NC-1900, an arginine–vasopressin analogue, ameliorates social behavior deficits and hyperlocomotion in MK-801-treated rats: Therapeutic implications for schizophrenia

Matsuoka, Tadasu; Sumiyoshi, Tomiki; Tanaka, Kodai; Tsunoda, Masahiko; Uehara, Takashi; Itoh, Hiroko; Kurachi, Masayoshi

doi:10.1016/j.brainres.2005.06.035

Cited by 37 publications

(25 citation statements)

References 40 publications

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“…MK-801 has been shown in some but not all studies to produce similar deficits in social behaviours in adult male rats following both acute treatment (0.2 mg/kg, ip; Rung et al, 2005) and a sub-chronic dosing regime (0.13 mg/kg/day ip for 14 days; Matsuoka et al, 2005). Sams-Dodd in 2004 used different dosing regimes of MK-801 (group 1: 0.063 or 0.5 mg/kg for 7 days, s.c with mini osmotic pumps) where the rats were tested in the social interaction test 21 days post drug administration and (group 2: 5mg/kg of MK-801, on alternate days for 4 days) with the rats were being tested following a 7 day washout period.…”

mentioning

confidence: 99%

Animal models of cognitive dysfunction and negative symptoms of schizophrenia: Focus on NMDA receptor antagonism

Neill

Barnes

Cook

et al. 2010

Pharmacology & Therapeutics

478

322

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Cognitive deficits in schizophrenia remain an unmet clinical need. Improved understanding of the neuro-and psychopathology of these deficits depends on the availability of carefully validated animal models which will assist the development of novel therapies. There is much evidence that at least some of the pathology and symptomatology (particularly cognitive and negative symptoms) of schizophrenia results from a dysfunction of the glutamatergic system which may be modelled in animals through the use of NMDA receptor antagonists. The current review examines the validity of this model in rodents. We review the ability of acute and sub-chronic treatment with three non-competitive NMDA antagonists; phencyclidine (PCP), ketamine and MK801 (dizocilpine) to produce cognitive disturbances of relevance to schizophrenia in rodents and their subsequent reversal by first-and second-generation antipsychotic drugs. Effects of NMDA receptor antagonists on the performance of rodents in behavioural tests assessing the various domains of cognition and negative symptoms are examined: novel object recognition for visual memory, reversal learning and attentional set shifting for problem solving and reasoning, 5-choice serial reaction time for attention and speed of processing; in addition to effects on social behaviour and neuropathology. The evidence strongly supports the use of NMDA receptor antagonists to model cognitive deficit and negative symptoms of schizophrenia as well as certain pathological disturbances seen in the illness. This will facilitate the evaluation of much-needed novel therapies for improved therapy of cognitive deficits and negative symptoms in schizophrenia.

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mentioning

confidence: 99%

Animal models of cognitive dysfunction and negative symptoms of schizophrenia: Focus on NMDA receptor antagonism

Neill

Barnes

Cook

et al. 2010

Pharmacology & Therapeutics

478

322

View full text Add to dashboard Cite

show abstract

“…These findings from our laboratory are consistent with Bielsky et al [16] who reported that re-expressing of V1a receptors in the lateral septum of V1a receptor knockout mice exhibits complete recovery from impaired social recognition. Down-regulation of the AVP gene in the amygdala of MK-801-treated rats may provide a basis for the ability of AVP-analogues to ameliorate the behavioral disturbances by blockade of NMDA receptor [17]. Similar benefits regarding social behavior have been reported for oxytocin [3; 13; 28; 29; 30].…”

Section: Sociality Deficits In Animal Models Of Schizophrenia; Effectmentioning

confidence: 81%

“…Accordingly, we reported that NC-1900, an AVP analogue and agonist at V1a receptors, ameliorates social interaction deficits in rats chronically treated with MK-801 [17] (Figure 4). This result from an animal model of schizophrenia is consistent with the observation, discussed above [18], that chronic administration of the NMDA antagonist phencyclidine reduces the density of V1a receptor binding sites in several brain regions, including the LS, in rats showing social interaction deficits.…”

Section: Sociality Deficits In Animal Models Of Schizophrenia; Effectmentioning

confidence: 85%

Role for Pituitary Neuropeptides in Social Behavior Disturbances of Schizophrenia

Sumiyoshi¹,

Matsuoka²,

Kurachi³

2012

Neuroendocrinology and Behavior

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“…Consistent with behavioral evidence, MK801 induced similar ERP changes in both WT and BRAT rats. deficits and hyperlocomotion [25,64].…”

Section: Response To Nmda Antagonist Treatmentmentioning

confidence: 97%

“…VP is also involved in behavioral outcomes important in the etiology of schizophrenia such as learning and memory, aggression, and sociality [23]. In addition, both glutamate and VP antagonism have been associated with negative symptoms of schizophrenia, suggesting a potential interaction between glutamate and VP signaling in the brain [24][25][26]. Moreover, there is evidence that VP activity in the hypothalamus may be regulated by glutamatergic signaling [22].…”

Section: Crossmarkmentioning

confidence: 99%

Differential sensitivity of the Brattleboro rat to glutamatergic and dopaminergic perturbation

Lin¹,

Ambler²,

Billingslea³

et al. 2014

J Psychiatry Brain Funct

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Background: The vasopressin deficient Brattleboro (BRAT) rats have behavioral impairments which mimic those seen in other schizophrenia models. However, the mechanism by which vasopressin produces these behavioral abnormalities is unclear. Notably, elevations in dopamine signaling as well as reductions in glutamatergic signaling have been associated with behavioral impairments consistent with those observed in the BRAT rats. Therefore, a potential mechanism for vasopressin induces behavioral abnormalities could be through modulation of dopamine or glutamate signaling. Consequently, the aim of this study was to assess the modulatory function of vasopressin on dopamine and NMDA signaling. Methods: Single intraperitoneal injection of amphetamine (0.5 mg/kg), a dopamine agonist, and MK801 (0.25 mg/kg), a NMDA antagonist, were used to assess vasopressin (VP) modulatory activity on dopaminergic and glutamatergic pre-pulse inhibition of startle (PPI), social interaction and auditory event related potential (ERPs) impairments in BRAT and littermate control WT rats. Results: MK801-induced impairments were consistent and not significantly different between WT and BRAT rats suggesting minimal modulatory activity of vasopressin on NMDA signaling. In contrast, amphetamine-induced deficits were genotype dependent. In control animals, amphetamine caused a statistically significant deficit in PPI and social interaction whereas there was no effect in BRAT rats. Conversely, ERP components were unaltered in control rats, whereas N40 amplitude, evoked gamma power, and gamma signal to noise ratio were all elevated in BRAT rats. Conclusions:The ERP component analyses of BRAT rats treated with amphetamine suggest modulation of auditory information processing through interplay between dopaminergic and vasopressin. However, the behavioral and electrophysiological evidence presented here also suggest that vasopressin does not modulate glutamatergic signaling through NMDA receptors. Further evidence in necessary to determine the interaction between vasopressin and dopamine signaling and future studies are necessary to comprehend glutamatergic interactions with vasopressin that are not NMDA-mediated.

show abstract

NC-1900, an arginine–vasopressin analogue, ameliorates social behavior deficits and hyperlocomotion in MK-801-treated rats: Therapeutic implications for schizophrenia

Cited by 37 publications

References 40 publications

Animal models of cognitive dysfunction and negative symptoms of schizophrenia: Focus on NMDA receptor antagonism

Animal models of cognitive dysfunction and negative symptoms of schizophrenia: Focus on NMDA receptor antagonism

Role for Pituitary Neuropeptides in Social Behavior Disturbances of Schizophrenia

Differential sensitivity of the Brattleboro rat to glutamatergic and dopaminergic perturbation

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