α1‐Adrenoceptor‐activated cation currents in neurones acutely isolated from rat cardiac parasympathetic ganglia
α1‐Adrenoceptor‐activated cation currents in neurones acutely isolated from rat cardiac parasympathetic ganglia
复制标题
从大鼠心脏副交感神经节中急性分离的神经元中α1-肾上腺素受体激活的阳离子电流
DOI:
10.1111/j.1469-7793.2003.00111.x
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发表时间:
2003
期刊:
影响因子:
--
通讯作者:
N. Akaike
中科院分区:
文献类型:
--
作者:
H. Ishibashi;M. Umezu;I. Jang;Y. Ito;N. Akaike
The noradrenaline (NA)‐induced cation current was investigated in neurones freshly isolated from rat cardiac parasympathetic ganglia using the nystatin‐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 Ca2+ or Mg2+, with a half‐maximal concentration of 13 μm for Ca2+ and 1.2 mm for Mg2+. Cirazoline mimicked the NA response, and prazosin and WB‐4101 inhibited the NA‐induced current, suggesting the contribution of an α1‐adrenoceptor. The NA‐induced current was inhibited by U73122, a phospholipase C (PLC) inhibitor. The membrane‐permeable IP3 receptor blocker xestospongin‐C also blocked the NA‐induced current. Furthermore, pretreatment with thapsigargin and BAPTA‐AM could inhibit the NA response while KN‐62, phorbol 12‐myristate 13‐acetate (PMA) and staurosporine had no effect. These results suggest that NA activates the extracellular Ca2+‐ and Mg2+‐sensitive cation channels via α1‐adrenoceptors in neurones freshly isolated from rat cardiac parasympathetic ganglia. This activation mechanism also involves phosphoinositide breakdown, release of Ca2+ from intracellular Ca2+ stores and calmodulin. The cation channels activated by NA may play an important role in neuronal membrane depolarization in rat cardiac ganglia.
影响因子:
--
作者:
ARDELL, JL;RANDALL, WC
通讯作者:
RANDALL, WC
影响因子:
2.5
作者:
Xu,ZJ;Adams,DJ
通讯作者:
Adams,DJ
影响因子:
2.5
作者:
Chen,C;Schofield,GG
通讯作者:
Schofield,GG