Distinct effects of d-amphetamine and phencyclidine on the social behaviour of rats

Sams-Dodd, Frank

doi:10.1097/00008877-199501000-00009

Cited by 128 publications

(91 citation statements)

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“…proximal contact behaviors (anogenital exploration, crawling over/under) with a novel male peer target. The lack of interest in social contacts induced by PCP agrees with observations from other laboratories (Sams-Dodd, 1995, 1997Qiao et al, 2001). Furthermore, the ability of OT to normalize the diminished social interaction in the chronic PCP model of schizophrenia is especially relevant as it confirms findings of symptom improvement noted when a bolus of OT was infused into the peripheral circulation of schizophrenic patients (Bujanow, 1974).…”

Section: Discussionsupporting

confidence: 86%

“…These changes appear to be neuroplastic because the behavioral and neurochemical changes are present in the animals without further drug treatment. Administration of PCP within 1 h of testing is known to disrupt social interaction behavior (Sams-Dodd, 1995, 1997. Furthermore, since PCP is a NMDA receptor antagonist, and activation of NMDA receptors stimulates acute release of AVP from the hypothalamus (Swenson et al, 1998), the behavioral and binding data in the Tanaka et al study may reflect the acute effects of NMDA antagonism within the hypothalamus.…”

Section: Discussionmentioning

confidence: 97%

“…This procedure was adapted from Sams-Dodd (1995). Male Sprague-Dawley rats (initial weight: 175-200 g) were housed two-three/cage and maintained as stated above.…”

Section: Animalsmentioning

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: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 97%

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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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“…23 Male NRG1 HET demonstrated a reduction in number of social investigation episodes, while the opposite effect was observed for females (NRG1 × sex, F(1,71) = 9.72, P = .002; supplementary figure 2). Male mice with simultaneous disruption to both genes (NRG1 HET /DISC1 HOM ) exhibited increased frequency of self-grooming behavior (NRG1 × DISC1 × sex, F(2,71) = 3.32, P = .04; figure 3C), which is considered indicative of anxiety-related behavior in a social context.…”

Section: Social Interactionmentioning

confidence: 90%

“…23,24 During the sociability phase, while 5 genotypes spent more time in (and made more entries into) the chamber containing the unfamiliar mouse relative to the opposite, empty chamber, this effect was absent in NRG1 HET /DISC1 HOM (NRG1 × DISC1, F(2, 60) = 3.72, P < .05; no sex or genotype × sex interaction; figure 3A). During the social novelty phase, both NRG1 heterozygosity and DISC1 heterozygosity (but not DISC1 homozygosity) were independently associated with loss of preference for spending more time in the chamber containing the new, unfamiliar mouse relative to the opposite chamber containing the previous, now familiar mouse (NRG1, F(1, 60) = 5.93, P = .03; DISC1, F(1, 60) = 2.69, P = .06; no sex or genotype × sex interaction; figure 3B).…”

Section: Social Interactionmentioning

confidence: 99%

Epistatic and Independent Effects on Schizophrenia-Related Phenotypes Following Co-disruption of the Risk Factors Neuregulin-1 × DISC1

O’Tuathaigh

Fumagalli

Desbonnet

et al. 2016

Schizophrenia Bulletin

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Few studies have addressed likely gene × gene (ie, epistatic) interactions in mediating risk for schizophrenia. Using a preclinical genetic approach, we investigated whether simultaneous disruption of the risk factors Neuregulin-1 (NRG1) and Disrupted-in-schizophrenia 1 (DISC1) would produce a disease-relevant phenotypic profile different from that observed following disruption to either gene alone. NRG1 heterozygotes exhibited hyperactivity and disruption to prepulse inhibition, both reversed by antipsychotic treatment, and accompanied by reduced striatal dopamine D2 receptor protein expression, impaired social cognition, and altered glutamatergic synaptic protein expression in selected brain areas. Single gene DISC1 mutants demonstrated a disruption in social cognition and nest-building, altered brain 5-hydroxytryptamine levels and hippocampal ErbB4 expression, and decreased cortical expression of the schizophrenia-associated microRNA miR-29b. Co-disruption of DISC1 and NRG1, indicative of epistasis, evoked an impairment in sociability and enhanced self-grooming, accompanied by changes in hypothalamic oxytocin/vasopressin gene expression. The findings indicate specific behavioral correlates and underlying cellular pathways downstream of main effects of DNA variation in the schizophrenia-associated genes NRG1 and DISC1.

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Antipsychotic Agents

Altar¹,

Martin²,

Thurkauf³

2003

Burger's Medicinal Chemistry and Drug Discovery

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Distinct effects of d-amphetamine and phencyclidine on the social behaviour of rats

Cited by 128 publications

References 0 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

Epistatic and Independent Effects on Schizophrenia-Related Phenotypes Following Co-disruption of the Risk Factors Neuregulin-1 × DISC1

Antipsychotic Agents

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