Norepinephrine increases rat mitral cell excitatory responses to weak olfactory nerve input via alpha-1 receptors in vitro

A rat olfactory bulb in vitro slice preparation was used to investigate the actions of norepinephrine on spontaneous and afferent (olfactory nerve) ev oked activity of mitral cells. Single olfactory nerve shocks elicited a cha racteristic mitral cell response consisting of distinct, early and late spi king components separated by a brief inhibitory epoch. Bath-applied norepin ephrine (1 mu M) increased the early spiking component elicited by perithre shold (79% increase, P<0.02), but not by suprathreshold (3% decrease, P>0.0 5), intensity olfactory nerve shocks. The facilitatory effect of norepineph rine was due to a reduction in the incidence of response failures to perith reshold intensity shocks. Norepinephrine also decreased the inhibitory epoc h separating the early and late spiking components by 44% (P<0.05). By cont rast, norepinephrine had no consistent effect on the spontaneous discharge rate of the mitral cells. The effects of norepinephrine were mimicked by th e alpha 1 receptor agonist phenylephrine (1 mu M, P<0.001). Both norepineph rine and phenylephrine modulation of mitral cell responses were blocked by the alpha 1 adrenergic antagonist WB-4101 (1 mu M). These findings are cons istent with observations that the main olfactory bulb exhibits the highest density of alpha 1 receptors in the brain. The alpha 2 receptor agonist clo nidine (100 nM) and the beta receptor agonist isoproterenol (1 mu M) had in consistent effects on mitral cell spontaneous and olfactory nerve-evoked ac tivity. These results indicate that norepinephrine increases mitral cell excitatory responses to weak but not strong olfactory nerve inputs in vitro via activ ation of al receptors. This is consistent with recent findings in vivo that synaptically released norepinephrine preferentially increases mitral cell excitatory responses to weak olfactory nerve inputs. Taken together, these results suggest that the release of norepinephrine in the olfactory bulb ma y increase the sensitivity of mitral cells to weak odors. Olfactory cues ev oke norepinephrine release in the main olfactory bulb, and norepinephrine p lays important roles in early olfactory learning and reproductive/maternal behaviors. By increasing mitral cell responses to olfactory nerve input, no repinephrine may play a critical role in modulating olfactory function, inc luding formation and/or recall of specific olfactory memories. (C) 1999 IBR O. Published by Elsevier Science Ltd.