GALANIN-5-HYDROXYTRYPTAMINE INTERACTIONS - ELECTROPHYSIOLOGICAL, IMMUNOHISTOCHEMICAL AND IN-SITU HYBRIDIZATION STUDIES ON RAT DORSAL RAPHE NEURONS WITH A NOTE ON GALANIN R1 AND R2 RECEPTORS

Galaninergic mechanisms related to 5-hydroxytryptamine neurons in the dorsal raphe nucleus of the rat were analysed using electrophysiology, immunohistochemistry and in situ hybridization. Galanin caused a dose -dependent hyperpolarization accompanied by a decrease in membrane res istance in most 5-hydroxytryptamine-sensitive dorsal raphe neurons. Th e galanin-induced outward current reversed at about -105 mV and shifte d to a more positive potential with increasing extracellular potassium concentrations. The 5-hydroxytryptamine-induced outward current was e nhanced and prolonged by preincubation with a low concentration of gal anin (1-10 nM). The immunohistochemical analysis showed (i) generally low levels of galanin in the 5-hydroxytriptamine cell bodies, (ii) mod erate numbers of galanin-positive nerve endings around the 5-hydroxytr yptamine cell bodies, (iii) presence of galanin-like immunoreactivity in 5-hydroxytryptamine-positive dendrites and (iv) galanin-positive, 5 -hydroxytryptamine-negative boutons making synaptic contact with 5-hyd roxytryptamine-positive dendrites. The in situ hybridization results s uggest that the galanin receptor present in the galanin/5-hydroxytrypt amine neurons is not of the recently cloned galanin-R1 type. Taken tog ether these results indicate that galanin exerts an inhibitory effect via an increase in K+ conductance in 5-hydroxytryptamine neurons by ac ting on a postsynaptic receptor. In addition, galanin at low, possibly physiological concentrations enhances the inhibitory effect of 5-hydr oxytryptamine at the cell soma level. We propose that galanin primaril y is released from adjacent galanin boutons lacking 5-hydroxytryptamin e and also from soma and dendrites of galanin/5-hydroxytryptamine dors al raphe neurons. Galanin may thus be involved in the manifold functio ns hitherto ascribed to ascending 5-hydroxytryptamine neurons, for exa mple in mood regulation. (C) 1998 IBRO. Published by Elsevier Science Ltd.