Phencyclidine-induced stereotyped behaviour and social isolation in rats

Sams-Dodd, Frank

doi:10.1097/00008877-199601000-00001

Cited by 218 publications

(101 citation statements)

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“…Several behavioral models claimed to model processes impaired in schizophrenia have been shown to discriminate between typical and atypical APD's, e.g., PCP-induced disruption of prepulse inhibition (Bakshi and Geyer 1995;Swerdlow et al 1996a), PCP-induced disruption of social interaction (Sams-Dodd 1996, 1997 and PCP-induced enhancement of immobility in the forced swim test (Noda et al 1995). If shown effective in further studies, the LI model would differ from these models in two important respects.…”

Section: Discussionmentioning

confidence: 99%

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

Shadach

2000

Neuropsychopharmacology

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Section: Discussionmentioning

confidence: 99%

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

Shadach

2000

Neuropsychopharmacology

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“…[63][64][65][66] For example, neonatal damage of the ventral hippocampus or amygdala, [67][68][69] administration of amphetamine 70 inducing disruption (and probably blocking) of latent inhibition, or phencyclidine 71 inducing changes in the startle response provided productive animal models with construct, face, and predictive validity for schizophrenia. It has been shown 72,73 that interference with neurogenesis in the mediotemporal allocortex of rat embryos, during the earliest stages of cortical proliferation, results not only in a thickness reduction of the adult entorhinal cortex and hippocampus 55,73 but also in other morphological characteristics resembling those observed in patients with schizophrenia.…”

Section: Bdnf and Animal Models Of Schizophreniamentioning

confidence: 99%

BDNF in schizophrenia, depression and corresponding animal models

2005

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Understanding the etiology and pathogenesis schizophrenia and depression is a major challenge facing psychiatry. One hypothesis is that these disorders are secondary to a malfunction of neurotrophic factors. Inappropriate neurotrophic support during brain development could lead to structural disorganisation in which neuronal networks are established in a nonoptimal manner. Inadequate neurotrophic support in adult individuals could ultimately be an underlying mechanism leading to decreased capacity of brain to adaptive changes and increased vulnerability to neurotoxic damage. Brain-derived neurotrophic factor (BDNF) is a mediator involved in neuronal survival and plasticity of dopaminergic, cholinergic, and serotonergic neurons in the central nervous system (CNS). In this review, we summarize findings regarding altered BDNF in schizophrenia and depression and animal models, as well as the effects of antipsychotic and antidepressive treatments on the expression of BDNF. Molecular Psychiatry (2005) 10, 345-352.

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“…Furthermore, we now demonstrate hyper-responsivity to the stimulant qualities of stress and amphetamine in PCP-treated rats, and schizophrenic subjects can show increased psychotic symptoms in response to stress and amphetamine (Angrist and Gershon 1977). Finally, abnormal social interactions have previously been characterized in rats after subchronic PCP administration (Sams-Dodd 1996) another classic symptom of schizophrenia. Neurobiologically, this model seems to mimic some observations of alterations in the schizophrenic brain.…”

Section: Validity Of the Subchronic Pcp-based Animal Model Of Schizopmentioning

confidence: 99%

“…Furthermore, several studies have generated data to suggest that the PCP model may have predictive validity, showing a qualitatively similar response to drug treatment as schizophrenia (Steinpreis et al 1994;Sams-Dodd 1996;Jentsch et al 1997c). …”

Section: Validity Of the Subchronic Pcp-based Animal Model Of Schizopmentioning

confidence: 99%

Subchronic Phencyclidine Administration Increases Mesolimbic Dopaminergic System Responsivity and Augments Stress- and Psychostimulant-Induced Hyperlocomotion

Jentsch

Taylor

Roth

1998

Neuropsychopharmacology

147

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Previous studies have shown that repeated exposures to phencyclidine (PCP) induces prefrontal cortical dopaminergic and cognitive deficits in rats and (Javitt and Zukin 1991); that is, administration of PCP or its congeners ketamine or dizocilpine can induce schizophrenic-like symptomatology in people (Luby et al. 1959;Krystal et al. 1994; Bunney et al. 1994) and precipitate psychosis in schizophrenics (Ital et al. 1967;Lahti et al. 1994). These compounds can stimulate both positive and negative symptoms of schizophrenia (Javitt and Zukin), including cognitive dysfunction (Cosgrove and Newell 1991). As such, PCP administration has been suggested to represent a drug-induced model of schizophrenia (Javitt and Zukin;Steinpreis 1996).The ability of PCP to simulate the symptomatology of schizophrenia in humans has led to the proposal that the behavioral pathologies evident in schizophrenia and PCP-exposed humans are caused by dysfunction of common neural substrates (Luby et al. 1959;Javitt and Zukin 1991). The effects of PCP on brain dopamine systems has received particular attention (Meltzer et al. 1980;Bowers and Hoffman 1984;Deutch et al. 1987;Hertel et al. 1996;Jentsch et al. 1997a) since alterations in dopaminergic systems have been hypothesized in schizophrenia (reviewed in Davis et al. 1991;Deutch 1992 Recent work has shown that long-term administration of PCP causes enduring cognitive dysfunction and cortical dopamine deficits in rats and monkeys (Jentsch et al. 1997b,c). These data correspond to reports of cognitive disturbances in schizophrenic subjects (Fey 1951;Goldman-Rakic 1991;Park and Holzman 1992), and recent in vivo imaging studies of the schizophrenic brain have revealed a failure of activation of frontal cortex during cognitive performance (termed "hypofrontality" by Weinberger and Berman 1996), effects that may be mediated by dopaminergic dysfunction Daniel et al. 1989 Daniel et al. , 1991Dolan et al. 1995). These data are also consistent with studies in nonhuman primates that have revealed that lesions of the prefrontal cortical dopamine innervation lead to working memory impairments (Brozoski et al. 1979), a cognitive process closely associated with this brain region (Goldman-Rakic 1987).Moreover, prefrontal cortical dopaminergic deficiencies may result in enhancement of activity of subcortical dopamine systems. Destruction of prefrontal cortical dopamine terminals has been shown to augment the response of the mesolimbic dopamine systems to stress ), amphetamine sensitization (Banks and Gratton 1994), high K ϩ -stimulation (Roberts et al. 1994), or haloperidol administration (Rosin et al. 1994). These data have supported an emerging neurochemical hypothesis of schizophrenia: cortical dopaminergic hypoactivity and subcortical dopaminergic hyperactivity (Robbins 1990;Grace 1991;Deutch 1992). Recent in vivo studies of the schizophrenic brain have revealed evidence for the subcortical component of this hypothesis; heightened responsivity to the dopamine-releasing properties of amphetamine ha...

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Phencyclidine-induced stereotyped behaviour and social isolation in rats

Cited by 218 publications

References 0 publications

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

The Latent Inhibition Model Dissociates between Clozapine, Haloperidol, and Ritanserin

BDNF in schizophrenia, depression and corresponding animal models

Subchronic Phencyclidine Administration Increases Mesolimbic Dopaminergic System Responsivity and Augments Stress- and Psychostimulant-Induced Hyperlocomotion

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