Voltage-gated calcium channels in adult rat inferior colliculus neurons

Abstract

The inferior colliculus (IC) plays a key role in the processing of auditory information and is thought to be an important site for genesis of wild running seizures that evolve into tonic–clonic seizures. IC neurons are known to have Ca 2+ channels but neither their types nor their pharmacological properties have been as yet characterized. Here, we report on biophysical and pharmacological properties of Ca 2+ channel currents in acutely dissociated neurons of adult rat IC, using electrophysiological and molecular techniques. Ca 2+ channels were activated by depolarizing pulses from a holding potential of −90 mV in 10 mV increments using 5 mM barium (Ba 2+) as the charge carrier. Both low (T-type, VA) and high (HVA) threshold Ca 2+ channel currents that could be blocked by 50 μM cadmium, were recorded. Pharmacological dissection of HVA currents showed that nifedipine (10 μM, L-type channel blocker), ω-conotoxin GVIA (1 μM, N-type channel blocker), and ω-agatoxin TK (30 nM, P-type channel blocker) partially suppressed the current by 21%, 29% and 22%, respectively. Since at higher concentration (200 nM) ω-agatoxin TK also blocks Q-type channels, the data suggest that Q-type Ca 2+ channels carry approximately 16% of HVA current. The fraction of current (approximately 12%) resistant to the above blockers, which was blocked by 30 μM nickel and inactivated with τ of 15–50 ms, was considered as R-type Ca 2+ channel current. Consistent with the pharmacological evidences, Western blot analysis using selective Ca 2+ channel antibodies showed that IC neurons express Ca 2+ channel α 1A, α 1B, α 1C, α 1D, and α 1E subunits. We conclude that IC neurons express functionally all members of HVA Ca 2+ channels, but only a subset of these neurons appear to have developed functional LVA channels.