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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

GABA, THIP and baclofen inhibition of Purkinje cells and cerebellar nuclei neurons.

The sensitivity of Purkinje cells (PCs) and neurons of the cerebellar nuclei (NCNs) to iontophoretic application of gamma-aminobutyric acid (GABA), 4,5,6,7-tetrahydroisoxazolo(5,4-c)pyridin-3-ol (THIP) and baclofen, i.e., GABAA and GABAB agonists respectively, have been studied in anesthetized rats. All the agonists produced dose-dependent firing rate depression of the PCs but with different potencies. The inhibitory actions of both GABA and THIP were specifically antagonized by bicuculline (Bic) and the baclofen-induced responses by 2-hydroxysaclofen. GABA and THIP also depressed the spontaneous activity of NCNs while baclofen was ineffective. The present results therefore suggest that GABAA receptors are involved in the GABA-induced inhibition in the cerebellar cortex and in the cerebellar nuclei and GABAB receptors are involved only in the cerebellar cortex.[1]


  1. GABA, THIP and baclofen inhibition of Purkinje cells and cerebellar nuclei neurons. Billard, J.M., Vigot, R., Batini, C. Neurosci. Res. (1993) [Pubmed]
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