Apart from their primary function as balance sensors, Hermissenda hair cells are presynaptic neurons involved in the Ca2+ -dependent neuronal plasticity in postsynaptic B photoreceptors that accompanies classical conditioning. With a view to beginning to understand presynaptic mechanisms of plasticity in the vestibulo-visual system, a locus for conditioning- induced neuronal plasticity, outward currents that may govern the excitability of hair cells were recorded by means of a whole-cell patch- clamp technique. Three K+ currents were characterized: a 4-aminopyridine- sensitive transient outward K+ current (I(A)), a tetraethyl ammonium- sensitive delayed rectifier K+ current (I(K,V)), and a Ca2+-activated K+ current (I(K,Ca)). I(A) activates and decays rapidly; the steady-state activation and inactivation curves of the current reveal a window current close to the apparent resting voltage of the hair cells, suggesting that the current is partially activated at rest. By modulating firing frequency and perhaps damping membrane oscillations, I(A) may regulate synaptic release at baseline. In contrast, I(K,V) and I(K,Ca) have slow onset and exhibit little or no inactivation. These two K+ currents may determine the duration of the repolarization phase of hair-cell action potentials and hence synaptic release via Ca2+ influx through voltage-gated Ca2+ channels. In addition, I(K,Ca) may be responsible for the afterhyperpolarization of hair cell membrane voltage following prolonged stimulation.
|Original language||English (US)|
|Number of pages||11|
|State||Published - Jan 1997|
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