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α 1 ‐Adrenoceptor‐activated cation currents in neurones acutely isolated from rat cardiac parasympathetic ganglia
Author(s) -
Ishibashi Hitoshi,
Umezu Mari,
Jang IlSung,
Ito Yushi,
Akaike Norio
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2003.00111.x
Subject(s) - medicine , chemistry , endocrinology , neuroscience , adrenergic receptor , biophysics , biology , receptor
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 Ca 2+ or Mg 2+ , with a half‐maximal concentration of 13 μ m for Ca 2+ and 1.2 m m for Mg 2+ . Cirazoline mimicked the NA response, and prazosin and WB‐4101 inhibited the NA‐induced current, suggesting the contribution of an α 1 ‐adrenoceptor. The NA‐induced current was inhibited by U73122, a phospholipase C (PLC) inhibitor. The membrane‐permeable IP 3 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 Ca 2+ ‐ and Mg 2+ ‐sensitive cation channels via α 1 ‐adrenoceptors in neurones freshly isolated from rat cardiac parasympathetic ganglia. This activation mechanism also involves phosphoinositide breakdown, release of Ca 2+ from intracellular Ca 2+ stores and calmodulin. The cation channels activated by NA may play an important role in neuronal membrane depolarization in rat cardiac ganglia.