1. The proposed mechanism of cellular plasticity underlying classical conditioning of Hermissenda involves Ca2+ influx through voltage-activated channels. This influx triggers several molecular cascades and leads to the phosphorylation of K+ channels in identified photoreceptors. We studied Ca2+ currents from isolated photoreceptors of Hermissenda with the whole cell patch-clamp technique. Two distinct Ca2+ currents were identified in isolated photoreceptors on the basis of differences in their voltage dependence, kinetics, and pharmacology. 2. One Ca2+ current was transient (I(Ca(t))), with a fast onset (~5 ms), activated at -50 mV from a holding potential of -90 mV, and peaked at 0 mV. The second Ca2+ current, designated as sustained (I(Ca(s))), exhibited a delayed time-to-peak, activated at -30 mV, and reached maximum at 30 mV. 3. Steady-state activation curves for both currents were generated from normalized currents and fitted with the Boltzmann function; estimates of half-activation voltages for I(Ca(t)) were -38.8 ± 6.7 mV (mean ± SD; n = 9) and 3.2 ± 8.2 mV for I(Ca(s)) (n = 11) with maximum slopes of 8.9 ± 1.6 mV (n = 9) and 11.0 ± 2.4 mV (n = 11). 4. The inactivation of I(Ca(s)) was slow (time constants >3 s) whereas I(Ca(t)) inactivated rapidly (time constant of inactivation at various voltages; 75-600 ms). 5. Ni2+ (0.8 mM), Gd3+ (0.5 mM), and amiloride (10 μM) produced a reversible block of I(Ca(t)) without affecting I(Ca(s)). ω-Conotoxin GVIA (10 nM) irreversibly blocked I(Ca(s)) whereas nitrendipine (20 μM) produced a reversible block. 6. I(Ca(t)) may be responsible for steady-state membrane potential oscillations, I(Ca(s)) may contribute to the maintenance of the amplitude of the plateau phase of the generator potential.
|Original language||English (US)|
|Number of pages||10|
|Journal||Journal of Neurophysiology|
|State||Published - 1994|
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