The role of fast inactivating (IA) voltage gated K+ channel function in shaping the fi ring activity of Purkinje cells (PCs) in ataxic rats was investigated. Ataxia was induced in 5 week-old male rats of Sprauge-Dawley by single injection of 3-acethylpyridine (65 mg/kg, i.p.). Four days following induction of ataxia, etheranesthetized rats were decapitated; brains rapidly removed and 300 μm thick parasagittal slices were prepared from the vermis of the cerebellum. Whole cell patch clamp recording was achieved in the presence of synaptic blockers. To prevent the induction of ataxia, 4-AP (2 mg/kg body weight), IA channel blocker, was injected prior to 3-AP treatment. Results indicated that in ataxic rats, the latency of the initial spike in PCs was signifi cantly increased (P<0.001), while both fi ring frequency and amplitude of Ca2+ spikes were (P<0.001) suppressed compared to control. However, pretreatment with 4-AP not only almost completely prevented the neuronal degeneration in PCs layer but also the development of ataxia, which occurred in ataxic rats. PCs in rats co-treated with 4-AP and 3-AP fi red predominantly in rhythmic bursts. The amplitude of Ca2+ spikes was signifi cantly (P<0.001) increased compared to ataxic rats. An increase in the intrinsic excitability of PCs was also observed as a signifi cant decrease in the fi rst spike latency (P<0.001). In 4-AP co-treated rats, the duration of action potential was also signifi cantly lengthened (P<0.001).
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