Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Nov;30(11):1141-1144.
doi: 10.1177/0269881116667668. Epub 2016 Sep 13.

Modelling the Cognitive and Neuropathological Features of Schizophrenia With Phencyclidine

Affiliations
Review

Modelling the Cognitive and Neuropathological Features of Schizophrenia With Phencyclidine

Gavin P Reynolds et al. J Psychopharmacol. .

Abstract

Here, Reynolds and Neill describe the studies that preceded and followed publication of this paper, which reported a deficit in parvalbumin (PV), a calcium-binding protein found in GABA interneurons known to be reduced in schizophrenia patients, in conjunction with a deficit in reversal learning in an animal model for schizophrenia. This publication resulted from common research interests: Reynolds in the neurotransmitter pathology of schizophrenia, and Neill in developing animal models for schizophrenia symptomatology. The animal model, using a sub-chronic dosing regimen (sc) with the non-competitive NMDA receptor antagonist PCP (phencyclidine), evolved from previous work in rats (for PCP) and primates (for cognition). The hypothesis of a PV deficit came from emerging evidence for a GABAergic dysfunction in schizophrenia, in particular a deficit in PV-containing GABA interneurons. Since this original publication, a PV deficit has been identified in other animal models for schizophrenia, and the PV field has expanded considerably. This includes mechanistic work attempting to identify the link between oxidative stress and GABAergic dysfunction using this scPCP model, and assessment of the potential of the PV neuron as a target for new antipsychotic drugs. The latter has included development of a molecule targeting KV3.1 channels located on PV-containing GABA interneurons which can restore both PV expression and cognitive deficits in the scPCP model.

Keywords: GABA; PCP; Schizophrenia; cognition; parvalbumin; rat.

Similar articles

See all similar articles

Cited by 5 articles

MeSH terms

LinkOut - more resources

Feedback