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Gentili, Giuliano (2016) Intranasal administration of neuropeptides as a new therapeutic strategy to treat social and cognitive alterations relevant to schizophrenia. [Tesi di dottorato]

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Abstract (inglese)

Schizophrenia is a chronic enduring disorder ranked among the most debilitating mental illnesses (Mueser & McGurk, 2004; Tandon, Keshavan, & Nasrallah, 2008). Although it has been vigorously studied over the past century, the etiology and pathophysiology of schizophrenia remains largely unknown and currently available treatments, in the form of antipsychotics, are mainly unsatisfactory (Insel, 2010; Tandon et al., 2008).
Schizophrenia is characterized by three broad types of symptoms: positive symptoms, negative symptoms, and cognitive deficits. While drugs currently available for the treatment of this disorder are effective for positive symptoms, negative symptoms (including social impairments) and cognitive deficits still remain mainly untreatable.(Keefe et al., 2007; Neill et al., 2010). Negative and cognitive symptoms are more pervasive, fluctuate less over time than psychotic symptoms and are strongly associated with poor psychosocial functioning in community living and work (Kasper & Resinger, 2003; Mueser & McGurk, 2004; Tandon, Nasrallah, & Keshavan, 2009).
Although there have been rapid progress in the development of non-invasive technologies to study human brain structure and function in the last two decades, there are still substantial limitations in our ability to investigate details of the physiology and molecular biology of the human brain (Nestler & Hyman, 2010a). To that end, it is imperative to have carefully validated animal models for continued progress in our understanding of pathophysiology and in the development and screening of novel therapeutic agents in order to enhance functional recovery of patients (Davis et al., 2013; Neill et al., 2010).
Neuropeptides have an important role in intracerebral signaling and might have the potential to be used as therapeutic agents in many psychiatric and neurological diseases(Bedse, Di Domenico, Serviddio, & Cassano, 2015; Erbaş, Çınar, Solmaz, Çavuşoğlu, & Ateş, 2015; Nishimura, Murayama, & Takahashi, 2015; Reglodi et al., 2015, 2015). Unfortunately, they usually can’t be administered systemically due to the elevated hydrophilicity and molecular weight that prevent them to overcame the blood brain barrier.
Intranasal administration might be a promising and non-invasive way of administration of neuropeptides: this administration route enables highly hydrophilic and high molecular weight molecules to bypass the blood-brain barrier permitting them to reach the brain in a non-invasive way. This way has been demonstrated in in humans that permits the delivery of biologically effective concentrations of many peptides to the brain without eliciting significantly eventual systemic hormone-like side effects (Born et al., 2002); This route of administration was tested also in mice and rats (Born et al., 2002; Neumann, Maloumby, Beiderbeck, Lukas, & Landgraf, 2013)and, recently, was successfully used specifically in the context of behavioural studies in in mice (Huang et al., 2014).
The aim of the studies described in this thesis is to investigate, through the use of clinically-relevant animal models of schizophrenia, the pharmacogenetics behavioral effects of intranasal administration of two different neuropeptides:
- oxytocin (OXT), a neurohypophyseal peptide suggested to have beneficial effects in social behaviors (Meyer-Lindenberg, Domes, Kirsch, & Heinrichs, 2011; Striepens, Kendrick, Maier, & Hurlemann, 2011) and currently in clinical studies for mental disorders characterized by social behavioral alterations such as autism (Anagnostou et al., 2012; Guastella et al., 2010) and schizophrenia (Feifel et al., 2010).
- CRF(6-33), a syntetic peptide designed to be an effective competitive antagonist for the binding between the endogenous CRF neuropeptide and its binding protein (CRFbp)(Sutton et al., 1995) suggested in preclinical ICV studies to be an effective pro cognitive agent with potential therapeutic applications (Stephen C. Heinrichs & Joppa, 2001; Stephen C. Heinrichs, 2003; Koob & Bloom, 1985)
In previous work from our laboratory (Huang et al., 2014), we already implemented, for the first time, the use of intranasal oxytocin in C57BL/6J mice, checking different behavioral effects. Thus, we now tested the effects of intransal OXT in the schizophrenia-relevant dysbindin-1 knockout mouse model.
Genetic variations of the dysbindin-1 gene (DTNBP 1) has been associated with susceptibility to schizophrenia (O’Tuathaigh et al., 2007; Ross, Margolis, Reading, Pletnikov, & Coyle, 2006; Straub et al., 2002) and severity of negative symptoms and cognitive dysfunction in schizophrenic patients (Burdick et al., 2007; DeRosse et al., 2006; Fanous et al., 2005; Straub et al., 2002). Thereafter, using a Dys knockout mutant mouse model, we demonstrated that both the heterozygous and homozygous knockout mice manifested a reduction in social interaction compared to wildtype mice. Similar social deficits in Dys mutant mice have been reported by other groups (Feng et al., 2008; Hattori et al., 2008).
Interestingly, both chronic and acute intranasal OXT treatments were able to ameliorate the social deficits observed in the Dys knockout mice. These data suggest that intranasal oxytocin might be beneficial to subjects with genetic modifications relevant to schizophrenia, while administration to healthy subjects has not significant behavioral effect or may eventually be detrimental (Huang et al., 2014).
This opens new ways of exploration in relationship to the beneficial effects of OXT treatment and its utility in the clinical setting.
The data (aforementioned) correlate well with the molecular data available. As a matter of fact, OXT receptors are downregulated in WT subjects that are chronically IN –OXT treated, and even mutant mice, though treated with the same therapeutic protocol, show that the receptors are not subject to variation , compared to the control subjects treated with the vehicle substance only. Indeed, after being chronically treated, WT mice showed a decrease in social behaviour, while mutant mice (under an equivalent OXT treatment) showed an increase in social behaviour.
For the CRF(6-33) part, in order to set the ground for future studies with genetically modified mice, disease-related mouse models and facilitate inter-laboratory comparisons, we first tested the effects of both chronic and acute intranasal CRF treatments in C57BL/6J mice. Considered that OXT did not show significant improvement in cognitive performance, we chose to target these functions with a different peptide that in previous intracerebroventricular studies had shown to improve cognitive functions (Behan et al., 1995; Eckart et al., 1999; S C Heinrichs et al., 1997; Stephen C Heinrichs & Koob, 2004; Stephen C. Heinrichs & Joppa, 2001; Stephen C. Heinrichs, 2003; Koob & Bloom, 1985; Lee, Lee, Wang, & Lin, 1993; Lee & Sung, 1989; Thompson, Erickson, Schulkin, & Rosen, 2004) had shown to improve cognitive functions . To asses cognitive functions we used a modified version of the 5-Choice Serial Reaction Time Task (5-csrtt), a rodent test designed as analog of the Continuous Performance Test (cpt) used to asses quantitatively attentional control in humans (Amitai & Markou, 2011). The modifications are intended to reduce the time needed to train the animals , reduce stressful manipulations as food restriction or single housing. Additionally, several new manipulations have been implemented to investigate various specific cognitive functions such as attention, broad monitoring / compulsivity, response disinhibition/ impulsivity, distractibility and processing speed.
We were able to demonstrate that the intranasal administration of CRF(6-33) can produce selective behavioral effects in mice. In particular, acute administration was able to improve accuracy of responses and reduce impulsivity, while chronic administrations produced a delay in correct responses. Gene expression studies with real time PCR are starting to suggest that the CRF(6-33) is able to reach the brain, as both CRFr1 and CRFbp were altered following intranasal CRF(6-33) in different and specific brain areas (i.e. Hippocampus and Prefrontal Cortex ).
Subsequent dose-response tests confirmed the ability of evocate behavioral effects with a much lower dose of CRF(6-33). Moreover, we discovered a rebound effect in impulsive behavior the day after administration of higher doses.. This detrimental effect was absent with the lowest doses that was still able to significantly reduce impulsive behavior.
Lastly we tested ability of CRF(6-33) to ameliorate an impulsive phenotype in a genetic modified mouse model of schizophrenia. The chosen model was a double mutant for Dysbindin and for the receptor D2. The D2 receptor that had proven in previous test to have an increased impulsive behaviour.
The dopamine D2 receptor (D2) gene is another important risk gene identified for schizophrenia. Functional genetic variants in the D2 gene have been found to be differently expressed in patients with schizophrenia (Kaalund et al., 2013) and might modulate schizophrenia-related phenotypes by modifying the ratio of the short isoform (D2S) to the long isoform (D2L) (Bertolino et al., 2009). Heterozigote mutant for D2L has an increased D2S (receptor D2 short form)/ D2L (receptor D2 long form) ratio.
From preliminary data CRF(6-33) was not able to significantly affect impulsive behaviour in double heterozygote Dys +/- D2L +/- . Interestigly, in single heterozygote Dys +/- was observed a trend of increased impulsivity il CRF(6-33) group suggesting a detrimental interaction with Dys deficient genotype.
From this studies we can conclude that both OXT than CRF(6-33) have the potential to be used for treatment, respectively of social and impulsivity deficits. For OXT so far we observed a positive interaction with Dys deficient genotype , that needs to be confirmed in other schizophrenia relevant mouse models of social deficits. CRF(6-33) so far has demonstrated only to improve social performance in WT mice. The preliminary study on mutated mouse,if confirmed, seems to suggest that it might worsen the phenotype in presence of certain genetic mutations. It should be important to define mechanisms of interaction of CRF(6-33) with genetics as to define when it could be positively used for therapy and when it shouldn’t in a view of a genetic driven personalized schizophrenia therapy.

Abstract (italiano)

La schizofrenia è un disturbo cronico duraturo classificato tra le malattie mentali più debilitanti (Mueser e McGurk, 2004; Tandon, Keshavan, e Nasrallah, 2008). Anche se è stato vigorosamente studiata nel corso dell'ultimo secolo, l'eziologia e fisiopatologia della schizofrenia rimane in gran parte sconosciute e attualmente i trattamenti disponibili, in forma di antipsicotici, sono fondamentalmente insoddisfacente (Insel, 2010; Tandon et al., 2008).
La schizofrenia è caratterizzata da tre grandi tipi di sintomi: sintomi positivi, i sintomi negativi e deficit cognitivi. Mentre i farmaci attualmente disponibili per il trattamento di questo disturbo sono efficaci per i sintomi positivi, sintomi negativi (compresi i deficit sociali) e deficit cognitivi rimangono principalmente incurabile. (Keefe et al, 2007;.. Neill et al, 2010). Sintomi negativi e cognitivi sono più pervasivi, fluttuano meno nel tempo dei sintomi psicotici e sono fortemente associati con scarso funzionamento psicosociale nella vita comunitaria e di lavoro (Kasper & Resinger, 2003; Mueser & McGurk, 2004; Tandon, Nasrallah, e Keshavan, 2009) .
Anche se ci sono stati rapidi progressi nello sviluppo di tecnologie non invasive per studiare la struttura del cervello umano e il suo funzionamento negli ultimi due decenni, ci sono ancora limitazioni sostanziali nella nostra capacità di indagare i dettagli della fisiologia e della biologia molecolare del cervello umano (Nestler & Hyman, 2010a). A tal fine, è indispensabile avere modelli animali accuratamente convalidati per proseguire i progressi nella nostra comprensione della fisiopatologia e nello sviluppo e lo screening di nuovi agenti terapeutici al fine di migliorare il recupero funzionale dei pazienti (Davis et al, 2013;. Neill et al ., 2010).
Neuropeptidi hanno un ruolo importante nella segnalazione intracerebrale e potrebbe avere il potenziale per essere utilizzati come agenti terapeutici in molte malattie psichiatriche e neurologiche (Bedse, Di Domenico, Serviddio, e Cassano, 2015; Erbas, Cinar, Solmaz, Cavusoglu, e Ates, 2015 , Nishimura, Murayama, e Takahashi, 2015;. Reglodi et al, 2015, 2015). Purtroppo, di solito non possono essere somministrati per via sistemica a causa della idrofilia elevata e peso molecolare che impediscono loro di superamento del la barriera ematoencefalica.
La via di somministrazione intranasale potrebbe essere un modo promettente e non invasivo di somministrazione di neuropeptidi: questa via di somministrazione permette molecole altamente idrofile e ad alto peso molecolare per bypassare la barriera emato-encefalica, consentendo loro di raggiungere il cervello in modo non invasivo. In questo modo è stato dimostrato in negli esseri umani che permette la consegna delle concentrazioni biologicamente efficaci di molti peptidi al cervello, senza suscitare in modo significativo eventuali effetti collaterali ormonali sistemici (Born et al., 2002); Questa via di somministrazione è stata testata anche in topi e ratti (Nato et al., 2002; Neumann, Maloumby, Beiderbeck, Lukas, e Landgraf, 2013) e, recentemente, è stato utilizzato con successo in particolare nel contesto degli studi comportamentali nei topi ( Huang et al., 2014).
Lo scopo dello studio descritto in questa tesi è di indagare, attraverso l'uso di modelli animali clinicamente rilevanti per la schizofrenia, la farmacogenetica degli effetti comportamentali della somministrazione intranasale di due neuropeptidi differenti:
- Ossitocina (OXT), un peptide neuroipofisario suggerito avere effetti benefici in comportamenti sociali (Meyer-Lindenberg, Domes, Kirsch, e Heinrichs, 2011; Striepens, Kendrick, Maier, e Hürlemann, 2011) e attualmente in studi clinici per i disturbi mentali caratterizzata da alterazioni comportamentali sociali come l'autismo (Anagnostou et al, 2012;.. Guastella et al, 2010) e la schizofrenia (Feifel et al., 2010).
- (. Sutton et al, 1995) CRF (6-33), un peptide sintetico progettato per essere un antagonista competitivo efficace per il legame tra il neuropeptide CRF endogena e la sua proteina legante (CRFbp) ha suggerito in studi preclinici ICV ad essere un efficace agente pro cognitivo con potenziali applicazioni terapeutiche (Stephen C. Heinrichs e Giaffa, 2001; Stephen C. Heinrichs, 2003; Koob & Bloom, 1985)
In un precedente lavoro del nostro laboratorio (Huang et al., 2014), abbiamo già implementato, per la prima volta, l'uso di ossitocina intranasale in C57BL / 6J, controllando effetti comportamentali diversi. Così, ora abbiamo testato gli effetti di OXT intransale nel modello di topo dysbindin-1 knockout rilevante per schizofrenia.
Variazioni genetiche del dysbindin-1 gene (DTNBP 1) è stato associato con la suscettibilità alla schizofrenia (O'Tuathaigh et al, 2007;. Ross, Margolis, lettura, Pletnikov, & Coyle, 2006;. Straub et al, 2002) e gravità dei sintomi negativi e disfunzioni cognitive nei pazienti schizofrenici (Burdick et al, 2007;. DeRosse et al, 2006;.. Fanous et al., 2005; Straub et al, 2002). Successivamente, utilizzando un modello di topo knockout mutante Dys, abbiamo dimostrato che sia i topi knockout eterozigoti e omozigoti manifestano una riduzione nell'interazione sociale rispetto ai topi di wild type. Deficit sociali simili a Dys topi mutanti sono stati segnalati da altri gruppi (Feng et al, 2008;. Hattori et al., 2008).
È interessante notare che entrambi i trattamenti intranasale OXT, cronici e acuti, sono stati in grado di migliorare i deficit sociali osservati nei topi knockout Dys. Questi dati suggeriscono che intranasale di ossitocina potrebbe essere utile ai soggetti con modificazioni genetiche rilevanti per la schizofrenia, mentre la somministrazione a soggetti sani non ha significativo effetto comportamentale o alla fine può essere dannoso (Huang et al., 2014).
Questo apre nuove vie di esplorazione in relazione agli effetti benefici del trattamento OXT e la sua utilità in ambito clinico.
I dati (di cui sopra) correlano bene con i dati molecolari disponibili. È un dato di fatto, recettori OXT sono inibiti in soggetti WT che sono cronicamente IN -OXT trattati, e persino topi mutanti, anche se trattata con lo stesso protocollo terapeutico, mostrano che i recettori non sono soggetti a variazioni, rispetto ai soggetti di controllo trattati con solo la sostanza veicolo. Infatti, dopo essere stati trattati cronicamente, WT topi hanno mostrato una diminuzione del comportamento sociale, mentre i topi mutanti (nel quadro di un trattamento OXT equivalente) hanno mostrato un aumento dei comportamenti sociali.
Per il CRF (6-33) parte, al fine di impostare le basi per futuri studi con i topi geneticamente modificati, modelli murini legati alla malattia e facilitare il confronto tra laboratori, in primo luogo abbiamo testato gli effetti di entrambi i trattamenti intranasale CRF cronici e acuti in C57BL / 6J. Considerato che OXT non ha mostrato un significativo miglioramento delle prestazioni cognitive, abbiamo scelto di indirizzare queste funzioni con un peptide diverso che in precedenti studi intracerebroventricolare aveva dimostrato di migliorare le funzioni cognitive (Behan et al, 1995;.. Eckart et al, 1999; SC Heinrichs et al, 1997;. Stephen C Heinrichs & Koob, 2004; Stephen C. Heinrichs e Giaffa, 2001; Stephen C. Heinrichs, 2003; Koob & Bloom, 1985; Lee, Lee, Wang, e Lin, 1993; Lee & Sung , 1989; Thompson, Erickson, Schulkin, e Rosen, 2004) aveva dimostrato di migliorare le funzioni cognitive. Per asini funzioni cognitive abbiamo utilizzato una versione modificata del 5 choice serial reaction time task (5-csrtt), un test per roditori progettato come analogo del Continuous Performance Test (cpt) utilizzato per testare quantitativamente il controllo dell'attenzione negli esseri umani (Amitai & Markou , 2011). Le modifiche sono destinate a ridurre il tempo necessario per addestrare gli animali, ridurre manipolazioni stressanti come restrizione alimentare o allevamento isolato. Inoltre, diverse nuove manipolazioni sono state implementate per studiare varie specifiche funzioni cognitive quali l'attenzione, broad monitoring / compulsività, risposta disinibizione / impulsività, distraibilità e velocità di elaborazione.
Siamo stati in grado di dimostrare che la somministrazione intranasale di CRF (6-33) in grado di produrre effetti comportamentali selettivi nei topi. In particolare, la somministrazione acuta è stata in grado di migliorare la precisione delle risposte e ridurre l'impulsività, mentre le amministrazioni croniche hanno prodotto un ritardo nelle risposte corrette. Gli studi di espressione genica con real time PCR stanno iniziando a suggerire che il CRF (6-33) è in grado di raggiungere il cervello, poiché l’espressione di molecole come CRFR1 e CRFbp sono state modificate in seguito intranasale CRF (6-33) in diverse e specifiche aree cerebrali (cioè Hippocampus e corteccia prefrontale).
Test dose-risposta successivi hanno confermato la possibilità di evocare effetti comportamentali con una dose molto più bassa di CRF (6-33). Inoltre, abbiamo scoperto un effetto di rimbalzo nel comportamento impulsivo il giorno dopo la somministrazione di dosi più elevate .. Questo effetto negativo è stato assente con le dosi più basse che ancora sono in grado di ridurre in modo significativo il comportamento impulsivo.
Infine abbiamo testato la capacità di CRF (6-33) di migliorare un fenotipo impulsivo in un modello genetico del topo modificato della schizofrenia. Il modello scelto è stato un doppio mutante per Dysbindin e per la D2 recettore. Il recettore D2 che aveva dimostrato in prova precedente per avere una maggiore comportamento impulsivo.
Il gene recettore D2 della dopamina (D2) è un altro importante gene rischi identificati per la schizofrenia. Varianti genetiche funzionali nel gene D2 sono stati trovati per essere espressi in modo diverso nei pazienti con schizofrenia (Kaalund et al., 2013) e possono modulare fenotipi correlato alla schizofrenia modificando il rapporto tra la breve isoforma (D2S) alla lunga isoforma (D2L ) (Bertolino et al., 2009). Mutante Heterozigote per D2L ha una maggiore rapporto D2S (recettore D2 forma breve) / D2L (recettore forma estesa D2).
Dai dati preliminari CRF (6-33) non è stato in grado di incidere in modo significativo il comportamento impulsivo in Dys doppi eterozigoti +/- D2L +/-. È interessante notare che, in Dys singoli eterozigote +/- è stata osservata una tendenza di aumento impulsività il CRF (6-33) del gruppo suggerisce una interazione dannoso con Dys genotipo carente.
Da questi studi si può concludere che sia OXT di CRF (6-33) hanno il potenziale per essere utilizzato per il trattamento, rispettivamente, di deficit sociali e impulsività. Per OXT finora abbiamo osservato una interazione positiva con il genotipo deficitario per Dys, che ha bisogno di essere confermata in altri modelli murini di schizofrenia rilevanti di deficit sociali. CRF (6-33) finora ha dimostrato solo per migliorare le prestazioni sociali in topi WT. Lo studio preliminare sul mouse mutato, se confermato, sembra suggerire che potrebbe peggiorare il fenotipo in presenza di alcune mutazioni genetiche. E’ importante quindi definire meccanismi di interazione di CRF (6-33) con la genetica per definire quando potrebbe essere utilizzato positivamente per la terapia e quando non dovrebbe in una visione di un regime terapeutico per la schizofrenia personalizzato e direzionato da test genetici.

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Tipo di EPrint:Tesi di dottorato
Relatore:Giusti, Pietro
Correlatore:Papaleo, Francesco
Dottorato (corsi e scuole):Ciclo 28 > Scuole 28 > SCIENZE FARMACOLOGICHE > FARMACOLOGIA MOLECOLARE E CELLULARE
Data di deposito della tesi:01 Febbraio 2016
Anno di Pubblicazione:01 Febbraio 2016
Parole chiave (italiano / inglese):CRF(6-33), CRF, Oxytocin, schizophrenia, SDY, Disbindin
Settori scientifico-disciplinari MIUR:Area 05 - Scienze biologiche > BIO/14 Farmacologia
Struttura di riferimento:Dipartimenti > Dipartimento di Scienze del Farmaco
Codice ID:9552
Depositato il:07 Ott 2016 09:59
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Le url contenute in alcuni riferimenti sono raggiungibili cliccando sul link alla fine della citazione (Vai!) e tramite Google (Ricerca con Google). Il risultato dipende dalla formattazione della citazione.

Allen, N. C., Bagade, S., McQueen, M. B., Ioannidis, J. P. A., Kavvoura, F. K., Khoury, M. J., … Bertram, L. (2008). Systematic meta-analyses and field synopsis of genetic association studies in schizophrenia: the SzGene database. Nature Genetics, 40(7), 827–34. doi:10.1038/ng.171 Cerca con Google

Amitai, N., & Markou, A. (2009). Increased impulsivity and disrupted attention induced by repeated phencyclidine are not attenuated by chronic quetiapine treatment. Pharmacology, Biochemistry, and Behavior, 93(3), 248–57. doi:10.1016/j.pbb.2008.08.025 Cerca con Google

Amitai, N., & Markou, A. (2011). Comparative effects of different test day challenges on performance in the 5-choice serial reaction time task. Behavioral Neuroscience, 125(5), 764–74. doi:10.1037/a0024722 Cerca con Google

Amitai, N., Semenova, S., & Markou, A. (2007). Cognitive-disruptive effects of the psychotomimetic phencyclidine and attenuation by atypical antipsychotic medications in rats. Psychopharmacology, 193(4), 521–37. doi:10.1007/s00213-007-0808-x Cerca con Google

Anagnostou, E., Soorya, L., Chaplin, W., Bartz, J., Halpern, D., Wasserman, S., … Hollander, E. (2012). Intranasal oxytocin versus placebo in the treatment of adults with autism spectrum disorders: a randomized controlled trial. Molecular Autism, 3(1), 16. doi:10.1186/2040-2392-3-16 Cerca con Google

Andari, E., Duhamel, J.-R., Zalla, T., Herbrecht, E., Leboyer, M., & Sirigu, A. (2010). Promoting social behavior with oxytocin in high-functioning autism spectrum disorders. Proceedings of the National Academy of Sciences of the United States of America, 107(9), 4389–94. doi:10.1073/pnas.0910249107 Cerca con Google

Arborelius, L., Owens, M. J., Plotsky, P. M., & Nemeroff, C. B. (1999). The role of corticotropin-releasing factor in depression and anxiety disorders. The Journal of Endocrinology, 160(1), 1–12. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9854171 Vai! Cerca con Google

Arguello, P. A., & Gogos, J. A. (2006). Modeling madness in mice: one piece at a time. Neuron, 52(1), 179–96. doi:10.1016/j.neuron.2006.09.023 Cerca con Google

Ayalew, M., Le-Niculescu, H., Levey, D. F., Jain, N., Changala, B., Patel, S. D., … Niculescu, A. B. (2012). Convergent functional genomics of schizophrenia: from comprehensive understanding to genetic risk prediction. Molecular Psychiatry, 17(9), 887–905. doi:10.1038/mp.2012.37 Cerca con Google

Baker, H., & Spencer, R. F. (1986). Transneuronal transport of peroxidase-conjugated wheat germ agglutinin (WGA-HRP) from the olfactory epithelium to the brain of the adult rat. Experimental Brain Research, 63(3), 461–73. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3758265 Vai! Cerca con Google

Balducci, C., Nurra, M., Pietropoli, A., Samanin, R., & Carli, M. (2003). Reversal of visual attention dysfunction after AMPA lesions of the nucleus basalis magnocellularis (NBM) by the cholinesterase inhibitor donepezil and by a 5-HT1A receptor antagonist WAY 100635. Psychopharmacology, 167(1), 28–36. doi:10.1007/s00213-002-1385-7 Cerca con Google

Bales, K. L., Perkeybile, A. M., Conley, O. G., Lee, M. H., Guoynes, C. D., Downing, G. M., … Mendoza, S. P. (2013). Chronic Intranasal Oxytocin Causes Long-Term Impairments in Partner Preference Formation in Male Prairie Voles. Biological Psychiatry, 74(3), 180–188. doi:10.1016/j.biopsych.2012.08.025 Cerca con Google

Bales, K. L., Solomon, M., Jacob, S., Crawley, J. N., Silverman, J. L., Larke, R. H., … Mendoza, S. P. (2014). Long-term exposure to intranasal oxytocin in a mouse autism model. Translational Psychiatry, 4(11), e480. doi:10.1038/tp.2014.117 Cerca con Google

Barbelivien, A., Ruotsalainen, S., & Sirviö, J. (2001). Metabolic alterations in the prefrontal and cingulate cortices are related to behavioral deficits in a rodent model of attention-deficit hyperactivity disorder. Cerebral Cortex (New York, N.Y. : 1991), 11(11), 1056–63. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11590115 Vai! Cerca con Google

Bedse, G., Di Domenico, F., Serviddio, G., & Cassano, T. (2015). Aberrant insulin signaling in Alzheimer’s disease: current knowledge. Frontiers in Neuroscience, 9, 204. doi:10.3389/fnins.2015.00204 Cerca con Google

Behan, D. P., Heinrichs, S. C., Troncoso, J. C., Liu, X. J., Kawas, C. H., Ling, N., & De Souza, E. B. (1995). Displacement of corticotropin releasing factor from its binding protein as a possible treatment for Alzheimer’s disease. Nature, 378(6554), 284–7. doi:10.1038/378284a0 Cerca con Google

Bertolino, A., Fazio, L., Caforio, G., Blasi, G., Rampino, A., Romano, R., … Sadee, W. (2009). Functional variants of the dopamine receptor D2 gene modulate prefronto-striatal phenotypes in schizophrenia. Brain : A Journal of Neurology, 132(Pt 2), 417–25. doi:10.1093/brain/awn248 Cerca con Google

Bielsky, I. F., & Young, L. J. (2004). Oxytocin, vasopressin, and social recognition in mammals. Peptides, 25(9), 1565–74. doi:10.1016/j.peptides.2004.05.019 Cerca con Google

Bissette, G., Reynolds, G. P., Kilts, C. D., Widerlöv, E., & Nemeroff, C. B. (1985). Corticotropin-releasing factor-like immunoreactivity in senile dementia of the Alzheimer type. Reduced cortical and striatal concentrations. JAMA, 254(21), 3067–9. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3877182 Vai! Cerca con Google

Born, J., Lange, T., Kern, W., McGregor, G. P., Bickel, U., & Fehm, H. L. (2002). Sniffing neuropeptides: a transnasal approach to the human brain. Nature Neuroscience, 5(6), 514–6. doi:10.1038/nn849 Cerca con Google

Bukovskaya, O., & Shmukler, A. (2015). Oxytocin and Social Cognitions in Schizophrenia: A Systematic Review. The Psychiatric Quarterly. doi:10.1007/s11126-015-9407-x Cerca con Google

Burdick, K. E., Goldberg, T. E., Funke, B., Bates, J. A., Lencz, T., Kucherlapati, R., & Malhotra, A. K. (2007). DTNBP1 genotype influences cognitive decline in schizophrenia. Schizophrenia Research, 89(1-3), 169–72. doi:10.1016/j.schres.2006.09.008 Cerca con Google

Burdick, K. E., Lencz, T., Funke, B., Finn, C. T., Szeszko, P. R., Kane, J. M., … Malhotra, A. K. (2006). Genetic variation in DTNBP1 influences general cognitive ability. Human Molecular Genetics, 15(10), 1563–8. doi:10.1093/hmg/ddi481 Cerca con Google

Burmeister, M. (1999). Basic concepts in the study of diseases with complex genetics. Biological Psychiatry, 45(5), 522–32. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10088042 Vai! Cerca con Google

Burmeister, M., McInnis, M. G., & Zöllner, S. (2008). Psychiatric genetics: progress amid controversy. Nature Reviews. Genetics, 9(7), 527–40. doi:10.1038/nrg2381 Cerca con Google

Carli, M., Calcagno, E., Mainini, E., Arnt, J., & Invernizzi, R. W. (2011). Sertindole restores attentional performance and suppresses glutamate release induced by the NMDA receptor antagonist CPP. Psychopharmacology, 214(3), 625–37. doi:10.1007/s00213-010-2066-6 Cerca con Google

Carli, M., Calcagno, E., Mainolfi, P., Mainini, E., & Invernizzi, R. W. (2011). Effects of aripiprazole, olanzapine, and haloperidol in a model of cognitive deficit of schizophrenia in rats: relationship with glutamate release in the medial prefrontal cortex. Psychopharmacology, 214(3), 639–52. doi:10.1007/s00213-010-2065-7 Cerca con Google

Charlton, S. T., Whetstone, J., Fayinka, S. T., Read, K. D., Illum, L., & Davis, S. S. (2008). Evaluation of Direct Transport Pathways of Glycine Receptor Antagonists and an Angiotensin Antagonist from the Nasal Cavity to the Central Nervous System in the Rat Model. Pharmaceutical Research, 25(7), 1531–1543. doi:10.1007/s11095-008-9550-2 Cerca con Google

Chen, X.-W., Feng, Y.-Q., Hao, C.-J., Guo, X.-L., He, X., Zhou, Z.-Y., … Zhou, Z. (2008). DTNBP1, a schizophrenia susceptibility gene, affects kinetics of transmitter release. The Journal of Cell Biology, 181(5), 791–801. doi:10.1083/jcb.200711021 Cerca con Google

Contarino, a, Heinrichs, S. C., & Gold, L. H. (1999). Understanding corticotropin releasing factor neurobiology: contributions from mutant mice. Neuropeptides, 33(1), 1–12. doi:10.1054/npep.1999.0001 Cerca con Google

Cornblatt, B. A., Risch, N. J., Faris, G., Friedman, D., & Erlenmeyer-Kimling, L. (1988). The continuous performance test, identical pairs version (CPT-IP): I. new findings about sustained attention in normal families. Psychiatry Research, 26(2), 223–238. doi:10.1016/0165-1781(88)90076-5 Cerca con Google

Cox, M. M., Tucker, A. M., Tang, J., Talbot, K., Richer, D. C., Yeh, L., & Arnold, S. E. (2009). Neurobehavioral abnormalities in the dysbindin-1 mutant, sandy, on a C57BL/6J genetic background. Genes, Brain, and Behavior, 8(4), 390–7. doi:10.1111/j.1601-183X.2009.00477.x Cerca con Google

D’Este, L., Casini, A., Puglisi-Allegra, S., Cabib, S., & Renda, T. G. (2007). Comparative immunohistochemical study of the dopaminergic systems in two inbred mouse strains (C57BL/6J and DBA/2J). Journal of Chemical Neuroanatomy, 33(2), 67–74. doi:10.1016/j.jchemneu.2006.12.005 Cerca con Google

Davies, W., Humby, T., Kong, W., Otter, T., Burgoyne, P. S., & Wilkinson, L. S. (2009). Converging Pharmacological and Genetic Evidence Indicates a Role for Steroid Sulfatase in Attention. Biological Psychiatry, 66(4), 360–367. doi:10.1016/j.biopsych.2009.01.001 Cerca con Google

Davis, M. C., Lee, J., Horan, W. P., Clarke, A. D., McGee, M. R., Green, M. F., & Marder, S. R. (2013). Effects of single dose intranasal oxytocin on social cognition in schizophrenia. Schizophrenia Research, 147(2-3), 393–7. doi:10.1016/j.schres.2013.04.023 Cerca con Google

de Bruin, N. M. W. J., Fransen, F., Duytschaever, H., Grantham, C., & Megens, A. A. H. P. (2006). Attentional performance of (C57BL/6Jx129Sv)F2 mice in the five-choice serial reaction time task. Physiology & Behavior, 89(5), 692–703. doi:10.1016/j.physbeh.2006.08.009 Cerca con Google

De Souza, E. B., Whitehouse, P. J., Kuhar, M. J., Price, D. L., & Vale, W. W. (1986). Reciprocal changes in corticotropin-releasing factor (CRF)-like immunoreactivity and CRF receptors in cerebral cortex of Alzheimer’s disease. Nature, 319(6054), 593–595. doi:10.1038/319593a0 Cerca con Google

DeRosse, P., Funke, B., Burdick, K. E., Lencz, T., Ekholm, J. M., Kane, J. M., … Malhotra, A. K. (2006). Dysbindin genotype and negative symptoms in schizophrenia. The American Journal of Psychiatry, 163(3), 532–4. doi:10.1176/appi.ajp.163.3.532 Cerca con Google

Dhuria, S. V., Hanson, L. R., & Frey, W. H. (2010). Intranasal delivery to the central nervous system: mechanisms and experimental considerations. Journal of Pharmaceutical Sciences, 99(4), 1654–73. doi:10.1002/jps.21924 Cerca con Google

Dickman, D. K., & Davis, G. W. (2009). The schizophrenia susceptibility gene dysbindin controls synaptic homeostasis. Science (New York, N.Y.), 326(5956), 1127–30. doi:10.1126/science.1179685 Cerca con Google

Eckart, K., Radulovic, J., Radulovic, M., Jahn, O., Blank, T., Stiedl, O., & Spiess, J. (1999). Actions of CRF and its analogs. Current Medicinal Chemistry, 6(11), 1035–53. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10519912 Vai! Cerca con Google

Elands, J., Barberis, C., Jard, S., Tribollet, E., Dreifuss, J. J., Bankowski, K., … Sawyer, W. H. (1988). 125I-labelled d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT: a selective oxytocin receptor ligand. European Journal of Pharmacology, 147(2), 197–207. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2835249 Vai! Cerca con Google

Erbaş, O., Çınar, B. P., Solmaz, V., Çavuşoğlu, T., & Ateş, U. (2015). The neuroprotective effect of erythropoietin on experimental Parkinson model in rats. Neuropeptides, 49, 1–5. doi:10.1016/j.npep.2014.10.003 Cerca con Google

Evans, S. L., Dal Monte, O., Noble, P., & Averbeck, B. B. (2014). Intranasal oxytocin effects on social cognition: A critique. Brain Research, 1580, 69–77. doi:10.1016/j.brainres.2013.11.008 Cerca con Google

Fallgatter, A. J., Herrmann, M. J., Hohoff, C., Ehlis, A.-C., Jarczok, T. A., Freitag, C. M., & Deckert, J. (2006). DTNBP1 (dysbindin) gene variants modulate prefrontal brain function in healthy individuals. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 31(9), 2002–10. doi:10.1038/sj.npp.1301003 Cerca con Google

Fanous, A. H., van den Oord, E. J., Riley, B. P., Aggen, S. H., Neale, M. C., O’Neill, F. A., … Kendler, K. S. (2005). Relationship between a high-risk haplotype in the DTNBP1 (dysbindin) gene and clinical features of schizophrenia. The American Journal of Psychiatry, 162(10), 1824–32. doi:10.1176/appi.ajp.162.10.1824 Cerca con Google

Feifel, D., Macdonald, K., Cobb, P., & Minassian, A. (2012). Adjunctive intranasal oxytocin improves verbal memory in people with schizophrenia. Schizophrenia Research, 139(1-3), 207–10. doi:10.1016/j.schres.2012.05.018 Cerca con Google

Feifel, D., Macdonald, K., Nguyen, A., Cobb, P., Warlan, H., Galangue, B., … Hadley, A. (2010). Adjunctive intranasal oxytocin reduces symptoms in schizophrenia patients. Biological Psychiatry, 68(7), 678–80. doi:10.1016/j.biopsych.2010.04.039 Cerca con Google

Feng, Y.-Q., Zhou, Z.-Y., He, X., Wang, H., Guo, X.-L., Hao, C.-J., … Li, W. (2008). Dysbindin deficiency in sandy mice causes reduction of snapin and displays behaviors related to schizophrenia. Schizophrenia Research, 106(2-3), 218–28. doi:10.1016/j.schres.2008.07.018 Cerca con Google

Ferguson, J. N., Young, L. J., Hearn, E. F., Matzuk, M. M., Insel, T. R., & Winslow, J. T. (2000). Social amnesia in mice lacking the oxytocin gene. Nature Genetics, 25(3), 284–8. doi:10.1038/77040 Cerca con Google

Ghiani, C. A., Starcevic, M., Rodriguez-Fernandez, I. A., Nazarian, R., Cheli, V. T., Chan, L. N., … Dell’Angelica, E. C. (2010). The dysbindin-containing complex (BLOC-1) in brain: developmental regulation, interaction with SNARE proteins and role in neurite outgrowth. Molecular Psychiatry, 15(2), 115, 204–15. doi:10.1038/mp.2009.58 Cerca con Google

Giancardo, L., Sona, D., Huang, H., Sannino, S., Managò, F., Scheggia, D., … Murino, V. (2013). Automatic Visual Tracking and Social Behaviour Analysis with Multiple Mice. PLoS ONE, 8(9), e74557. doi:10.1371/journal.pone.0074557 Cerca con Google

Gigliucci, V., Leonzino, M., Busnelli, M., Luchetti, A., Palladino, V. S., D’Amato, F. R., & Chini, B. (2014). Region specific up-regulation of oxytocin receptors in the opioid oprm1 (-/-) mouse model of autism. Frontiers in Pediatrics, 2, 91. doi:10.3389/fped.2014.00091 Cerca con Google

Gobira, P. H., Ropke, J., Aguiar, D. C., Crippa, J. A. S., & Moreira, F. A. (2013). Animal models for predicting the efficacy and side effects of antipsychotic drugs. Revista Brasileira de Psiquiatria (São Paulo, Brazil : 1999), 35 Suppl 2, S132–9. doi:10.1590/1516-4446-2013-1164 Cerca con Google

Gold, J. M., & Thaker, G. K. (2002). Current progress in schizophrenia research: cognitive phenotypes of schizophrenia: attention. The Journal of Nervous and Mental Disease, 190(9), 638–9. doi:10.1097/01.NMD.0000030569.71581.A9 Cerca con Google

Green, J. J., & Hollander, E. (2010). Autism and oxytocin: New developments in translational approaches to therapeutics. Neurotherapeutics, 7(3), 250–257. doi:10.1016/j.nurt.2010.05.006 Cerca con Google

Guastella, A. J., Einfeld, S. L., Gray, K. M., Rinehart, N. J., Tonge, B. J., Lambert, T. J., & Hickie, I. B. (2010). Intranasal Oxytocin Improves Emotion Recognition for Youth with Autism Spectrum Disorders. Biological Psychiatry, 67(7), 692–694. doi:10.1016/j.biopsych.2009.09.020 Cerca con Google

Guastella, A. J., Mitchell, P. B., & Dadds, M. R. (2008). Oxytocin increases gaze to the eye region of human faces. Biological Psychiatry, 63(1), 3–5. doi:10.1016/j.biopsych.2007.06.026 Cerca con Google

Hahn, B., Robinson, B. M., Harvey, A. N., Kaiser, S. T., Leonard, C. J., Luck, S. J., & Gold, J. M. (2012). Visuospatial attention in schizophrenia: deficits in broad monitoring. Journal of Abnormal Psychology, 121(1), 119–28. doi:10.1037/a0023938 Cerca con Google

Hahn, B., Ross, T. J., & Stein, E. A. (2006). Neuroanatomical dissociation between bottom-up and top-down processes of visuospatial selective attention. NeuroImage, 32(2), 842–53. doi:10.1016/j.neuroimage.2006.04.177 Cerca con Google

Harrison, P. J., Pritchett, D., Stumpenhorst, K., Betts, J. F., Nissen, W., Schweimer, J., … Tunbridge, E. M. (2012). Genetic mouse models relevant to schizophrenia: taking stock and looking forward. Neuropharmacology, 62(3), 1164–7. doi:10.1016/j.neuropharm.2011.08.009 Cerca con Google

Harvey, P. D., & Bowie, C. R. (2003). Cognitive deficits in schizophrenia: early course and treatment. Clinical Neuroscience Research, 3(1-2), 17–22. doi:10.1016/S1566-2772(03)00015-X Cerca con Google

Hashimoto, R., Noguchi, H., Hori, H., Nakabayashi, T., Suzuki, T., Iwata, N., … Kunugi, H. (2010). A genetic variation in the dysbindin gene (DTNBP1) is associated with memory performance in healthy controls. The World Journal of Biological Psychiatry : The Official Journal of the World Federation of Societies of Biological Psychiatry, 11(2 Pt 2), 431–8. doi:10.1080/15622970902736503 Cerca con Google

Hashimoto, R., Noguchi, H., Hori, H., Ohi, K., Yasuda, Y., Takeda, M., & Kunugi, H. (2009). Association between the dysbindin gene (DTNBP1) and cognitive functions in Japanese subjects. Psychiatry and Clinical Neurosciences, 63(4), 550–6. doi:10.1111/j.1440-1819.2009.01985.x Cerca con Google

Hattori, S., Murotani, T., Matsuzaki, S., Ishizuka, T., Kumamoto, N., Takeda, M., … Hashimoto, R. (2008). Behavioral abnormalities and dopamine reductions in sdy mutant mice with a deletion in Dtnbp1, a susceptibility gene for schizophrenia. Biochemical and Biophysical Research Communications, 373(2), 298–302. doi:10.1016/j.bbrc.2008.06.016 Cerca con Google

Heaton, R. K., Gladsjo, J. A., Palmer, B. W., Kuck, J., Marcotte, T. D., & Jeste, D. V. (2001). Stability and course of neuropsychological deficits in schizophrenia. Archives of General Psychiatry, 58(1), 24–32. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11146755 Vai! Cerca con Google

Heinrichs, S. C. (2003). Modulation of social learning in rats by brain corticotropin-releasing factor. Brain Research, 994(1), 107–14. doi:10.1016/j.brainres.2003.09.028 Cerca con Google

Heinrichs, S. C., & Joppa, M. (2001). Dissociation of arousal-like from anxiogenic-like actions of brain corticotropin-releasing factor receptor ligands in rats. Behavioural Brain Research, 122(1), 43–50. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11287075 Vai! Cerca con Google

Heinrichs, S. C., Joppa, M., Lapsansky, J., Jeske, K., Nelson, R., & De Souza, E. (2001). Selective stimulatory actions of corticotropin-releasing factor ligands on correlates of energy balance. Physiology & Behavior, 74(1-2), 5–13. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11564446 Vai! Cerca con Google

Heinrichs, S. C., & Koob, G. F. (2004). Corticotropin-releasing factor in brain: a role in activation, arousal, and affect regulation. The Journal of Pharmacology and Experimental Therapeutics, 311(2), 427–40. doi:10.1124/jpet.103.052092 Cerca con Google

Heinrichs, S. C., Vale, E. A., Lapsansky, J., Behan, D. P., McClure, L. V, Ling, N., … Schulteis, G. (1997). Enhancement of performance in multiple learning tasks by corticotropin-releasing factor-binding protein ligand inhibitors. Peptides, 18(5), 711–6. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9213365 Vai! Cerca con Google

Horowitz, L. F., Montmayeur, J.-P., Echelard, Y., & Buck, L. B. (1999). A genetic approach to trace neural circuits. Proceedings of the National Academy of Sciences, 96(6), 3194–3199. doi:10.1073/pnas.96.6.3194 Cerca con Google

Horta de Macedo, L. R., Zuardi, A. W., Machado-de-Sousa, J. P., Chagas, M. H. N., & Hallak, J. E. C. (2014). Oxytocin does not improve performance of patients with schizophrenia and healthy volunteers in a facial emotion matching task. Psychiatry Research, 220(1-2), 125–8. doi:10.1016/j.psychres.2014.07.082 Cerca con Google

Huang, H., Michetti, C., Busnelli, M., Managò, F., Sannino, S., Scheggia, D., … Papaleo, F. (2014). Chronic and acute intranasal oxytocin produce divergent social effects in mice. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 39(5), 1102–14. doi:10.1038/npp.2013.310 Cerca con Google

Iizuka, Y., Sei, Y., Weinberger, D. R., & Straub, R. E. (2007). Evidence that the BLOC-1 protein dysbindin modulates dopamine D2 receptor internalization and signaling but not D1 internalization. The Journal of Neuroscience : The Official Journal of the Society for Neuroscience, 27(45), 12390–5. doi:10.1523/JNEUROSCI.1689-07.2007 Cerca con Google

Illum, L. (2004). Is nose-to-brain transport of drugs in man a reality? Journal of Pharmacy and Pharmacology, 56(1), 3–17. doi:10.1211/0022357022539 Cerca con Google

Ilott, N. E., Schneider, T., Mill, J., Schalkwyk, L., Brolese, G., Bizarro, L., … Asherson, P. (2014). Long-Term Effects of Gestational Nicotine Exposure and Food-Restriction on Gene Expression in the Striatum of Adolescent Rats. PLoS ONE, 9(2), e88896. doi:10.1371/journal.pone.0088896 Cerca con Google

Insel, T. R. (2010). Rethinking schizophrenia. Nature, 468(7321), 187–93. doi:10.1038/nature09552 Cerca con Google

Jahn, O., Radulovic, J., Stiedl, O., Tezval, H., Eckart, K., & Spiess, J. (2005). Corticotropin-releasing factor binding protein--a ligand trap? Mini Reviews in Medicinal Chemistry, 5(10), 953–60. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/16250837 Vai! Cerca con Google

Jentsch, J. D., Trantham-Davidson, H., Jairl, C., Tinsley, M., Cannon, T. D., & Lavin, A. (2009). Dysbindin modulates prefrontal cortical glutamatergic circuits and working memory function in mice. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 34(12), 2601–8. doi:10.1038/npp.2009.90 Cerca con Google

Ji, Y., Yang, F., Papaleo, F., Wang, H.-X., Gao, W.-J., Weinberger, D. R., & Lu, B. (2009). Role of dysbindin in dopamine receptor trafficking and cortical GABA function. Proceedings of the National Academy of Sciences of the United States of America, 106(46), 19593–8. doi:10.1073/pnas.0904289106 Cerca con Google

Jin, D., Liu, H.-X., Hirai, H., Torashima, T., Nagai, T., Lopatina, O., … Higashida, H. (2007). CD38 is critical for social behaviour by regulating oxytocin secretion. Nature, 446(7131), 41–45. doi:10.1038/nature05526 Cerca con Google

Kaalund, S. S., Newburn, E. N., Ye, T., Tao, R., Li, C., Deep-Soboslay, a, … Kleinman, J. E. (2013). Contrasting changes in DRD1 and DRD2 splice variant expression in schizophrenia and affective disorders, and associations with SNPs in postmortem brain. Molecular Psychiatry, (October), 1–9. doi:10.1038/mp.2013.165 Cerca con Google

Kane, J. M., & Correll, C. U. (2010). Pharmacologic treatment of schizophrenia. Dialogues in Clinical Neuroscience, 12(3), 345–57. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/20954430 Vai! Cerca con Google

Karlsgodt, K. H., Robleto, K., Trantham-Davidson, H., Jairl, C., Cannon, T. D., Lavin, A., & Jentsch, J. D. (2011). Reduced dysbindin expression mediates N-methyl-D-aspartate receptor hypofunction and impaired working memory performance. Biological Psychiatry, 69(1), 28–34. doi:10.1016/j.biopsych.2010.09.012 Cerca con Google

Kasper, S., & Resinger, E. (2003). Cognitive effects and antipsychotic treatment. Psychoneuroendocrinology, 28, 27–38. doi:10.1016/S0306-4530(02)00115-4 Cerca con Google

Keefe, R. S. E., Bilder, R. M., Davis, S. M., Harvey, P. D., Palmer, B. W., Gold, J. M., … Neurocognitive Working Group. (2007). Neurocognitive effects of antipsychotic medications in patients with chronic schizophrenia in the CATIE Trial. Archives of General Psychiatry, 64(6), 633–47. doi:10.1001/archpsyc.64.6.633 Cerca con Google

Kirby, B. P., Waddington, J. L., & O’Tuathaigh, C. M. P. (2010). Advancing a functional genomics for schizophrenia: psychopathological and cognitive phenotypes in mutants with gene disruption. Brain Research Bulletin, 83(3-4), 162–76. doi:10.1016/j.brainresbull.2009.09.010 Cerca con Google

Koob, G. F., & Bloom, F. E. (1985). Corticotropin-releasing factor and behavior. Federation Proceedings, 44(1 Pt 2), 259–63. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3871412 Vai! Cerca con Google

Kumamoto, N., Matsuzaki, S., Inoue, K., Hattori, T., Shimizu, S., Hashimoto, R., … Tohyama, M. (2006). Hyperactivation of midbrain dopaminergic system in schizophrenia could be attributed to the down-regulation of dysbindin. Biochemical and Biophysical Research Communications, 345(2), 904–9. doi:10.1016/j.bbrc.2006.04.163 Cerca con Google

Kvajo, M., McKellar, H., & Gogos, J. A. (2012). Avoiding mouse traps in schizophrenia genetics: lessons and promises from current and emerging mouse models. Neuroscience, 211, 136–64. doi:10.1016/j.neuroscience.2011.07.051 Cerca con Google

Le Pen, G., Grottick, A. J., Higgins, G. A., & Moreau, J.-L. (2003). Phencyclidine exacerbates attentional deficits in a neurodevelopmental rat model of schizophrenia. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, 28(10), 1799–809. doi:10.1038/sj.npp.1300208 Cerca con Google

Lee, E. H., Lee, C. P., Wang, H. I., & Lin, W. R. (1993). Hippocampal CRF, NE, and NMDA system interactions in memory processing in the rat. Synapse (New York, N.Y.), 14(2), 144–53. doi:10.1002/syn.890140207 Cerca con Google

Lee, E. H., & Sung, Y. J. (1989). Differential influences of corticotropin-releasing factor on memory retention of aversive learning and appetitive learning in rats. Behavioral and Neural Biology, 52(3), 285–94. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2556103 Vai! Cerca con Google

Lehmann, O., Grottick, A. J., Cassel, J.-C., & Higgins, G. A. (2003). A double dissociation between serial reaction time and radial maze performance in rats subjected to 192 IgG-saporin lesions of the nucleus basalis and/or the septal region. The European Journal of Neuroscience, 18(3), 651–66. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12911761 Vai! Cerca con Google

Lewis, D. A., & Gonzalez-Burgos, G. (2006). Pathophysiologically based treatment interventions in schizophrenia. Nature Medicine, 12(9), 1016–22. doi:10.1038/nm1478 Cerca con Google

Lim, M. M., Bielsky, I. F., & Young, L. J. (2005). Neuropeptides and the social brain: potential rodent models of autism. International Journal of Developmental Neuroscience, 23(2-3), 235–243. doi:10.1016/j.ijdevneu.2004.05.006 Cerca con Google

Love, T. M. (2014). Oxytocin, motivation and the role of dopamine. Pharmacology, Biochemistry, and Behavior, 119, 49–60. doi:10.1016/j.pbb.2013.06.011 Cerca con Google

Luciano, M., Miyajima, F., Lind, P. A., Bates, T. C., Horan, M., Harris, S. E., … Payton, A. (2009). Variation in the dysbindin gene and normal cognitive function in three independent population samples. Genes, Brain, and Behavior, 8(2), 218–27. doi:10.1111/j.1601-183X.2008.00462.x Cerca con Google

Ludwig, M., Tobin, V. A., Callahan, M. F., Papadaki, E., Becker, A., Engelmann, M., & Leng, G. (2013). Intranasal application of vasopressin fails to elicit changes in brain immediate early gene expression, neural activity and behavioural performance of rats. Journal of Neuroendocrinology, 25(7), 655–67. doi:10.1111/jne.12046 Cerca con Google

MacDonald, E., Dadds, M. R., Brennan, J. L., Williams, K., Levy, F., & Cauchi, A. J. (2011). A review of safety, side-effects and subjective reactions to intranasal oxytocin in human research. Psychoneuroendocrinology, 36(8), 1114–26. doi:10.1016/j.psyneuen.2011.02.015 Cerca con Google

Markov, V., Krug, A., Krach, S., Jansen, A., Eggermann, T., Zerres, K., … Kircher, T. (2010). Impact of schizophrenia-risk gene dysbindin 1 on brain activation in bilateral middle frontal gyrus during a working memory task in healthy individuals. Human Brain Mapping, 31(2), 266–75. doi:10.1002/hbm.20862 Cerca con Google

Markov, V., Krug, A., Krach, S., Whitney, C., Eggermann, T., Zerres, K., … Kircher, T. (2009). Genetic variation in schizophrenia-risk-gene dysbindin 1 modulates brain activation in anterior cingulate cortex and right temporal gyrus during language production in healthy individuals. NeuroImage, 47(4), 2016–2022. doi:10.1016/j.neuroimage.2009.05.067 Cerca con Google

Meyer-Lindenberg, A., Domes, G., Kirsch, P., & Heinrichs, M. (2011). Oxytocin and vasopressin in the human brain: social neuropeptides for translational medicine. Nature Reviews Neuroscience, 12(9), 524–538. doi:10.1038/nrn3044 Cerca con Google

Mitchell, A. J. (1998). The role of corticotropin releasing factor in depressive illness: a critical review. Neuroscience and Biobehavioral Reviews, 22(5), 635–51. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9662725 Vai! Cerca con Google

Mueser, K. T., & McGurk, S. R. (2004). Schizophrenia. Lancet (London, England), 363(9426), 2063–72. doi:10.1016/S0140-6736(04)16458-1 Cerca con Google

Murphy, E. R., Dalley, J. W., & Robbins, T. W. (2005). Local glutamate receptor antagonism in the rat prefrontal cortex disrupts response inhibition in a visuospatial attentional task. Psychopharmacology, 179(1), 99–107. doi:10.1007/s00213-004-2068-3 Cerca con Google

Navarra, R., Graf, R., Huang, Y., Logue, S., Comery, T., Hughes, Z., & Day, M. (2008). Effects of atomoxetine and methylphenidate on attention and impulsivity in the 5-choice serial reaction time test. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 32(1), 34–41. doi:10.1016/j.pnpbp.2007.06.017 Cerca con Google

Neill, J. C., Barnes, S., Cook, S., Grayson, B., Idris, N. F., McLean, S. L., … Harte, M. K. (2010). Animal models of cognitive dysfunction and negative symptoms of schizophrenia: focus on NMDA receptor antagonism. Pharmacology & Therapeutics, 128(3), 419–32. doi:10.1016/j.pharmthera.2010.07.004 Cerca con Google

Nestler, E. J., & Hyman, S. E. (2010a). Animal models of neuropsychiatric disorders. Nature Neuroscience, 13(10), 1161–9. doi:10.1038/nn.2647 Cerca con Google

Nestler, E. J., & Hyman, S. E. (2010b). Animal models of neuropsychiatric disorders. Nature Neuroscience, 13(10), 1161–9. doi:10.1038/nn.2647 Cerca con Google

Neumann, I. D., Maloumby, R., Beiderbeck, D. I., Lukas, M., & Landgraf, R. (2013). Increased brain and plasma oxytocin after nasal and peripheral administration in rats and mice. Psychoneuroendocrinology, 38(10), 1985–93. doi:10.1016/j.psyneuen.2013.03.003 Cerca con Google

Nguyen, P. V. (2000). Strain-dependent Differences in LTP and Hippocampus-dependent Memory in Inbred Mice. Learning & Memory, 7(3), 170–179. doi:10.1101/lm.7.3.170 Cerca con Google

Nielsen, R. E. (2011). Cognition in schizophrenia – a systematic review. Drug Discovery Today: Therapeutic Strategies, 8(1-2), 43–48. doi:10.1016/j.ddstr.2011.09.004 Cerca con Google

Nishimura, K., Murayama, S., & Takahashi, J. (2015). Identification of Neurexophilin 3 as a Novel Supportive Factor for Survival of Induced Pluripotent Stem Cell-Derived Dopaminergic Progenitors. Stem Cells Translational Medicine, 4(8), 932–44. doi:10.5966/sctm.2014-0197 Cerca con Google

Nithianantharajah, J., Komiyama, N. H., McKechanie, A., Johnstone, M., Blackwood, D. H., Clair, D. S., … Grant, S. G. N. (2012). Synaptic scaffold evolution generated components of vertebrate cognitive complexity. Nature Neuroscience, 16(1), 16–24. doi:10.1038/nn.3276 Cerca con Google

Nuechterlein, K. H., & Dawson, M. E. (1984). Information processing and attentional functioning in the developmental course of schizophrenic disorders. Schizophrenia Bulletin, 10(2), 160–203. doi:10.1093/schbul/10.2.160 Cerca con Google

Nuechterlein, K. H., & Dawson, M. E. (1984). Information processing and attentional functioning in the developmental course of schizophrenic disorders. Schizophrenia Bulletin, 10(2), 160–203. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/6729409 Vai! Cerca con Google

Nuechterlein, K. H., Green, M. F., Kern, R. S., Baade, L. E., Barch, D. M., Cohen, J. D., … Marder, S. R. (2008). The MATRICS Consensus Cognitive Battery, part 1: test selection, reliability, and validity. The American Journal of Psychiatry, 165(2), 203–13. doi:10.1176/appi.ajp.2007.07010042 Cerca con Google

Numakawa, T., Yagasaki, Y., Ishimoto, T., Okada, T., Suzuki, T., Iwata, N., … Hashimoto, R. (2004). Evidence of novel neuronal functions of dysbindin, a susceptibility gene for schizophrenia. Human Molecular Genetics, 13(21), 2699–708. doi:10.1093/hmg/ddh280 Cerca con Google

O’Carroll, R. (2000). Cognitive impairment in schizophrenia. Advances in Psychiatric Treatment, 6(3), 161–168. doi:10.1192/apt.6.3.161 Cerca con Google

O’Connell, G., Lawrie, S. M., McIntosh, A. M., & Hall, J. (2011). Schizophrenia risk genes: Implications for future drug development and discovery. Biochemical Pharmacology, 81(12), 1367–73. doi:10.1016/j.bcp.2010.11.009 Cerca con Google

O’Tuathaigh, C. M. P., Babovic, D., O’Meara, G., Clifford, J. J., Croke, D. T., & Waddington, J. L. (2007). Susceptibility genes for schizophrenia: characterisation of mutant mouse models at the level of phenotypic behaviour. Neuroscience and Biobehavioral Reviews, 31(1), 60–78. doi:10.1016/j.neubiorev.2006.04.002 Cerca con Google

O’Tuathaigh, C. M. P., Desbonnet, L., Moran, P. M., & Waddington, J. L. (2012). Susceptibility genes for schizophrenia: mutant models, endophenotypes and psychobiology. Current Topics in Behavioral Neurosciences, 12, 209–50. doi:10.1007/7854_2011_194 Cerca con Google

Owen, M. J., & O’Donovan, M. C. (2005). Genetics of schizophrenia. Psychiatry, 4(10), 14–17. doi:10.1383/psyt.2005.4.10.14 Cerca con Google

Owen, M. J., Williams, N. M., & O’Donovan, M. C. (2004). The molecular genetics of schizophrenia: new findings promise new insights. Molecular Psychiatry, 9(1), 14–27. doi:10.1038/sj.mp.4001444 Cerca con Google

Paine, T. A., & Carlezon, W. A. (2009). Effects of antipsychotic drugs on MK-801-induced attentional and motivational deficits in rats. Neuropharmacology, 56(4), 788–97. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/19705572 Vai! Cerca con Google

Papaleo, F., Erickson, L., Liu, G., Chen, J., & Weinberger, D. R. (2012). Effects of sex and COMT genotype on environmentally modulated cognitive control in mice. Proceedings of the National Academy of Sciences of the United States of America, 109(49), 20160–5. doi:10.1073/pnas.1214397109 Cerca con Google

Papaleo, F., Lipska, B. K., & Weinberger, D. R. (2012). Mouse models of genetic effects on cognition: relevance to schizophrenia. Neuropharmacology, 62(3), 1204–20. doi:10.1016/j.neuropharm.2011.04.025 Cerca con Google

Papaleo, F., & Weinberger, D. R. (2011). Dysbindin and Schizophrenia: it’s dopamine and glutamate all over again. Biological Psychiatry, 69(1), 2–4. doi:10.1016/j.biopsych.2010.10.028 Cerca con Google

Papaleo, F., Yang, F., Garcia, S., Chen, J., Lu, B., Crawley, J. N., & Weinberger, D. R. (2012). Dysbindin-1 modulates prefrontal cortical activity and schizophrenia-like behaviors via dopamine/D2 pathways. Molecular Psychiatry, 17(1), 85–98. doi:10.1038/mp.2010.106 Cerca con Google

Pardridge, W. M. (2005). The blood-brain barrier: Bottleneck in brain drug development. NeuroRX, 2(1), 3–14. doi:10.1602/neurorx.2.1.3 Cerca con Google

Patel, S., Stolerman, I. P., Asherson, P., & Sluyter, F. (2006). Attentional performance of C57BL/6 and DBA/2 mice in the 5-choice serial reaction time task. Behavioural Brain Research, 170(2), 197–203. doi:10.1016/j.bbr.2006.02.019 Cerca con Google

Pomara, N., Singh, R. R., Deptula, D., LeWitt, P. A., Bissette, G., Stanley, M., & Nemeroff, C. B. (1989). CSF corticotropin-releasing factor (CRF) in Alzheimer’s disease: its relationship to severity of dementia and monoamine metabolites. Biological Psychiatry, 26(5), 500–4. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2477071 Vai! Cerca con Google

Popik, P., Vetulani, J., & Van Ree, J. M. (1996). Facilitation and attenuation of social recognition in rats by different oxytocin-related peptides. European Journal of Pharmacology, 308(2), 113–6. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/8840121 Vai! Cerca con Google

Reglodi, D., Renaud, J., Tamas, A., Tizabi, Y., Socías, S. B., Del-Bel, E., & Raisman-Vozari, R. (2015). Novel tactics for neuroprotection in Parkinson’s disease: Role of antibiotics, polyphenols and neuropeptides. Progress in Neurobiology. doi:10.1016/j.pneurobio.2015.10.004 Cerca con Google

Robbins, T. W. (2002). The 5-choice serial reaction time task: behavioural pharmacology and functional neurochemistry. Psychopharmacology, 163(3-4), 362–80. doi:10.1007/s00213-002-1154-7 Cerca con Google

Ross, C. A., Margolis, R. L., Reading, S. A. J., Pletnikov, M., & Coyle, J. T. (2006). Neurobiology of schizophrenia. Neuron, 52(1), 139–53. doi:10.1016/j.neuron.2006.09.015 Cerca con Google

Rubino, T., Forlani, G., Viganò, D., Zippel, R., & Parolaro, D. (2005). Ras/ERK signalling in cannabinoid tolerance: from behaviour to cellular aspects. Journal of Neurochemistry, 93(4), 984–91. doi:10.1111/j.1471-4159.2005.03101.x Cerca con Google

Rugh, R. (1990). The mouse: its reproduction and development. Oxford science publications CN - QL737.R666 R8 1990. Oxford [England] ; New York: Oxford University Press. Cerca con Google

Sakka, L., Coll, G., & Chazal, J. (2011). Anatomy and physiology of cerebrospinal fluid. European Annals of Otorhinolaryngology, Head and Neck Diseases, 128(6), 309–316. doi:10.1016/j.anorl.2011.03.002 Cerca con Google

Sala, M., Braida, D., Donzelli, A., Martucci, R., Busnelli, M., Bulgheroni, E., … Chini, B. (2013). Mice Heterozygous for the Oxytocin Receptor Gene ( Oxtr +/− ) Show Impaired Social Behaviour but not Increased Aggression or Cognitive Inflexibility: Evidence of a Selective Haploinsufficiency Gene Effect. Journal of Neuroendocrinology, 25(2), 107–118. doi:10.1111/j.1365-2826.2012.02385.x Cerca con Google

Sala, M., Braida, D., Donzelli, A., Martucci, R., Busnelli, M., Bulgheroni, E., … Chini, B. (2013). Mice heterozygous for the oxytocin receptor gene (Oxtr(+/-)) show impaired social behaviour but not increased aggression or cognitive inflexibility: evidence of a selective haploinsufficiency gene effect. Journal of Neuroendocrinology, 25(2), 107–18. doi:10.1111/j.1365-2826.2012.02385.x Cerca con Google

Sala, M., Braida, D., Lentini, D., Busnelli, M., Bulgheroni, E., Capurro, V., … Chini, B. (2011a). Pharmacologic Rescue of Impaired Cognitive Flexibility, Social Deficits, Increased Aggression, and Seizure Susceptibility in Oxytocin Receptor Null Mice: A Neurobehavioral Model of Autism. Biological Psychiatry, 69(9), 875–882. doi:10.1016/j.biopsych.2010.12.022 Cerca con Google

Sala, M., Braida, D., Lentini, D., Busnelli, M., Bulgheroni, E., Capurro, V., … Chini, B. (2011b). Pharmacologic rescue of impaired cognitive flexibility, social deficits, increased aggression, and seizure susceptibility in oxytocin receptor null mice: a neurobehavioral model of autism. Biological Psychiatry, 69(9), 875–82. doi:10.1016/j.biopsych.2010.12.022 Cerca con Google

Scattoni, M. L., Crawley, J., & Ricceri, L. (2009). Ultrasonic vocalizations: a tool for behavioural phenotyping of mouse models of neurodevelopmental disorders. Neuroscience and Biobehavioral Reviews, 33(4), 508–15. doi:10.1016/j.neubiorev.2008.08.003 Cerca con Google

Scattoni, M. L., Ricceri, L., & Crawley, J. N. (2011). Unusual repertoire of vocalizations in adult BTBR T+tf/J mice during three types of social encounters. Genes, Brain, and Behavior, 10(1), 44–56. doi:10.1111/j.1601-183X.2010.00623.x Cerca con Google

Scearce-Levie, K., Roberson, E. D., Gerstein, H., Cholfin, J. A., Mandiyan, V. S., Shah, N. M., … Mucke, L. (2008). Abnormal social behaviors in mice lacking Fgf17. Genes, Brain, and Behavior, 7(3), 344–54. doi:10.1111/j.1601-183X.2007.00357.x Cerca con Google

Schwab, S. G., Knapp, M., Mondabon, S., Hallmayer, J., Borrmann-Hassenbach, M., Albus, M., … Wildenauer, D. B. (2003). Support for association of schizophrenia with genetic variation in the 6p22.3 gene, dysbindin, in sib-pair families with linkage and in an additional sample of triad families. American Journal of Human Genetics, 72(1), 185–90. doi:10.1086/345463 Cerca con Google

Sharma, T., & Antonova, L. (2003). Cognitive function in schizophrenia. Deficits, functional consequences, and future treatment. The Psychiatric Clinics of North America, 26(1), 25–40. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12683258 Vai! Cerca con Google

Shipley, M. T. (1985). Transport of molecules from nose to brain: Transneuronal anterograde and retrograde labeling in the rat olfactory system by wheat germ agglutinin-horseradish peroxidase applied to the nasal epithelium. Brain Research Bulletin, 15(2), 129–142. doi:10.1016/0361-9230(85)90129-7 Cerca con Google

Smid, H. G. O. M., de Witte, M. R., Homminga, I., & van den Bosch, R. J. (2006). Sustained and Transient Attention in the Continuous Performance Task. Journal of Clinical and Experimental Neuropsychology, 28(6), 859–883. doi:10.1080/13803390591001025 Cerca con Google

Smid, H. G. O. M., Martens, S., de Witte, M. R., & Bruggeman, R. (2013). Inflexible minds: impaired attention switching in recent-onset schizophrenia. PloS One, 8(10), e78062. doi:10.1371/journal.pone.0078062 Cerca con Google

Steinman, M. Q., Duque-Wilckens, N., Greenberg, G. D., Hao, R., Campi, K. L., Laredo, S. A., … Trainor, B. C. (2015). Sex-Specific Effects of Stress on Oxytocin Neurons Correspond With Responses to Intranasal Oxytocin. Biological Psychiatry, 1–9. doi:10.1016/j.biopsych.2015.10.007 Cerca con Google

Straub, R. E., Jiang, Y., MacLean, C. J., Ma, Y., Webb, B. T., Myakishev, M. V, … Kendler, K. S. (2002). Genetic variation in the 6p22.3 gene DTNBP1, the human ortholog of the mouse dysbindin gene, is associated with schizophrenia. American Journal of Human Genetics, 71(2), 337–48. doi:10.1086/341750 Cerca con Google

Striepens, N., Kendrick, K. M., Maier, W., & Hurlemann, R. (2011). Prosocial effects of oxytocin and clinical evidence for its therapeutic potential. Frontiers in Neuroendocrinology, 32(4), 426–450. doi:10.1016/j.yfrne.2011.07.001 Cerca con Google

Sutton, S. W., Behan, D. P., Lahrichi, S. L., Kaiser, R., Corrigan, A., Lowry, P., … Vale, W. W. (1995). Ligand requirements of the human corticotropin-releasing factor-binding protein. Endocrinology, 136(3), 1097–1102. doi:10.1210/endo.136.3.7867564 Cerca con Google

Takahashi, L. K. (2001). Role of CRF1 and CRF2 receptors in fear and anxiety. Neuroscience and Biobehavioral Reviews, 25(2001), 627–636. doi:10.1016/S0149-7634(01)00046-X Cerca con Google

Takao, K., Toyama, K., Nakanishi, K., Hattori, S., Takamura, H., Takeda, M., … Hashimoto, R. (2008). Impaired long-term memory retention and working memory in sdy mutant mice with a deletion in Dtnbp1, a susceptibility gene for schizophrenia. Molecular Brain, 1, 11. doi:10.1186/1756-6606-1-11 Cerca con Google

Takayanagi, Y., Yoshida, M., Bielsky, I. F., Ross, H. E., Kawamata, M., Onaka, T., … Nishimori, K. (2005). Pervasive social deficits, but normal parturition, in oxytocin receptor-deficient mice. Proceedings of the National Academy of Sciences of the United States of America, 102(44), 16096–101. doi:10.1073/pnas.0505312102 Cerca con Google

Talbot, K. (2009). The sandy (sdy) mouse: a dysbindin-1 mutant relevant to schizophrenia research. Progress in Brain Research, 179, 87–94. doi:10.1016/S0079-6123(09)17910-4 Cerca con Google

Talbot, K., Eidem, W. L., Tinsley, C. L., Benson, M. A., Thompson, E. W., Smith, R. J., … Arnold, S. E. (2004). Dysbindin-1 is reduced in intrinsic, glutamatergic terminals of the hippocampal formation in schizophrenia. The Journal of Clinical Investigation, 113(9), 1353–63. doi:10.1172/JCI20425 Cerca con Google

Tamborski, S., Mintz, E. M., & Caldwell, H. K. (2016). Sex differences in the embryonic development of the central oxytocin system in mice. Journal of Neuroendocrinology, n/a–n/a. doi:10.1111/jne.12364 Cerca con Google

Tandon, R., Keshavan, M. S., & Nasrallah, H. A. (2008). Schizophrenia, “just the facts” what we know in 2008. 2. Epidemiology and etiology. Schizophrenia Research, 102(1-3), 1–18. doi:10.1016/j.schres.2008.04.011 Cerca con Google

Tandon, R., Nasrallah, H. A., & Keshavan, M. S. (2009). Schizophrenia, “just the facts” 4. Clinical features and conceptualization. Schizophrenia Research, 110(1-3), 1–23. doi:10.1016/j.schres.2009.03.005 Cerca con Google

Tang, J., LeGros, R. P., Louneva, N., Yeh, L., Cohen, J. W., Hahn, C.-G., … Talbot, K. (2009). Dysbindin-1 in dorsolateral prefrontal cortex of schizophrenia cases is reduced in an isoform-specific manner unrelated to dysbindin-1 mRNA expression. Human Molecular Genetics, 18(20), 3851–63. doi:10.1093/hmg/ddp329 Cerca con Google

Thompson, B. L., Erickson, K., Schulkin, J., & Rosen, J. B. (2004). Corticosterone facilitates retention of contextually conditioned fear and increases CRH mRNA expression in the amygdala. Behavioural Brain Research, 149(2), 209–15. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15129783 Vai! Cerca con Google

Thorne, R. G., Pronk, G. J., Padmanabhan, V., & Frey, W. H. (2004). Delivery of insulin-like growth factor-I to the rat brain and spinal cord along olfactory and trigeminal pathways following intranasal administration. Neuroscience, 127(2), 481–496. doi:10.1016/j.neuroscience.2004.05.029 Cerca con Google

Timofeeva, E., Deshaies, Y., Picard, F., & Richard, D. (1999). Corticotropin-releasing hormone-binding protein in brain and pituitary of food-deprived obese (fa/fa) Zucker rats. The American Journal of Physiology, 277, R1749–R1759. Cerca con Google

Tribollet, E., Barberis, C., & Arsenijevic, Y. (1997). Distribution of vasopressin and oxytocin receptors in the rat spinal cord: sex-related differences and effect of castration in pudendal motor nuclei. Neuroscience, 78(2), 499–509. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/9145805 Vai! Cerca con Google

Usiello, A., Baik, J. H., Rougé-Pont, F., Picetti, R., Dierich, A., LeMeur, M., … Borrelli, E. (2000). Distinct functions of the two isoforms of dopamine D2 receptors. Nature, 408(6809), 199–203. doi:10.1038/35041572 Cerca con Google

Van Den Bogaert, A., Schumacher, J., Schulze, T. G., Otte, A. C., Ohlraun, S., Kovalenko, S., … Cichon, S. (2003). The DTNBP1 (dysbindin) gene contributes to schizophrenia, depending on family history of the disease. American Journal of Human Genetics, 73(6), 1438–43. doi:10.1086/379928 Cerca con Google

Veening, J. G., & Olivier, B. (2013). Intranasal administration of oxytocin: behavioral and clinical effects, a review. Neuroscience and Biobehavioral Reviews, 37(8), 1445–65. doi:10.1016/j.neubiorev.2013.04.012 Cerca con Google

Walitza, S., Melfsen, S., Herhaus, G., Scheuerpflug, P., Warnke, A., Müller, T., … Gerlach, M. (2007). Association of Parkinson’s disease with symptoms of attention deficit hyperactivity disorder in childhood. In Neuropsychiatric Disorders An Integrative Approach (pp. 311–315). Vienna: Springer Vienna. doi:10.1007/978-3-211-73574-9_38 Cerca con Google

Weickert, C. S., Rothmond, D. A., Hyde, T. M., Kleinman, J. E., & Straub, R. E. (2008). Reduced DTNBP1 (dysbindin-1) mRNA in the hippocampal formation of schizophrenia patients. Schizophrenia Research, 98(1-3), 105–10. doi:10.1016/j.schres.2007.05.041 Cerca con Google

Weickert, C. S., Straub, R. E., McClintock, B. W., Matsumoto, M., Hashimoto, R., Hyde, T. M., … Kleinman, J. E. (2004). Human dysbindin (DTNBP1) gene expression in normal brain and in schizophrenic prefrontal cortex and midbrain. Archives of General Psychiatry, 61(6), 544–55. doi:10.1001/archpsyc.61.6.544 Cerca con Google

Winslow, J. T., & Insel, T. R. (2002). The social deficits of the oxytocin knockout mouse. Neuropeptides, 36(2-3), 221–9. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12359512 Vai! Cerca con Google

Winterer, G., & Weinberger, D. R. (2004). Genes, dopamine and cortical signal-to-noise ratio in schizophrenia. Trends in Neurosciences, 27(11), 683–90. doi:10.1016/j.tins.2004.08.002 Cerca con Google

Young, J. W., Powell, S. B., Risbrough, V., Marston, H. M., & Geyer, M. A. (2009). Using the MATRICS to guide development of a preclinical cognitive test battery for research in schizophrenia. Pharmacology & Therapeutics, 122(2), 150–202. doi:10.1016/j.pharmthera.2009.02.004 Cerca con Google

Zhang, Y., Bertolino, A., Fazio, L., Blasi, G., Rampino, A., Romano, R., … Sadée, W. (2007). Polymorphisms in human dopamine D2 receptor gene affect gene expression, splicing, and neuronal activity during working memory. Proceedings of the National Academy of Sciences of the United States of America, 104(51), 20552–7. doi:10.1073/pnas.0707106104 Cerca con Google

Zvyagintsev, M., Parisi, C., Chechko, N., Nikolaev, A. R., & Mathiak, K. (2013). Attention and multisensory integration of emotions in schizophrenia. Frontiers in Human Neuroscience, 7, 674. doi:10.3389/fnhum.2013.00674 Cerca con Google

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