Effect of apamin, a toxin that inhibits Ca(2+)-dependent K+ channels, on learning and memory processes.
Apamin, a neurotoxin extracted from bee venom, specifically binds to a particular class of Ca(2+)-activated K+ channels which are involved in the slow afterhyperpolarization (S-AHP) that follows action potentials in many excitable cells. We tested in mice the effects of apamin on learning and memory processes. The results showed that pre-training injection of apamin accelerated the acquisition of a bar-pressing response but also increased the bar-pressing rates of the animals. This latter result suggests that apamin accelerated acquisition because it increased behavioral activity in general and the number of bar-presses in particular. Post-training apamin injection retroactively and non-contingently facilitated memory processes taking place shortly after training in a bar-pressing task. The lack of an effect of the delayed apamin injection showed that apamin did not act proactively on memory retrieval processes. These results suggest that apamin-sensitive KCa channels may contribute to memory processes.
Messier
C
C
Laboratoire de Psychophysiologie, URA CNRS no. 339, Université de Bordeaux I, Talence, France.
Mourre
C
C
Bontempi
B
B
Sif
J
J
Lazdunski
M
M
Destrade
C
C
D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects; D002118:Calcium / Q000502:physiology*; D007858:Learning / Q000187:drug effects*; D008297:Male; D008568:Memory / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D015221:Potassium Channels / Q000378:metabolism*
D015221:Potassium Channels; D001030:Apamin; D002118:Calcium