Properties of ligand-gated potassium channels in neurons of rat dorsolateral septal nucleus.

Properties of ligand-gated K+ channels were examined in neurons of rat dorsolateral septal nucleus (DLSN). Application of muscarine (30 microM), 5-hydroxytryptamine (5-HT, 10 microM), adenosine (100 microM), baclofen (10 microM) and norepinephrine (NE, 10 microM) 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 Ba(2+)-sensitive K+ channels, probably the GTP-binding protein (G-protein) activated inward rectifier K+ (GIRK) channels in DLSN neurons.