A number of studies have suggested the existence of multiple benzodiazepine binding sites in the brain1-20. We have recently reported the physical separation of two apparent benzodiazepine binding site subtypes 21, the pharmacological properties, and distribution in tissue sections of which correspond to the putative type I and type II sites 20,22. Benzodiazepine and γ-aminobutyric acid (GABA) receptors have been shown to interact23, and lesions of the GABAergic striatonigral pathway, which lead to GABA supersensitivity24,25, both increase the numbers of GABA binding sites24,26 and enhance GABA-stimulated benzodiazepine binding27. We demonstrate here that degeneration of striatonigral fibres increases the density of putative type I benzodiazepine binding sites in the substantia nigra and decreases the density of the putative type II sites. This suggests that type I sites that increase after denervation are postsynaptic, whereas the type II sites reduced by the lesion may be localized to axons or terminals of the striatonigral pathways.
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