GABA and benzodiazepine receptors in the cat motor thalamus after lesioning of nigro- and pallidothalamic pathways.

Binding parameters of [3H]muscimol ([3H]MUS) and [3H]flunitrazepam ([ 3H]FLU) were determined in the thalamic area of overlap of nigro- and pallidothalamic pathways at short- (1-10 weeks) and long-term (6-11 months) survival times after kainic acid lesioning of substantia nigra pairs reticularis (SNr) and/or entopeduncular nucleus (EPN). No statistically significant lesion-induced changes in Kd could be established in any of the lesioned groups. Bmax values for both binding sites, when corrected for nerve cell densities, revealed some changes in all but one instance (no statistically significant changes in the number of [3H]MUS binding sites were detected after SNr lesions). Significant bilateral increase in the number of [3H]MUS binding sites was found after unilateral EPN and combined EPN + SNr lesions. In the first group the changes were transient; in the second, the number of binding sites appeared to be still on the rise at 8 months postlesion. The latter increase was interpreted as resulting from plasticity type changes in GABAergic local circuit neurons in response to massive deafferentation from extrinsic inhibitory inputs. Changes in [3H]FLU binding sites were of different character and of extremely low magnitude compared to changes in [3H]MUS binding sites. Subtle, but statistically significant, ipsilateral increase in the number of [3H]FLU binding sites as a function of time postlesion was found in the SNr lesioned group. In two other lesioned groups small magnitude increase occurred bilaterally, although in the EPN lesioned group it was more pronounced on the operated side. The results are consistent with earlier suggestion that [3H]MUS and [3H]FLU binding sites in the motor thalamus appear to be associated with different types of GABAergic synapses with none of them being directly associated with the basal ganglia thalamic pathways.