ИСТИНА |
Войти в систему Регистрация |
|
ИПМех РАН |
||
In previous studies we have shown that Ca2+ entering the terminal through L-type Ca2+-channels triggers the release of intracellular Ca2+ from ryanodine stores, which in turn leads to depression of ACh release in reinnervated mouse neuromuscular junctions. Ca2+-dependent protein kinase C which is known (along with other substrates) to modulate the activity of voltage-dependent K+-channels (Kv) was considered as a possible target for this Ca2+ signal.