Alpha 1-adrenoceptor-activated cation currents in neurones acutely isolated from @entity35 cardiac parasympathetic XXXX .

@entity2426 @entity1025 @entity13397 @entity141 @entity3159 @entity9423 @entity9422 @entity11008 @entity1359 @entity10756 @entity4515 @entity4385 @entity866 @entity35 @entity21 @entity1063 @entity8701 @entity20253
The @entity1063 (NA)-induced cation current was investigated in neurones freshly isolated from @entity35 cardiac parasympathetic @entity21 using the @entity8701 -perforated patch recording configuration. Under current-clamp conditions, NA depolarized the membrane, eliciting repetitive action potentials. NA evoked an inward cation current under voltage-clamp conditions at a holding potential of -60 mV. The NA-induced current was inhibited by extracellular @entity141 or @entity1025 , with a half-maximal concentration of 13 microM for @entity141 and 1.2 mM for @entity1025 . @entity20253 mimicked the NA response, and @entity3159 and @entity13397 inhibited the NA-induced current, suggesting the contribution of an alpha1-adrenoceptor. The NA-induced current was inhibited by @entity4385 , a phospholipase C (PLC) inhibitor. The membrane-permeable @entity9423 blocker @entity9422 also blocked the NA-induced current. Furthermore, pretreatment with @entity2426 and @entity11008 could inhibit the NA response while @entity10756 , @entity1359 ( @entity4515 ) and @entity866 had no effect. These results suggest that NA activates the extracellular @entity141 - and @entity1025 -sensitive cation channels via alpha 1-adrenoceptors in neurones freshly isolated from @entity35 cardiac parasympathetic @entity21 . This activation mechanism also involves phosphoinositide breakdown, release of @entity141 from intracellular @entity141 stores and calmodulin. The cation channels activated by NA may play an important role in neuronal membrane depolarization in @entity35 cardiac @entity21 .
