抄録
Cerebellar Purkinje cells highly express B-type G-protein-coupled γ-aminobutyric acid receptors (GABABR). However, the functional contribution of GABABR is not fully elucidated in this cell type. Here we identified a GABABR agonist (baclofen)-induced inwardly rectifying current (Ibacl) in cultured mouse Purkinje cells, using a ruptured-patch whole-cell technique. Ibacl is coupled to GABABR via Gi/o-proteins as it is not inducible in pertussis toxin-treated cells. Ibacl is carried by K+ but not Na+. Ibacl is blocked by Ba2+, Cs+, and tertiapin-Q. Ibacl is activated rapidly upon hyperpolarization with a double-exponential time-course (time constants, 0.8 and 80 ms). These results indicate that Ibacl is mediated by G-protein-coupled inwardly rectifying K+ channels. Perforated-patch recordings demonstrate that Ibacl hyperpolarizes the resting potential and the peak level of glutamate-evoked potentials initiated in the dendrites. Moreover, cell-attached recordings in cerebellar slices demonstrate that Ibacl slows down the rate of spontaneous firing. Ibacl activation via GABABR reduces the postsynaptic and intrinsic excitability of Purkinjes and may thereby influence the integration of motor information conveyed by excitatory parallel and climbing fibers. [Jpn J Physiol 55 Suppl:S150 (2005)]
