Abstract
Injections of cAMP-dependent, Ca2+/calmodulin-dependent, or Ca2+/phospholipid-dependent protein kinases into Hermissenda crassicornis type B photoreceptors are sufficient to induce many of the changes in B-cell excitability produced by associative conditioning. We report that inhibitors of Ca2+/phospholipid-dependent protein kinases, but not inhibitors of cyclic nucleotide- or Ca2+/calmodulin-dependent protein kinases, prevent the induction as well as continued expression of learning-produced changes in type-B-cell excitability: reductions of voltage-dependent and Ca2(+)-activated K+ currents. Our results represent a direct demonstration of long-term (days) experientially induced modulation of ion-channel activity that is dependent upon persistent kinase activity.
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