Subchronic phencyclidine administration alters central vasopressin receptor binding and social interaction in the rat

Tanaka, Kodai; Suzuki, Michio; Sumiyoshi, Tomiki; Murata, Masahiko; Tsunoda, Masahiko; Kurachi, Masayoshi

doi:10.1016/j.brainres.2003.08.050

Cited by 37 publications

(27 citation statements)

References 44 publications

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“…There was a significant decrease of approximately 20% in V1aR binding in the CeA after chronic PCP treatment (t-test, t ¼ 4.00, df ¼ 9, po0.003). As first reported by Tanaka et al (2003), following chronic PCP treatment, the binding of the V1aR specific ligand in LS was decreased by 58% following chronic PCP treatment (t-test, t ¼ 4.03, df ¼ 12, po0.002).…”

Section: Oxytocinergic and Vasopressinergic Marker Mrna Expression Insupporting

confidence: 73%

“…Brattleboro rats, a rat naturally lacking the ability to synthesize functional AVP, also exhibit PPI deficits (Feifel and Priebe, 2001). Thus, the successful treatment of sensorimotor gating disturbances with a neuropeptide along with the V1aR binding results of Tanaka et al (2003) are significant because they reaffirm the distinct possibility that, in animal models of schizophrenia, neuropeptides are altered by many different pharmacological and experiential manipulations purported to model schizophrenogenic insults. Furthermore, it predicts the potential efficacy of central-acting AVP or OT analogues as potential schizophrenia treatments.…”

Section: Introductionmentioning

confidence: 81%

“…A recent published study (Tanaka et al, 2003) reported that administration of a chronic low dose (2 mg/kg) of PCP to Wistar rats was associated with diminished social interaction and lowered V1aR binding in several brain regions. In contrast to our data, their study did not, however, find a decrease in V1aR binding within the CeA.…”

Section: Discussionmentioning

confidence: 99%

“…Tanaka et al (2003) have reported that chronic PCP administration causes a reduction in V1aR binding in the lateral septum (LS), substantia nigra, bed nucleus of the stria terminalis, and other regions. In rats, subcutaneous administration of OT dose dependently normalized reductions in prepulse inhibition (PPI) of the startle response caused by amphetamine or an NMDA receptor antagonist (Feifel and Reza, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Social Interaction Deficits Caused by Chronic Phencyclidine Administration are Reversed by Oxytocin

Lee

Brady

Shapiro

et al. 2005

Neuropsychopharmacol

184

105

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Chronic administration of phencyclidine (PCP) has been advanced as a valid animal model of the social deficit symptoms of schizophrenia. In these studies, the cumulative time that male rats treated once a day for 14 days with PCP actively engaged in social behavior was decreased approximately 75% relative to saline-treated control animals. In addition, these socially impaired rats had an increase in the relative amount of noncontact interactions compared with saline-injected peers. Social behaviors were preferentially affected by PCP treatment because in two anxiety-related behavioral assays, the open field and light/dark emergence tests, there was a failure to differentiate between the PCP-treated rats and saline-injected control rats. Considering the general importance of the neuropeptides oxytocin and vasopressin in male social behaviors, studies of molecular markers related to these neuropeptides were performed. Hypothalamic oxytocin mRNA expression was significantly decreased while oxytocin receptor binding was increased in the central nucleus of the amygdala following chronic PCP treatment. Given the significance of central nucleus of the amygdala in social behavior, oxytocin was infused into the central nucleus of experimental and control male rats, and their postinfusion social interaction and open field behaviors were analyzed. A bilateral infusion of 1 mg of oxytocin into the central amygdala selectively restored the normal quantity and quality of social behavior in chronic PCP-treated male rats without altering open field behaviors. These findings suggest that deficits in the central oxytocinergic system may underlie the social impairment exhibited in this animal model of schizophrenia.

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Section: Oxytocinergic and Vasopressinergic Marker Mrna Expression Insupporting

confidence: 73%

Section: Introductionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Social Interaction Deficits Caused by Chronic Phencyclidine Administration are Reversed by Oxytocin

Lee

Brady

Shapiro

et al. 2005

Neuropsychopharmacol

184

105

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“…Vasopressin in species such as the prairie vole, is a potent mediator of a variety of social behaviors (Witt et al, 1990, Young et al, 1997, Cho et al, 1999, Bales and Carter, 2003. In addition, vasopressin has been implicated in the social deficits in rats following repeated phencyclidine administration (Tanaka et al, 2003). How the present data integrate with the data from Tanaka and colleagues remains unclear.…”

Section: Discussionmentioning

confidence: 61%

Prenatal stress generates deficits in rat social behavior: Reversal by oxytocin

Lee¹,

Brady²,

Shapiro³

et al. 2007

Brain Research

237

188

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Neurodevelopmental changes induced by environmental stress exposure play a significant but poorly defined role in the etiology of schizophrenia. Exposure of pregnant female rats to a series of unpredictable stresses during the final week of pregnancy generates behavioral deficits and molecular changes in the offspring similar to those observed in schizophrenic individuals. We used this rat prenatal stress preparation to investigate social withdrawal behaviors that may have relevance to the negative symptoms of schizophrenia. The cumulative time adult male offspring of stress-exposed pregnant female rats actively interacted with a weight-matched, same-sex peer was decreased approximately 76% relative to non-stress exposed control rats. Prenatal stress exposure also diminished the quality of the social interaction behavior indicative of reduced social drive. Analysis of the oxytocinergic system in the prenatally stressed male rats revealed significantly less oxytocin mRNA in the paraventricular nucleus and increased oxytocin receptor binding in the central amygdala. Moreover, oxytocin, but not vasopressin, administration into the central amygdala reversed the social incompetence of the prenatally stressed rats without increasing behavior in nonstressed control animals. In addition, cross-fostering pups from prenatally stressed mothers to nonstressed mothers failed to improve the social deficit of the prenatally stressed male offspring. Two behavioral assays designed to measure anxiety did not differentiate the prenatally stressed rats from non-stressed controls. These data indicate that prenatal stress may be an etiologically appropriate animal model for some aspects of schizophrenic social withdrawal. Furthermore, unpredictable prenatal stress exposure selectively degrades social interaction behaviors without increasing anxiety measures.

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Schizophrenia

Depoortère¹,

Moser²

2014

In Vivo Models for Drug Discovery

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Subchronic phencyclidine administration alters central vasopressin receptor binding and social interaction in the rat

Cited by 37 publications

References 44 publications

Social Interaction Deficits Caused by Chronic Phencyclidine Administration are Reversed by Oxytocin

Social Interaction Deficits Caused by Chronic Phencyclidine Administration are Reversed by Oxytocin

Prenatal stress generates deficits in rat social behavior: Reversal by oxytocin

Schizophrenia

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