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

• Published in: Neuroscience Vol. 90; no. 2; pp. 595 - 606
• Main Authors: Ciombor, K.J, Ennis, M, Shipley, M.T
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.05.1999; Elsevier
• Subjects: adrenergic receptor; Afferent Pathways - physiology; Animals; Biological and medical sciences; brain slice; clonidine; Electric Stimulation; Evoked Potentials - drug effects; Evoked Potentials - physiology; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; locus coeruleus; Male; mitral cells; Neurons - drug effects; Neurons - physiology; Norepinephrine - pharmacology; odors; olfaction; olfactory bulb; Olfactory Bulb - drug effects; Olfactory Bulb - physiology; Olfactory Nerve - physiology; Olfactory system and olfaction. Gustatory system and gustation; phenylephrine; Phenylephrine - pharmacology; Prosencephalon - drug effects; Prosencephalon - physiology; Rats; Rats, Sprague-Dawley; Receptors, Adrenergic, alpha-1 - drug effects; Receptors, Adrenergic, alpha-1 - physiology; Sensory Thresholds; Smell; Vertebrates: nervous system and sense organs; olfactory bulb; ON, olfactory nerve; adrenergic receptor; olfaction; LC, locus coeruleus; locus coeruleus; ACSF, artificial cerebrospinal fluid; odors; NE, norepinephrine; EPL, external plexiform layer; MOB, main olfactory bulb; phenylephrine; IPL, internal plexiform layer; PSTH, peristimulus time histogram; MCL, mitral cell layer; GCL, granule cell layer; Vertebrata; Mammalia; Olfactory pathway; Mitral neuron; Rat; Rodentia; Olfactory nerve; Olfaction; Electrophysiology; α1-Adrenergic receptor; Norepinephrine; Catecholamine
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/S0306-4522(98)00437-0

A rat olfactory bulb in vitro slice preparation was used to investigate the actions of norepinephrine on spontaneous and afferent (olfactory nerve) evoked activity of mitral cells. Single olfactory nerve shocks elicited a characteristic mitral cell response consisting of distinct, early and late spiking components separated by a brief inhibitory epoch. Bath-applied norepinephrine (1 μM) increased the early spiking component elicited by perithreshold (79% increase, P<0.02), but not by suprathreshold (3% decrease, P>0.05), intensity olfactory nerve shocks. The facilitatory effect of norepinephrine was due to a reduction in the incidence of response failures to perithreshold intensity shocks. Norepinephrine also decreased the inhibitory epoch separating the early and late spiking components by 44% ( P<0.05). By contrast, norepinephrine had no consistent effect on the spontaneous discharge rate of the mitral cells. The effects of norepinephrine were mimicked by the α1 receptor agonist phenylephrine (1 μM, P<0.001). Both norepinephrine and phenylephrine modulation of mitral cell responses were blocked by the α1 adrenergic antagonist WB-4101 (1 μM). These findings are consistent with observations that the main olfactory bulb exhibits the highest density of α1 receptors in the brain. The α2 receptor agonist clonidine (100 nM) and the β receptor agonist isoproterenol (1 μM) had inconsistent effects on mitral cell spontaneous and olfactory nerve-evoked activity. These results indicate that norepinephrine increases mitral cell excitatory responses to weak but not strong olfactory nerve inputs in vitro via activation of α1 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 may increase the sensitivity of mitral cells to weak odors. Olfactory cues evoke norepinephrine release in the main olfactory bulb, and norepinephrine plays important roles in early olfactory learning and reproductive/maternal behaviors. By increasing mitral cell responses to olfactory nerve input, norepinephrine may play a critical role in modulating olfactory function, including formation and/or recall of specific olfactory memories.