NORADRENALINE MODIFIES THE SPONTANEOUS SPIKING ACTIVITY OF RED NUCLEUS NEURONS IN THE RAT BY ACTIVATION OF ALPHA(2)-ADRENOCEPTOR AND BETA-ADRENOCEPTOR

We have investigated the effects of noradrenaline (NA) on the spontane ous firing activity of red nucleus (RN) neurons recorded extracellular ly in anesthetized rats by using an in vivo electrophysiological techn ique. Microiontophoretic applications of NA (5-100 nA for 30 s) modifi ed the background firing rate in 99 out of 124 neurons and three diffe rent patterns of response were observed in distinct cells. In 61% of t he responding neurons NA decreased the mean firing rate, whereas 22% o f the neurons responded to NA application with an increase of their sp iking activity; in a smaller group of cells (17%) NA exerted a biphasi c inhibitory/excitatory effect on the spontaneous firing rate. The eff ects of NA were reversible and dose-dependent. From histological exami nation, the neurons responding to NA with a purely inhibitory effect w ere scattered throughout the RN. On the other hand, the neurons respon ding to NA with an excitation were found to be more numerous in the do rso-medial part of the RN, whereas the neurons in which NA induced bip hasic effects appeared to be segregated in the outer lateral portion o f the RN. The alpha(2)-adrenoceptor antagonist yohimbine completely bl ocked the inhibitory effect of NA but was unable to antagonize the exc itatory response. In addition, the inhibitory effect of NA was mimicke d by clonidine, a selective agonist of alpha(2)-adrenoceptors; clonidi ne had no effect on those cells which responded to NA with an increase of the mean firing rate. The excitatory effect of NA was mimicked by the P-receptor agonist isoprenaline and was antagonized by timolol, a selective antagonist of beta-adrenoceptors. Isoprenaline was ineffecti ve in those cells in which NA exerted inhibitory responses. Taken toge ther, our results indicate that the inhibitory effects of NA on the fi ring activity of rat RN neurons were mediated by alpha(2)-adrenoceptor s, whereas beta-adrenoceptors were responsible for the excitatory effe cts.