GALANIN RECEPTORS INHIBIT THE SPONTANEOUS FIRING OF LOCUS-CERULEUS NEURONS AND INTERACT WITH MU-OPIOID RECEPTORS

Electrophysiological experiments were performed in a pontine slice preparation of rat brain containing the locus coeruleus (LC). The extracellular part of this study showed that galanin (0.003-0.1 mumol/1), [Met5]enkephalin (0.01-10 mumol/l) and noradrenaline (0.1-100 mumol/l) concentration dependently inhibited the firing rate. Noradrenaline (1 and 3 mumol/l) had the same effect both before and during the application of galanin (0.001 or 0.01 mumol/l). Similarly, [Met5]enkephalin (0.03 and 0.1 mumol/l) produced identical inhibition, regardless of the presence or absence of 0.01 mumol/l galanin. Whereas rauwolscine (1 mumol/l) potentiated the effect of galanin (0.03 mumol/l), idazoxan (1 mumol/l) was inactive. In contrast, both naloxone (0.1 mumol/l) and beta-funaltrexamine (0.1 mumol/l) facilitated the galanin-induced inhibition. In the intracellular experiments, galanin (0.3 mumol/l) abolished the spontaneous discharge of action potentials, hyperpolarized the cells and decreased their input resistance. In conclusion, galanin may depress the firing rate by increasing a potassium permeability. Moreover, galanin receptors appear to interact with mu-opioid receptors but not with alpha2-adrenoceptors.