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Resting and depolarization-induced 45CaCl2 accumulation was compared for synaptosomes isolated from hibernating and nonhibernating ground squirrels. Channel subtype antagonists were used to identify the active voltage-sensitive calcium channel subtypes in these preparations. There was significantly less 45Ca2+ accumulation in synaptosomes isolated from hibernating as compared to cold-adapted nonhibernating ground squirrels in both basal (p < 0.005) and depolarizing (p < 0.03) media over a 30 sec to 5 min incubation period. The elevation in 45Ca2+ accumulation triggered by K+ depolarization was blocked by 50 microM CdCl2, 1 microM omega-conotoxin MVIIC or 1 microM omega-agatoxin IVA. Inhibition was not observed with 1 microM nifedipine or with 1 microM omega-conotoxin GVIA. These results suggest that hibernation is associated with reduced presynaptic 45Ca2+ conductance via voltage-sensitive channels with a pharmacological sensitivity that is different from the established L-, N-, and P-types in other systems but share features of the recently described Q-type calcium channel. This decrease may reflect a cellular adaptation that helps confer tolerance to the near total cerebral ischemia associated with hibernation.
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