GABA-induced responses in Purkinje cell dendrites of the rabbit cerebellar slice

Abstract

Pressure applications of GABA localized to Purkinje cell somas in a rabbit cerebellar slice produced uniphasic hyperpolarizing responses, whereas applications of GABA that were directed at the Purkinje cell dendrites produced complex, triphasic responses with hyperpolarizing and depolarizing components. Both somatic and dendritic application of GABA elicited fast hyperpolarization (GABA hf), but dendritic application also elicited a slower depolarization (GABA d) and a later, long-lasting hyperpolarization (GABA hf). All three types of responses were accompanied by increased conductance. Use of either GABA antagonist, bicuculline or picrotoxin, eliminated the GABA hf and GABA d responses but left the GABA hl response intact. Pressure delivery of the GABA agonist, baclofen, to the dendrites but not the soma elicited a GABA hl response. Application of baclofen paired with membrane depolarization sufficient to elicit local, calcium-dependent dendritic spiking produced a persistent reduction in the GABA hl response, whereas alternating presentations of baclofen and membrane depolarization or presentations of baclofen alone could not. The fact that GABA and baclofen inhibited Purkinje cell activity in the rabbit cerebellar slice and that picrotoxin and bicuculline eliminated some, but not all of the components of the GABA response suggests the presence of both GABA A and GABA B receptors. The ability of baclofen to inhibit Purkinje cells if it was applied to the applied to the soma suggests that GABA B receptors are located predominantly on Purkinje cell dendrites. The pairing-specific change in the baclofen response suggests the existence of GABA B-mediated modifiability of Purkinje cell dendrites. Taken together, the present data provide the first electrophysiological evidence that (1) GABA A receptors are located predominantly at the Purkinje cell soma, (2) GABA B receptors are located predominantly on Purkinje cell dendrites, and (3) these GABA B receptors may be susceptible to modification.