1997 Volume 44 Issue 2 Pages 125-133
Properties of ligand-gated K+ channels were examined in neurons of rat dorsolateral septal nucleus (DLSN). Application of muscarine (30μM), 5-hydroxytryptamine (5-HT, 10μM), adenosine (100μM), baclofen (10μM) and norepinephrine (NE, 10μM) to DLSN neurons caused hyperpolarizing responses associated with decreased membrane resistance. Hyperpolarizations induced by muscarine increased their amplitudes at membrane potential between -70 and -50 mV. Baclofen- and NE-induced hyperpolarizations were less sensitive to voltage. The agonist-induced hyperpolarizations decrease in amplitudes and reversed at a membrane potential between -90 and -100 mV. Ba2+ (1 mM) blocked all agonist-induced hyperpolarizations in DLSN neurons. Tetraethylammonium (TEA, 3 mM) blocked the muscarine-induced hyperpolarization but not the hyperpolarizations induced by the other agonists. Extracellular Cs+ and glibenclamide did not block the agonist-induced hyperpolarizations. These results suggest that muscarine, 5-HT, adenosine, baclofen and NE cause the hyperpolarization by increasing the activity of Ba2+-sensitive K+ channels, probably the GTP-binding protein (G-protein) activated inward rectifier K+ (GIRK) channels in DLSN neurons.
