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 (IK(DR)) 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. IK(DR) was smaller in rutabaga (368 +/- 11 pA) than in wild-type (541 +/- 14 pA) neurons, measured in a Ca(2+)-free solution. IK(DR) was clearly activated at approximately 0 mV in the two genotypes. IK(DR) typically reached its peak within 10-20 msec after the start of the pulse (60 mV). There was no difference in inactivation of IK(DR) for wild-type (14 +/- 3%) and rutabaga (19 +/- 3%). After application of 10 mM TEA, in wild-type, IK(DR) was reduced by 46 +/- 5%, whereas in rutabaga, IK(DR) was reduced by 28 +/- 3%. Our results suggest that IK(DR) 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.
