In vivo release of [ 3H]GABA in cat caudate nucleus and substantia nigra. II. Involvement of different thalamic nuclei in the bilateral changes induced by a nigral application of muscimol

Abstract

The contribution of motor and intralaminar thalamic nuclei to the changes of [ 3H]GABA release evoked in both caudate nuclei (CN) and both substantia nigra (SN) by a unilateral nigral application of muscimol (10 −6 M) was investigated on halothane-anaesthetized cats. Acute lesions were performed on one side of the thalamus at the level of either the ventralis medialis and ventralis lateralis (motor nuclei) or the centralis lateralis and paralamellar zone of the medialis dorsalis (intralaminar nuclei). The release of [ 3H]GABA neosynthesized from [ 3H]glutamine was measured by perfusing continuously a [ 3H]glutamine-enriched physiological medium through a push-pull cannula implanted in the 4 structures under investigation. After two hours of superfusion, muscimol (10 −6 M) was delivered for 60 min through the nigral push-pull cannula implanted ipsilaterally to the thalamic lesion. Evoked changes of [ 3H]GABA release were analyzed either in motor or intralaminar nuclei lesioned cats and compared to those observed in intact animals. Whatever the localization of the thalamic lesions was, an increased release of [ 3H]GABA was elicited locally in the SN and distally in the ipsilateral CN as in intact animals, suggesting that the responses induced ipsilaterally did not require nigro-thalamic pathways. On the contrary, in the contralateral CN changes of [ 3H]GABA release evoked by the nigral muscimol application were reversed by both types of thalamic lesion. Instead of a decreased release of [ 3H]GABA observed in intact cats, and increased release of [ 3H]GABA was detected in lesioned animals. In the contralateral SN, the response was reversed only after the intralaminar nuclei lesion. In this situation nigral muscimol application induced a decreased release of [ 3H]GABA in contrast to the enhanced release observed in intact and motor thalamic lesioned cats. The parallel increased release of [ 3H]GABA observed in the contralateral CN and SN in motor thalamic nuclei lesioned cats suggests an activation of the striatonigral cells by the nigral muscimol treatment. The asymmetrical changes of [ 3H]GABA release measured in the contralateral CN and SN in intact and intralaminar nuclei lesioned cats could indicate a presynaptic modulation of the [ 3H]GABA release acting either at the CN or the SN levels. The possible pathways involved in the interhemispheric transfer of information originating from one SN to the contralateral basal ganglia components are also discussed.