IONIC MECHANISM OF ACTION OF ADENOSINE ON THE RAT SUPERIOR CERVICAL-GANGLION

1 The ionic mechanism responsible for hyperpolarization of the rat sup erior cervical ganglion (SCG) and depression of the depolarizing respo nse to muscarine by adenosine was studied using an extracellular greas e-gap recording technique. 2 Both the hyperpolarizations to adenosine and 2-chloroadenosine and the depression of the response to muscarine by adenosine were potentiated in reduced external calcium (Ca2+). Hype rpolarizations to adenosine were either unaltered or potentiated in th e presence of the dihydropyridine Ca2+ channel antagonists, nitrendipi ne or (+)PN200 110 respectively. Hyperpolarizations to adenosine were unaltered by inorganic Ca2+ channel antagonists except for cobalt, whi ch also antagonized hyperpolarizations to carbachol and depolarization s to muscarine. 3 Hyperpolarizations to adenosine were unaltered in no minally magnesium (Mg2+)-free or in reduced external chloride (Cl-) me dia. When sodium ions (Na+) were replaced by lithium ions (Li+) maxima l responses to adenosine were initially enhanced, returning to pretrea tment levels and subsequently reduced in their duration. In contrast, responses to adenosine were significantly enhanced in nominally potass ium (K+)-free medium and reduced upon doubling the extracellular K+. 4 Hyperpolarisations were enhanced in the presence of the K+ channel an tagonists, 4-aminopyridine and 3,4-diaminopyridine, and reduced by a l ow concentration (2 mM) of tetraethylammonium (TEA), but not in 10 mm TEA. 5 The results support the hypothesis that adenosine-mediated hype rpolarization of postganglionic neurones of the rat SCG is by a Ca2+-i ndependent mechanism and is probably mediated via an increase of a Kcurrent. The results also indicate that adenosine-induced hyperpolariz ations of the rat SCG are independent of the presence of extracellular magnesium.