. Cerca con Google

[36] W. Adriani and G. Laviola, “Elevated levels of impulsivity and reduced place conditioning with d-amphetamine: Two behavioral features of adolescence in mice,” Behav. Neurosci., vol. 117, no. 4, pp. 695–703, 2003. Cerca con Google

[37] F. Papaleo, L. Erickson, G. Liu, J. Chen, and D. R. Weinberger, “Effects of sex and COMT genotype on environmentally modulated cognitive control in mice,” pp. 2–7, 2012. Cerca con Google

[38] V. Anderson, “Assessing executive functions in children: Biological, psychological, and developmental considerations,” Pediatr. Rehabil., vol. 4, no. 3, pp. 119–136, 2001. Cerca con Google

[39] T. J. Simon, Z. Wu, B. Avants, H. Zhang, J. C. Gee, and G. T. Stebbins, “Atypical cortical connectivity and visuospatial cognitive impairments are related in children with chromosome 22q11.2 deletion syndrome,” Behav. Brain Funct., vol. 4, pp. 1–11, 2008. Cerca con Google

[40] B. Hahn, T. J. Ross, and E. A. Stein, “Neuroanatomical dissociation between bottom-up and top-down processes of visuospatial selective attention,” Neuroimage, vol. 32, no. 2, pp. 842–853, 2006. Cerca con Google

[41] B. Hahn et al., “Visuospatial attention in schizophrenia: Deficits in broad monitoring.,” J. Abnorm. Psychol., vol. 121, no. 1, pp. 119–128, 2012. Cerca con Google

[42] E. Macaluso and F. Doricchi, “Attention and predictions: control of spatial attention beyond the endogenous-exogenous dichotomy,” Front. Hum. Neurosci., vol. 7, no. October, pp. 75–80, 2013. Cerca con Google

[43] I. Dumontheil, B. Hassan, S. J. Gilbert, and S.-J. Blakemore, “Development of the Selection and Manipulation of Self-Generated Thoughts in Adolescence,” J. Neurosci., vol. 30, no. 22, pp. 7664–7671, 2010. Cerca con Google

[44] C. L. Frame and T. F. Oltmanns, “Serial recall by schizophrenic and affective patients during and after psychotic episodes,” J. Abnorm. Psychol., vol. 91, no. 5, pp. 311–318, 1982. Cerca con Google

[45] P. Harvey, K. C. Winters, S. Weintraub, and J. M. Neale, “Distractibility in children vulnerable to psychopathology,” J. Abnorm. Psychol., vol. 90, no. 4, pp. 298–304, 1981. Cerca con Google

[46] O. Slobodin, H. Cassuto, and I. Berger, “Age-Related Changes in Distractibility: Developmental Trajectory of Sustained Attention in ADHD,” J. Atten. Disord., 2015. Cerca con Google

[47] H. Huang et al., “A schizophrenia relevant 5-Choice Serial Reaction Time Task for mice assessing broad monitoring, distractibility and impulsivity,” Psychopharmacology (Berl)., vol. 234, no. 13, pp. 2047–2062, 2017. Cerca con Google

[48] M. Mereu et al., “Dopamine transporter (DAT) genetic hypofunction in mice produces alterations consistent with ADHD but not schizophrenia or bipolar disorder,” Neuropharmacology, vol. 121, pp. 179–194, 2017. Cerca con Google

[49] D. Scheggia, S. Sannino, M. Luisa Scattoni, and F. Papaleo, “COMT as a Drug Target for Cognitive Functions and Dysfunctions,” CNS Neurol. Disord. - Drug Targets, vol. 11, no. 3, pp. 209–221, 2012. Cerca con Google

[50] N. M. W. J. de Bruin, F. Fransen, H. Duytschaever, C. Grantham, and A. A. H. P. Megens, “Attentional performance of (C57BL/6J × 129Sv)F2 mice in the five-choice serial reaction time task,” Physiol. Behav., vol. 89, no. 5, pp. 692–703, 2006. Cerca con Google

[51] T. W. Robbins, “The 5-choice serial reaction time task: Behavioural pharmacology and functional neurochemistry,” Psychopharmacology, vol. 163, no. 3–4. pp. 362–380, 2002. Cerca con Google

[52] J. Davis et al., “A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis,” Neurosci. Biobehav. Rev., vol. 65, pp. 185–194, 2016. Cerca con Google

[53] L. Desbonnet et al., “Gut microbiota depletion from early adolescence in mice: Implications for brain and behaviour,” Brain. Behav. Immun., vol. 48, pp. 165–173, 2015. Cerca con Google

[54] M. B. Zimmermann, “The role of iodine in human growth and development,” Semin. Cell Dev. Biol., vol. 22, no. 6, pp. 645–652, 2011. Cerca con Google

[55] P. E. Orndorff, T. S. Hamrick, I. W. Smoak, and E. A. Havell, “Host and bacterial factors in listeriosis pathogenesis,” Vet. Microbiol., vol. 114, no. 1–2, pp. 1–15, 2006. Cerca con Google

[56] L. A. Newman and J. Mcgaughy, “Adolescent rats show cognitive rigidity in a test of attentional set shifting,” Dev. Psychobiol., vol. 53, no. 4, pp. 391–401, 2011. Cerca con Google

[57] E. Remmelink, U. Chau, A. B. Smit, M. Verhage, and M. Loos, “A one-week 5-choice serial reaction time task to measure impulsivity and attention in adult and adolescent mice,” Sci. Rep., vol. 7, no. January, pp. 1–13, 2017. Cerca con Google

[58] N. Amitai and A. Markou, “Comparative effects of different test day challenges on performance in the 5-choice serial reaction time task,” Behav. Neurosci., vol. 125, no. 5, pp. 764–774, 2011. Cerca con Google

[59] M. J. Millan et al., “Altering the course of schizophrenia: Progress and perspectives,” Nat. Rev. Drug Discov., vol. 15, no. 7, pp. 485–515, 2016. Cerca con Google

[60] J.-Q. Engle, K. M.; Mei, T-S.; Wasa, M.; Yu, “NIH Public Access,” Acc. Chem. Res., vol. 45, no. 6, pp. 788–802, 2008. Cerca con Google

[61] D. W. Bayless, J. S. Darling, W. J. Stout, and J. M. Daniel, “Sex differences in attentional processes in adult rats as measured by performance on the 5-choice serial reaction time task,” Behav. Brain Res., vol. 235, no. 1, pp. 48–54, 2012. Cerca con Google

[62] Y. Chudasama and T. W. Robbins, “Dissociable contributions of the orbitofrontal and infralimbic cortex to pavlovian autoshaping and discrimination reversal learning: further evidence for the functional heterogeneity of the rodent frontal cortex.,” J. Neurosci., vol. 23, no. 25, pp. 8771–8780, 2003. Cerca con Google

[63] S. J. Blakemore and S. Choudhury, “Development of the adolescent brain: Implications for executive function and social cognition,” J. Child Psychol. Psychiatry Allied Discip., vol. 47, no. 3–4, pp. 296–312, 2006. Cerca con Google

[64] P. J. Olesen, J. Macoveanu, J. Tegnér, and T. Klingberg, “Brain activity related to working memory and distraction in children and adults,” Cereb. Cortex, vol. 17, no. 5, pp. 1047–1054, 2007. Cerca con Google

[65] B. Luna, A. Padmanabhan, and K. O. Hearn, “Sturio_Publi_Symposium_Albufeira_2000.Pdf,” vol. 72, no. 1, pp. 1–28, 2011. Cerca con Google

[66] G. C. Harris and J. E. Levine, “Pubertal acceleration of pulsatile gonadotropin-releasing hormone release in male rats as revealed by microdialysis,” Endocrinology, vol. 144, no. 1, pp. 163–171, 2003. Cerca con Google

[67] S. Sannino et al., “Adolescence is the starting point of sex-dichotomous COMT genetic effects,” Transl. Psychiatry, vol. 7, no. 5, 2017. Cerca con Google

[68] C. L. Sisk, H. N. Richardson, P. E. Chappell, and J. E. Levine, “In vivo gonadotropin-releasing hormone secretion in female rats during peripubertal development and on proestrus,” Endocrinology, vol. 142, no. 7, pp. 2929–2936, 2001. Cerca con Google

[69] M. Arain et al., “NDT-39776-maturation-of-the-adolescent-brain,” Neuropsychiatr. Dis. Treat., vol. 9, pp. 449–461, 2013. Cerca con Google

[70] J. W. Dalley et al., “Nucleus Accumbens D2/3 Receptors Predict Trait Impulsivity and Cocaine Reinforcement,” Science (80-. )., vol. 315, no. 5816, pp. 1267–1270, 2007. Cerca con Google

[71] F. Papaleo, S. Sannino, F. Piras, and G. Spalletta, “Sex-dichotomous effects of functional COMT genetic variations on cognitive functions disappear after menopause in both health and schizophrenia,” Eur. Neuropsychopharmacol., vol. 25, no. 12, pp. 2349–2363, 2015. Cerca con Google

[72] E. Jacobs and M. D’Esposito, “Estrogen Shapes Dopamine-Dependent Cognitive Processes: Implications for Women’s Health,” J. Neurosci., vol. 31, no. 14, pp. 5286–5293, 2011. Cerca con Google

[73] K. D. Foust and B. K. Kaspar, “NIH Public Access,” vol. 8, no. 24, pp. 4017–4018, 2010. Cerca con Google

[74] J. B. Becker, “Gender differences in dopaminergic function in striatum and nucleus accumbens,” Pharmacol. Biochem. Behav., vol. 64, no. 4, pp. 803–812, 1999. Cerca con Google

[75] B. Hooks, “Feminist Theory: From Margin to Center,” vol. 8, no. January, p. 179, 2000. Cerca con Google

Chapter 4 Cerca con Google

[1] T. Kitamura et al., “Adult Neurogenesis Modulates the Hippocampus-Dependent Period of Associative Fear Memory,” Cell, vol. 139, no. 4, pp. 814–827, 2009. Cerca con Google

[2] P. W. Frankland and B. Bontempi, “The organization of recent and remote memories,” Nature Reviews Neuroscience. 2005. Cerca con Google

[3] C. L. Beeman, P. S. Bauer, J. L. Pierson, and J. J. Quinn, “Hippocampus and medial prefrontal cortex contributions to trace and contextual fear memory expression over time,” Learn. Mem., vol. 20, no. 6, pp. 336–343, 2013. Cerca con Google

[4] F. Papaleo, B. K. Lipska, and D. R. Weinberger, “Mouse models of genetic effects on cognition: Relevance to schizophrenia,” Neuropharmacology, vol. 62, no. 3, pp. 1204–1220, Mar. 2012. Cerca con Google

[5] T. W. Robbins and S. Kousta, “Uncovering the genetic underpinnings of cognition,” Trends Cogn. Sci., vol. 15, no. 9, pp. 375–377, 2011. Cerca con Google

[6] W. Davies, T. Humby, S. Trent, J. B. Eddy, O. a Ojarikre, and L. S. Wilkinson, “Genetic and pharmacological modulation of the steroid sulfatase axis improves response control; comparison with drugs used in ADHD.,” Neuropsychopharmacology, vol. 39, no. 11, pp. 2622–32, 2014. Cerca con Google

[7] R. Cools and M. D’Esposito, “Inverted-U-shaped dopamine actions on human working memory and cognitive control,” Biol. Psychiatry, vol. 69, no. 12, pp. e113–e125, 2011. Cerca con Google

[8] D. Shohamy and R. A. Adcock, “Dopamine and adaptive memory,” Trends Cogn. Sci., vol. 14, no. 10, pp. 464–472, 2010. Cerca con Google

[9] E. M. Tunbridge, P. J. Harrison, and D. R. Weinberger, “Catechol-o-Methyltransferase, Cognition, and Psychosis: Val158Met and Beyond,” Biol. Psychiatry, vol. 60, no. 2, pp. 141–151, 2006. Cerca con Google

[10] L. Yavich, M. M. Forsberg, M. Karayiorgou, J. A. Gogos, and P. T. Mannisto, “Site-Specific Role of Catechol-O-Methyltransferase in Dopamine Overflow within Prefrontal Cortex and Dorsal Striatum,” J. Neurosci., vol. 27, no. 38, pp. 10196–10209, 2007. Cerca con Google

[11] F. Papaleo et al., “Genetic dissection of the role of catechol-O-methyltransferase in cognition and stress reactivity in mice.,” J. Neurosci., vol. 28, no. 35, pp. 8709–23, 2008. Cerca con Google

[12] E. M. Tunbridge, “Catechol-O-Methyltransferase Inhibition Improves Set-Shifting Performance and Elevates Stimulated Dopamine Release in the Rat Prefrontal Cortex,” J. Neurosci., vol. 24, no. 23, pp. 5331–5335, 2004. Cerca con Google

[13] M. Matsumoto et al., “Catechol O-methyltransferase mRNA expression in human and rat brain: evidence for a role in cortical neuronal function.,” Neuroscience, vol. 116, no. 1, pp. 127–137, 2003. Cerca con Google

[14] A. G. Nackley et al., “Human Catechol-&lt;em&gt;O&lt;/em&gt;-Methyltransferase Haplotypes Modulate Protein Expression by Altering mRNA Secondary Structure,” Science (80-. )., vol. 314, no. 5807, p. 1930 LP-1933, Dec. 2006. Cerca con Google

[15] I. Dumontheil, B. Hassan, S. J. Gilbert, and S.-J. Blakemore, “Development of the Selection and Manipulation of Self-Generated Thoughts in Adolescence,” J. Neurosci., vol. 30, no. 22, pp. 7664–7671, 2010. Cerca con Google

[16] J. H. Barnett, P. B. Jones, T. W. Robbins, and U. Müller, “Effects of the catechol-O-methyltransferase Val158Met polymorphism on executive function: A meta-analysis of the Wisconsin Card Sort Test in schizophrenia and healthy controls,” Mol. Psychiatry, vol. 12, no. 5, pp. 502–509, 2007. Cerca con Google

[17] A. Bertolino et al., “Prefrontal-Hippocampal Coupling During Memory Processing Is Modulated by COMT Val158Met Genotype,” Biol. Psychiatry, vol. 60, no. 11, pp. 1250–1258, 2006. Cerca con Google

[18] C. Rothe et al., “Association of the Val158Met catechol O-methyltransferase genetic polymorphism with panic disorder,” Neuropsychopharmacology, vol. 31, no. 10, pp. 2237–2242, 2006. Cerca con Google

[19] I. T. Kolassa, S. Kolassa, V. Ertl, A. Papassotiropoulos, and D. J. F. De Quervain, “The Risk of Posttraumatic Stress Disorder After Trauma Depends on Traumatic Load and the Catechol-O-Methyltransferase Val158Met Polymorphism,” Biol. Psychiatry, vol. 67, no. 4, pp. 304–308, 2010. Cerca con Google

[20] J. A. Wojtalik and D. M. Barch, “An FMRI study of the influence of a history of substance abuse on working memory-related brain activation in schizophrenia,” Front. psychiatry, vol. 5, p. 1, Jan. 2014. Cerca con Google

[21] M. Morena and P. Campolongo, “The endocannabinoid system: An emotional buffer in the modulation of memory function,” Neurobiol. Learn. Mem., vol. 112, pp. 30–43, 2014. Cerca con Google

[22] G. Marsicano et al., “The endogenous cannabinoid system controls extinction of aversive memories,” Nature, vol. 418, no. 6897, pp. 530–534, 2002. Cerca con Google

[23] A. Caspi et al., “Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: Longitudinal evidence of a gene X environment interaction,” Biol. Psychiatry, vol. 57, no. 10, pp. 1117–1127, 2005. Cerca con Google

[24] P. W. Frankland, B. Bontempi, L. E. Talton, L. Kaczmarek, and A. J. Silva, “The Involvement of the Anterior Cingulate Cortex in Remote Contextual Fear Memory,” Science (80-. )., vol. 304, no. 5672, p. 881 LP-883, May 2004. Cerca con Google

[25] S. Tambaro, M. L. Tomasi, and M. Bortolato, “Long-term CB1receptor blockade enhances vulnerability to anxiogenic-like effects of cannabinoids,” Neuropharmacology, vol. 70, pp. 268–277, 2013. Cerca con Google

[26] F. Managò et al., “Genetic Disruption of Arc/Arg3.1 in Mice Causes Alterations in Dopamine and Neurobehavioral Phenotypes Related to Schizophrenia,” Cell Rep., vol. 16, no. 8, pp. 2116–2128, 2016. Cerca con Google

[27] G. Paxinos, K. B. J. Franklin, K. B. J. Paxinos, G and Franklin, G. Paxinos, and K. B. J. Franklin, Mouse Brain in Stereotaxic Coordinates. 2001. Cerca con Google

[28] G. Astarita and D. Piomelli, “Lipidomic analysis of endocannabinoid metabolism in biological samples,” Journal of Chromatography B: Analytical Technologies in the Biomedical and Life Sciences. 2009. Cerca con Google

[29] E. Zamberletti, M. Gabaglio, P. Prini, T. Rubino, and D. Parolaro, “Cortical neuroinflammation contributes to long-term cognitive dysfunctions following adolescent delta-9-tetrahydrocannabinol treatment in female rats,” Eur. Neuropsychopharmacol., vol. 25, no. 12, pp. 2404–2415, 2015. Cerca con Google

[30] S. Bolte and F. P. Cordelières, “A guided tour into subcellular colocalization analysis in light microscopy,” Journal of Microscopy. 2006. Cerca con Google

[31] A. K. Hall, U. Rutishauser, and D. Biol, “Modality-Specific Retrograde Amnesia of Fear Author ( s ): Jeansok J . Kim and Michael S . Fanselow Published by : American Association for the Advancement of Science Stable URL : https://www.jstor.org/stable/2876873 JSTOR is a not-for-profit service that,” vol. 256, no. 5057, pp. 675–677, 2018. Vai! Cerca con Google

[32] J. J. Quinn, Q. D. Ma, M. R. Tinsley, C. Koch, and M. S. Fanselow, “Inverse temporal contributions of the dorsal hippocampus and medial prefrontal cortex to the expression of long-term fear memories,” Learn. Mem., vol. 15, no. 5, pp. 368–372, 2008. Cerca con Google

[33] L. Restivo, G. Vetere, B. Bontempi, and M. Ammassari-Teule, “The Formation of Recent and Remote Memory Is Associated with Time-Dependent Formation of Dendritic Spines in the Hippocampus and Anterior Cingulate Cortex,” J. Neurosci., vol. 29, no. 25, pp. 8206–8214, 2009. Cerca con Google

[34] M. R. Milad and G. J. Quirk, “58005 51..106,” vol. 420, no. NOVEMBER, pp. 1–5, 2002. Cerca con Google

[35] F. Papaleo et al., “Genetic Dissection of the Role of Catechol- O - Methyltransferase in Cognition and Stress Reactivity in Mice,” vol. 28, no. 35, pp. 8709–8723, 2008. Cerca con Google

[36] J. A. Gogos et al., “Catechol-O-methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior,” Proc. Natl. Acad. Sci., vol. 95, no. 17, pp. 9991–9996, 1998. Cerca con Google

[37] A. Gozzi et al., “A neural switch for active and passive fear,” Neuron, vol. 67, no. 4, pp. 656–666, 2010. Cerca con Google

[38] V. Di Marzo, N. Stella, and A. Zimmer, “Endocannabinoid signalling and the deteriorating brain,” Nat. Rev. Neurosci., vol. 16, no. 1, pp. 30–42, 2015. Cerca con Google

[39] J. Gräff et al., “Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories,” Cell, vol. 156, no. 1–2, pp. 261–276, 2014. Cerca con Google

[40] E. H. Simpson et al., “Genetic variation in COMT activity impacts learning and dopamine release capacity in the striatum,” Learn. Mem., vol. 21, no. 4, pp. 205–214, 2014. Cerca con Google

[41] A. Contarino and F. Papaleo, “The corticotropin-releasing factor receptor-1 pathway mediates the negative affective states of opiate withdrawal,” Proc. Natl. Acad. Sci., vol. 102, no. 51, pp. 18649–18654, 2005. Cerca con Google

[42] B. H. Schott, “The Dopaminergic Midbrain Participates in Human Episodic Memory Formation: Evidence from Genetic Imaging,” J. Neurosci., vol. 26, no. 5, pp. 1407–1417, 2006. Cerca con Google

[43] M. Wimber et al., “Prefrontal dopamine and the dynamic control of human long-term memory,” Transl. Psychiatry, vol. 1, no. June, pp. 1–7, 2011. Cerca con Google

[44] F. Papaleo, S. Sannino, F. Piras, and G. Spalletta, “Sex-dichotomous effects of functional COMT genetic variations on cognitive functions disappear after menopause in both health and schizophrenia,” Eur. Neuropsychopharmacol., vol. 25, no. 12, pp. 2349–2363, 2015. Cerca con Google

[45] F. Papaleo, L. Erickson, G. Liu, J. Chen, and D. R. Weinberger, “Effects of sex and COMT genotype on environmentally modulated cognitive control in mice,” pp. 2–7, 2012. Cerca con Google

[46] S. Sannino et al., “COMT genetic reduction produces sexually divergent effects on cortical anatomy and working memory in mice and humans,” Cereb. Cortex, vol. 25, no. 9, pp. 2529–2541, 2015. Cerca con Google

[47] E. Jacobs and M. D’Esposito, “Estrogen Shapes Dopamine-Dependent Cognitive Processes: Implications for Women’s Health,” J. Neurosci., vol. 31, no. 14, pp. 5286–5293, 2011. Cerca con Google

[48] T. P. White et al., “Sex differences in COMT polymorphism effects on prefrontal inhibitory control in adolescence,” Neuropsychopharmacology, vol. 39, no. 11, pp. 2560–2569, 2014. Cerca con Google

[49] D. Scheggia, A. Bebensee, D. R. Weinberger, and F. Papaleo, “The ultimate intra-/extra-dimensional attentional set-shifting task for mice,” Biol. Psychiatry, vol. 75, no. 8, pp. 660–670, 2014. Cerca con Google

[50] G. E. Bruder et al., “Catechol-O-methyltransferase (COMT) genotypes and working memory: Associations with differing cognitive operations,” Biol. Psychiatry, vol. 58, no. 11, pp. 901–907, 2005. Cerca con Google

[51] M. F. Egan et al., “Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia,” Pnas, vol. 98, no. 12, pp. 6917–6922, 2001. Cerca con Google

[52] A. K. Malhotra, L. J. Kestler, C. Mazzanti, J. A. Bates, T. Goldberg, and D. Goldman, “A functional polymorphism in the COMT gene and performance on a test of prefrontal cognition,” Am. J. Psychiatry, 2002. Cerca con Google

[53] D. Durstewitz and J. K. Seamans, “The Dual-State Theory of Prefrontal Cortex Dopamine Function with Relevance to Catechol-<em>O</em>-Methyltransferase Genotypes and Schizophrenia,” Biol. Psychiatry, vol. 64, no. 9, pp. 739–749, Sep. 2017. Cerca con Google

[54] D. Mueller, J. T. Porter, and G. J. Quirk, “Noradrenergic Signaling in Infralimbic Cortex Increases Cell Excitability and Strengthens Memory for Fear Extinction,” J. Neurosci., vol. 28, no. 2, pp. 369–375, 2008. Cerca con Google

[55] C. Y. Kao, G. Stalla, J. Stalla, C. T. Wotjak, and E. Anderzhanova, “Norepinephrine and corticosterone in the medial prefrontal cortex and hippocampus predict PTSD-like symptoms in mice,” Eur. J. Neurosci., vol. 41, no. 9, pp. 1139–1148, 2015. Cerca con Google

[56] R. Clark et al., “Predicting post-traumatic stress disorder in veterans: Interaction oftraumatic load with COMT gene variation,” J. Psychiatr. Res., vol. 47, no. 12, pp. 1849–1856, 2013. Cerca con Google

[57] K. L. Humphreys, M. S. Scheeringa, and S. S. Drury, “Race Moderates the Association of Catechol- O -methyltransferase Genotype and Posttraumatic Stress Disorder in Preschool Children,” J. Child Adolesc. Psychopharmacol., 2014. Cerca con Google

[58] E. A. Winkler et al., “COMT Val158Met polymorphism is associated with post-traumatic stress disorder and functional outcome following mild traumatic brain injury,” J. Clin. Neurosci., vol. 35, pp. 109–116, 2017. Cerca con Google

[59] S. Sannino et al., “Adolescence is the starting point of sex-dichotomous COMT genetic effects,” Transl. Psychiatry, vol. 7, no. 5, 2017. Cerca con Google

[60] C. O. Val et al., “Val 158 Met Genotype and Neural Mechanisms Related to Affective Arousal and Regulation,” Imaging, vol. 63, no. 12, pp. 1396–406, 2006. Cerca con Google

[61] A. Heinz and M. N. Smolka, “The effects of catechol O-methyltransferase genotype on brain activation elicited by affective stimuli and cognitive tasks.,” Rev. Neurosci., vol. 17, no. 3, pp. 359–67, 2006. Cerca con Google

[62] M. Koenigs et al., “Focal brain damage protects against post-traumatic stress disorder in combat veterans,” Nat. Neurosci., vol. 11, no. 2, pp. 232–237, 2008. Cerca con Google

[63] H. Y. Tan, J. H. Callicott, and D. R. Weinberger, “Dysfunctional and compensatory prefrontal cortical systems, genes and the pathogenesis of schizophrenia,” Cereb. Cortex, vol. 17, no. SUPPL. 1, pp. 171–181, 2007. Cerca con Google

[64] D. M. Barch and A. Ceaser, “Cognition in schizophrenia: Core psychological and neural mechanisms,” Trends Cogn. Sci., vol. 16, no. 1, pp. 27–34, 2012. Cerca con Google

[65] B. Lutz, G. Marsicano, R. Maldonado, and C. J. Hillard, “The endocannabinoid system in guarding against fear, anxiety and stress,” Nat. Rev. Neurosci., vol. 16, no. 12, pp. 705–718, 2015. Cerca con Google

[66] M. Morena et al., “Endogenous cannabinoid release within prefrontal-limbic pathways affects memory consolidation of emotional training,” Proc. Natl. Acad. Sci., vol. 111, no. 51, pp. 18333–18338, 2014. Cerca con Google

[67] J. F. Oliveira da Cruz, L. M. Robin, F. Drago, G. Marsicano, and M. Metna-Laurent, “Astroglial type-1 cannabinoid receptor (CB1): A new player in the tripartite synapse,” Neuroscience, vol. 323, pp. 35–42, 2016. Cerca con Google

[68] C. D. Paspalas, “Presynaptic D1 Dopamine Receptors in Primate Prefrontal Cortex: Target-Specific Expression in the Glutamatergic Synapse,” J. Neurosci., vol. 25, no. 5, pp. 1260–1267, 2005. Cerca con Google

[69] J. K. Seamans and C. R. Yang, “The principal features and mechanisms of dopamine modulation in the prefrontal cortex,” Prog. Neurobiol., vol. 74, no. 1, pp. 1–57, 2004. Cerca con Google

[70] H. C. Bergstrom, “The neurocircuitry of remote cued fear memory,” Neurosci. Biobehav. Rev., vol. 71, pp. 409–417, 2016. Cerca con Google

[71] S. Duvarci and D. Pare, “Amygdala microcircuits controlling learned fear,” Neuron, vol. 82, no. 5, pp. 966–980, 2014. Cerca con Google

[72] S. Tanimoto, T. Nakagawa, Y. Yamauchi, M. Minami, and M. Satoh, “Differential contributions of the basolateral and central nuclei of the amygdala in the negative affective component of chemical somatic and visceral pains in rats,” Eur. J. Neurosci., vol. 18, no. 8, pp. 2343–2350, 2003. Cerca con Google

[73] M. N. Smolka, “Catechol-O-Methyltransferase val158met Genotype Affects Processing of Emotional Stimuli in the Amygdala and Prefrontal Cortex,” J. Neurosci., vol. 25, no. 4, pp. 836–842, 2005. Cerca con Google

[74] H. Tan, N. M. Lauzon, S. F. Bishop, N. Chi, M. Bechard, and S. R. Laviolette, “Cannabinoid Transmission in the Basolateral Amygdala Modulates Fear Memory Formation via Functional Inputs to the Prelimbic Cortex,” J. Neurosci., vol. 31, no. 14, pp. 5300–5312, 2011. Cerca con Google

Cerca con Google

Chapter 5 Cerca con Google

[1] Dunbar, R.I. The social brain hypothesis and its implications for social evolution. Annals of human biology 36, 562-572 (2009). Cerca con Google

[2] Henry, J.D., von Hippel, W., Molenberghs, P., Lee, T. & Sachdev, P.S. Clinical assessment of social cognitive function in neurological disorders. Nature reviews. Neurology 12, 28-39 (2016). Cerca con Google

[3] Kennedy, D.P. & Adolphs, R. Perception of emotions from facial expressions in high-functioning adults with autism. Neuropsychologia 50, 3313-3319 (2012). Cerca con Google

[4] Green, M.F., Horan, W.P. & Lee, J. Social cognition in schizophrenia. Nature reviews. Neuroscience 16, 620-631 (2015). Cerca con Google

[5] Fett, A.K. et al. The relationship between neurocognition and social cognition with functional outcomes in schizophrenia: a meta-analysis. Neuroscience and biobehavioral reviews 35, 573-588 (2011). Cerca con Google

[6] Kurtz, M.M. & Richardson, C.L. Social cognitive training for schizophrenia: a meta-analytic investigation of controlled research. Schizophr Bull 38, 1092-1104 (2012). Cerca con Google

[7] Fletcher-Watson, S., McConnell, F., Manola, E. & McConachie, H. Interventions based on the Theory of Mind cognitive model for autism spectrum disorder (ASD). The Cochrane database of systematic reviews, CD008785 (2014). Cerca con Google

[8] Tate, A.J., Fischer, H., Leigh, A.E. & Kendrick, K.M. Behavioural and neurophysiologicalevidence for face identity and face emotion processing in animals. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 361, 2155-2172 (2006). Cerca con Google

[9] Burkett, J.P. et al. Oxytocin-dependent consolation behavior in rodents. Science 351, 375-378 (2016). Cerca con Google

[10] Langford, D.J. et al. Social modulation of pain as evidence for empathy in mice. Science 312, 1967-1970 (2006). Cerca con Google

[11] Pisansky, M.T., Hanson, L.R., Gottesman, II & Gewirtz, J.C. Oxytocin enhances observational fear in mice. Nature communications 8, 2102 (2017). Cerca con Google

[12] Sterley, T.L. et al. Social transmission and buffering of synaptic changes after stress. Nature neuroscience (2018). Cerca con Google

[13] Prochazkova, E. & Kret, M.E. Connecting minds and sharing emotions through mimicry: A neurocognitive model of emotional contagion. Neuroscience and biobehavioral reviews 80, 99-114 (2017). Cerca con Google

[14] Bossong MG, vanHella HH, Jagera G, Hahnd RS, Ramseya NF, Jansmaa JM (2013) The endocannabinoid system and emotional processing: a pharmacological fMRI study with Δ9-tetrahydrocannabinol. European Neuropsychopharmacology (2013) 23, 1687–1697 Cerca con Google

[15] Hindocha C, Wollenberg O, Carter Leno V, Alvarez BO, Curran HV and Freeman TP Emotional processing deficits in chronic cannabis use: A replication and extension. J Psychopharmacol, doi: 10.1177/0269881114527359 (2013) Cerca con Google

[16] Bayrakçıa A, Sertb E, Zorlua N, Erola A, Sarıçiçeka A, Metea L. Facial emotion recognition deficits in abstinent cannabis dependent patients. Comprehensive Psychiatry 58 (2015) 160–164 Cerca con Google

[17] de Almeida V, Martins- de- Sousa (2018) Cannabinoids and glial cells: possible mechanism to understand schizophrenia. European Archives of Psychiatry and Clinical Neuroscience Cerca con Google

https://doi.org/10.1007/s00406-018-0874-6 Vai! Cerca con Google

[18] Petrelli, F et al. Dysfunction of homeostatic control of dopamine by astrocytes in the developing prefrontal cortex leads to cognitive impairments. Molecular psychiatry (2018) Cerca con Google

[19] Scheggia, D. et al. Remote memories are enhanced by COMT activity through dysregulation of the endocannabinoid system in the prefrontal cortex. Molecular psychiatry (2018). Cerca con Google

[20] Rogers-Carter, M.M. et al. Insular cortex mediates approach and avoidance responses to social affective stimuli. Nature neuroscience 21, 404-414 (2018). Cerca con Google

[21] Huang, H. et al. Chronic and acute intranasal oxytocin produce divergent social effects in mice. Neuropsychopharmacology : official publication of the American College of Cerca con Google

[22] Contarino, A., Kitchener, P., Vallee, M., Papaleo, F. & Piazza, P.V. CRF1 receptor-deficiency increases cocaine reward. Neuropharmacology 117, 41-48 (2017). Cerca con Google

[23] Cecilione, J.L. et al. Test-retest reliability of the facial expression labeling task. Psychol Assess 29, 1537-1542 (2017). Cerca con Google

[24] Anderson, D.J. & Adolphs, R. A framework for studying emotions across species. Cell 157, 187-200 (2014). Cerca con Google

[25] Portfors, C.V. Types and functions of ultrasonic vocalizations in laboratory rats and mice. J Am Assoc Lab Anim Sci 46, 28-34 (2007). Cerca con Google

[26] Blanchard, R.J. & Blanchard, D.C. Attack and defense in rodents as ethoexperimental models for the study of emotion. Prog Neuropsychopharmacol Biol Psychiatry 13 Suppl, S3-14 (1989). Cerca con Google

[27] Sadananda, M., Wohr, M. & Schwarting, R.K. Playback of 22-kHz and 50-kHz ultrasonic vocalizations induces differential c-fos expression in rat brain. Neurosci Lett 435, 17-23 (2008). Cerca con Google

[28] Zalaquett, C. & Thiessen, D. The effects of odors from stressed mice on conspecif Cerca con Google

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