Reduced delayed-rectifier K+ current in the learning mutant rutabaga

Abstract

In the Drosophila mutant rutabaga, short-term memory is deficient and intracellular cyclic adenosine monophosphate (cAMP) concentration is reduced. We characterized the delayed-rectifier potassium current (IKDR) in rutabaga as compared with the wild-type. The conventional whole-cell patch-clamp technique was applied to cultured Drosophila neurons derived from embryonic neuroblasts. IKDR was smaller in rutabaga (368 ± 11 pA) than in wild-type (541 ± 14 pA) neurons, measured in a Ca2+-free solution. IKDR was clearly activated at ∼0 mV in the two genotypes. IKDR typically reached its peak within 10-20 msec after the start of the pulse (60 mV). There was no difference in inactivation of IKDR for wild-type (14 ± 3%) and rutabaga (19 ± 3%). After application of 10 mM TEA, in wild-type, IKDR was reduced by 46 ± 5%, whereas in rutabaga, IKDR was reduced by 28 ± 3%. Our results suggest that IKDR is carried by two different types of channels, one which is TEA-sensitive, whereas the other is TEA-insensitive. Apparently, the TEA-sensitive channel is less expressed in rutabaga neurons than in wild-type neurons. Conceivably, altered neuronal excitability in the rutabaga mutant could disrupt the processing of neural signals necessary for learning and memory.