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The effects of single and repeated phencyclidine administration on [125I] iomazenil binding in the rat brain.

K Kaneko, A Kuramaji, H Shibuya, Toshitaka Nabeshima, M Toru

Neurochemistry International September 1996 DOI: 10.1016/0197-0186(96)00006-x (opens in new tab)

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Characteristics Animal experimental study (in vitro quantitative autoradiographic receptor binding assay) Peer reviewed
Population Rats, 37 discrete brain areas examined
Intervention Phencyclidine (PCP)
Dose 7.5 mg/kg single dose; 7.5 mg/kg/day for 14 days
Duration Single treatment and repeated treatment for 14 days
Measures [125I] iomazenil binding (quantitative autoradiographic receptor binding assay)
Key findings Single and repeated PCP treatment produced region-specific changes in [125I] iomazenil binding to central-type benzodiazepine receptors, generally larger after repeated dosing. Binding increased in parietal cortex layers I-IV in both groups and in hippocampal CA1 after repeated treatment, and decreased in piriform cortex after repeated treatment. The authors suggest these are compensatory changes from NMDA receptor blockade, with regional differences reflecting differing glutamate-GABA receptor organization.

Abstract

We measured [125I] iomazenil binding, labeling the central-type benzodiazepine receptor in 37 discrete rat brain areas following single (7.5 mg/kg, i.p.) and repeated (7.5 mg/kg/day x 14 days, i.p.) treatment with phencyclidine (PCP), a non-competitive antagonist of the N-methyl-D-aspartate(NMDA)-type glutamate receptor, using in vitro quantitative autoradiographic receptor binding assay. Both single and repeated PCP treatment produced heterogeneous changes in the rat brain in a similar manner, the magnitude of change in [125I] iomazenil binding being generally greater in the repeated treatment group than in the single treatment group. A significant increase in [125I] iomazenil binding was observed in the superficial layer (layer I-IV) of the parietal cortex in both of the PCP treatment groups and the CA1 of the hippocampus of the repeated PCP-treated group. There was a significant decrease in [125I] iomazenil binding in the piriform cortex of the repeated PCP-treated group. These results suggest that the blockade of NMDA receptor-mediated glutamatergic neurotransmission by PCP produces the compensational alterations in the central-type benzodiazepine receptor antagonist binding, and that the observed diversity may be due to dissimilar modes of organizations between glutamatergic and the GABA(gamma-aminobutyric acid)-benzodiazepine receptor complex.

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