Involvement of γ-aminobutyric acid neurotransmission in phencyclidine-induced dopamine release in the medial prefrontal cortex

Yonezawa, Yuji; Kuroki, Tetsuo; Kawahara, Teppei; Tashiro, Nobutada; Uchimura, Hideyuki

doi:10.1016/s0014-2999(97)01435-0

Cited by 119 publications

(93 citation statements)

References 59 publications

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“…In a slice preparation of rat hippocampal CA1 neurons, it has been shown that MK-801 preferentially reduces alvear stimulation-induced long-term potentiation in local-circuit neurons relative to pyramidal cells (Grunze et al 1994), suggesting that the NMDA receptor antagonists preferentially reduce GABAergic transmission. This, indeed, seems to be the case, because, in prefrontal cortex, PCP increases glutamate release (Moghaddam et al 1997); whereas, profoundly reducing GABA release (Yonezawa et al 1998). These findings concur with the hypothesis that NMDA receptors primarily regulate the function of local circuit, GABAergic neurons (Olney and Farber 1995).…”

Section: Glutamatergic and Gabaergic Dysfunctionsupporting

confidence: 77%

“…Likewise, PCP itself increases the firing rate of dopaminergic neurons (Freedman and Bunney 1984; French 1994). The available data suggest that acute administration of PCP may reduce cortical GABAergic function (Grunze et al 1994;Yonezawa et al 1998), disinhibiting glutamatergic transmission in the prefrontal cortex (Moghaddam et al 1997) and ventral tegmental area (Mathe et al 1998). This increase in glutamatergic transmission would then stimulate mesocorticolimbic dopaminergic transmission and locomotor behavior (Jentsch et al 1998d).…”

Section: Neurochemistry Cortical Dopamine Dysfunctionmentioning

confidence: 99%

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The Neuropsychopharmacology of Phencyclidine From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia

Jentsch

Roth²

1999

Neuropsychopharmacology

1,201

772

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Administration of noncompetitive NMDA ր glutamate receptor antagonists, such as phencyclidine (PCP) and ketamine, to humans induces a broad range of schizophrenic-like symptomatology, findings that have contributed to a hypoglutamatergic hypothesis of schizophrenia. Moreover, a history of experimental investigations of the effects of these drugs in animalsBiological psychiatric research has seen the development of many putative animal models of schizophrenia. The etiological bases of these models have varied widely from the administration of purportedly psychotomimetic drugs (Snyder 1988; Javitt and Zukin 1991; Jentsch et al. 1998a), to perinatal insults (Lipska et al. 1993;El-Khodor and Boksa 1997;Moore and Grace 1997; Bertolino et al. 1997), to chronic social isolation or stress (Jones et al. 1990), and beyond. The administration of psychotomimetic drugs to humans and animals represents probably the most widely accepted and utilized class of schizophrenia models. These "pharmacological" models seem to represent methods for the induction of psychopathology in humans and aberrant (potentially related) behavior in animals.At the behavioral level, there seems to be some heterogeneity in the effects of different psychotomimetic drug classes. The psychomotor stimulants, such as amphetamine and cocaine, can clearly induce a form of 20 , NO . 3 paranoid psychosis in human subjects after high-dose or long-term administration, but evidence regarding the ability of these agents to induce "deficit" state symptoms is conflicting (Angrist and Gershon 1970;Everitt et al., 1997); moreover, there is evidence that amphetamine may actually alleviate negative and cognitive symptoms in schizophrenic patients (Angrist et al. 1982;Goldberg et al. 1991; Carter et al. 1997). Psychotomimetic indoleamines, such as lysergic acid diethylamide, can induce profound sensory hallucinations without causing any apparent deficit state in normal subjects (Geyer and Markou 1994) and without precipitating symptomatology in schizophrenic patients (Cohen et al. 1962). In contrast, the noncompetitive antagonists of the N-methyl-D-aspartate (NMDA) ր glutamate receptor, including phencyclidine (PCP) and ketamine, seem to be capable of inducing both positive and negative symptoms of schizophrenia, including cognitive dysfunction in normal humans (Snyder 1980; Javitt and Zukin 1991;Tamminga 1998); these drugs also profoundly exacerbate both positive and negative symptoms in schizophrenic patients (Itil et al. 1967;Lahti et al. 1994;Malhotra et al. 1997a).Because of the more comprehensive psychopathology induced by PCP, many researchers have studied the effects of NMDA receptor antagonists in humans and animals to gain insights into the neurobiology of schizophrenia. In this review, the validity of NMDA receptor antagonist-induced models of schizophrenia in humans and animals are considered, and the applicability of acute versus chronic administration of PCP as a more precise model is assessed. The neurobiological substrates of the observed behavior...

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Section: Glutamatergic and Gabaergic Dysfunctionsupporting

confidence: 77%

Section: Neurochemistry Cortical Dopamine Dysfunctionmentioning

confidence: 99%

The Neuropsychopharmacology of Phencyclidine From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia

Jentsch

Roth²

1999

Neuropsychopharmacology

1,201

772

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“…Thus, all these findings suggest that NMDA receptor antagonists would attenuate the tonic activation of inhibitory (GABA) neurons (possibly, though not exclusively, in the hippocampus and/or the thalamus), which would result in a disinhibition of glutamatergic input to the mPFC (Olney and Farber, 1995;Moghaddam et al, 1997;Krystal et al, 2003). In fact, GABAergic neurons are very sensitive to NMDA antagonism (Grunze et al, 1996;Li et al, 2002), and PCP and MK-801 are able to reduce dialysate GABA in the mPFC (Yonezawa et al, 1998) and striatum (Hondo et al, 1995). Our results would suggest that the GABAergic control of glutamate efflux within the mPFC would not have a tonic nature.…”

Section: Discussionmentioning

confidence: 96%

“…In fact, GABAergic interneurons in limbic cortex and hippocampus are extremely responsive to NMDA receptor antagonists in comparison with pyramidal neurons (Grunze et al, 1996;Li et al, 2002), and PCP is able to reduce cortical GABAergic function (Yonezawa et al, 1998). It remains to be determined whether this feature can be applied to other GABAergic cells throughout the brain.…”

Section: Introductionmentioning

confidence: 99%

Clozapine and Haloperidol Differently Suppress the MK-801-Increased Glutamatergic and Serotonergic Transmission in the Medial Prefrontal Cortex of the Rat

López-Gil

Babot

Amargós-Bosch

et al. 2007

Neuropsychopharmacol

170

162

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The administration of noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists such as phencyclidine and ketamine has been shown to increase the extracellular concentration of glutamate and serotonin (5-HT) in the medial prefrontal cortex (mPFC). In the present work, we used in vivo microdialysis to examine the effects of the more potent noncompetitive NMDA receptor antagonist, MK-801, on the efflux of glutamate and 5-HT in the mPFC, and whether the MK-801-induced changes in the cortical efflux of both transmitters could be blocked by clozapine and haloperidol given systemically or intra-mPFC. The systemic, but not the local administration of MK-801, induced an increased efflux of 5-HT and glutamate, which suggests that the NMDA receptors responsible for these effects are located outside the mPFC, possibly in GABAergic neurons that tonically inhibit glutamatergic inputs to the mPFC. The MK-801-induced increases of extracellular glutamate and 5-HT were dependent on nerve impulse and the activation of mPFC AMPA/ kainate receptors as they were blocked by tetrodotoxin and NBQX, respectively. Clozapine and haloperidol blocked the MK-801-induced increase in glutamate, whereas only clozapine was able to block the increased efflux of 5-HT. The local effects of clozapine and haloperidol paralleled those observed after systemic administration, which emphasizes the relevance of the mPFC as a site of action of these antipsychotic drugs in offsetting the neurochemical effects of MK-801. The ability of clozapine to block excessive cortical 5-HT efflux elicited by MK-801 might be related to the superior efficacy of this drug in treating negative/cognitive symptoms of schizophrenia.

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“…PCP and its structural analogue ketamine produce inactivation of inhibitory control by decreasing GABA release [58]. This disinhibition of excitatory neurotransmission is referred to as NMDA receptor hypofunction [32,45,46].…”

Section: Introductionmentioning

confidence: 99%

A preliminary investigation into the effects of antipsychotics on sub-chronic phencyclidine-induced deficits in attentional set-shifting in female rats

McLean

Beck

Woolley

et al. 2008

Behavioural Brain Research

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Rationale: The NMDA receptor antagonist, phencyclidine (PCP), has been shown to induce symptoms characteristic of schizophrenia. A loss in executive function and the ability to shift attention between stimulus dimensions is impaired in schizophrenia; this can be assessed in rodents by the perceptual attentional set-shifting task. Objective: The aim of this study was to investigate whether the deficits induced by sub-chronic PCP in attentional set-shifting could be reversed by sub-chronic administration of clozapine, risperidone or haloperidol. Methods: Adult female hooded-Lister rats received subchronic PCP (2 mg/kg) or vehicle (1 ml/kg) i.p. twice daily for seven days, followed by a seven-day washout period. PCP-treated rats then received clozapine, risperidone, haloperidol or vehicle once daily for seven days and were then tested in the perceptual set-shifting task. Results: PCP significantly (p<0.01) increased the number of trials to reach criterion in the EDS phase when compared to vehicle and this deficit was significantly (p<0.01) attenuated by sub-chronic clozapine (2.5 mg/kg) and risperidone (0.2 mg/kg), but not by sub-chronic haloperidol treatment (0.05 mg/kg). Conclusions:These data show that sub-chronic PCP produced a robust deficit within the EDS phase in the attentional set-shifting task, in female rats. Atypical antipsychotics, clozapine and risperidone, but not the classical agent, haloperidol, significantly improved the PCPinduced cognitive deficit.

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Involvement of γ-aminobutyric acid neurotransmission in phencyclidine-induced dopamine release in the medial prefrontal cortex

Cited by 119 publications

References 59 publications

The Neuropsychopharmacology of Phencyclidine From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia

The Neuropsychopharmacology of Phencyclidine From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia

Clozapine and Haloperidol Differently Suppress the MK-801-Increased Glutamatergic and Serotonergic Transmission in the Medial Prefrontal Cortex of the Rat

A preliminary investigation into the effects of antipsychotics on sub-chronic phencyclidine-induced deficits in attentional set-shifting in female rats

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