Transient increase in [3H]Ro 15-4513 specific binding in the superficial gray layer of the rat superior colliculus induced by visual deafferentation.

The imidazodiazepine compound [3H]Ro 15-4513, a partial inverse agonist of benzodiazepine receptors of the central type, binds with high affinity (order of 10(-8) M) to a single population of benzodiazepine binding sites in the mammalian central nervous system. A quantitative autoradiographic study was carried out to determine the effects of one eye removal on [3H]Ro 15-4513 specific binding to rat brain sections in the superficial gray layer or stratum griseum superficiale (SGS) of the superior colliculus. Retinal afferent degeneration due to right eye removal, performed 3 and 7 days before sacrifice, led to a significant and symmetrical increase in the [3H]Ro 15-4513 specific binding in both right and left SGS by enhancing the binding affinity of the radioligand. This transient phenomenon disappeared when a longer survival period of 45 days was allowed to elapse. Conversely, unilateral lesion of the primary visual areas had no apparent effects on the specific binding of the radioligand. The absence of any loss of binding sites after either type of lesion suggests that the benzodiazepine receptors are probably not situated on the optic nerve axon terminals, nor on the cortical axon terminals originating from primary visual areas. In the SGS, as in other rat brain structures, benzodiazepine receptors of the central type are functionally coupled with GABAA receptors and form 'GABAA receptors/benzodiazepine receptors/chloride channel' complexes. The involvement of the local GABAergic system in the postlesion plasticity of benzodiazepine receptors was studied by testing the effects of exogenously applied GABA on [3H]Ro 15-4513 specific binding.(ABSTRACT TRUNCATED AT 250 WORDS)