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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
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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