Norepinephrine inhibits a subset of hippocampal interneurons.
The inhibitory effect of NE on these interneurons is mediated by an [alpha] adrenergic receptor (AR), as the effect of NE was mimicked by the [alpha] AR agonist 6-fluoronorepinephrine, but not the [beta] AR agonist isoproterenol. The AR appears to be an [[alpha].sub.2] subtype, as the selective [[alpha].sub.2] AR agonists, [alpha]-methylnorepinephrine and oxymetazoline, similarly hyperpolarized these cells. In addition, the NE-induced hyperpolarization was inhibited by atipamezole, a selective [[alpha].sub.2] AR antagonist, but not by YM-12617, a selective [[alpha].sub.1] AR antagonist. The amplitude of pharmacologically isolated late inhibitory postsynaptic potentials (IPSPs) evoked in CA 1 pyramidal neurons was reduced by NE. This effect also was blocked by atipamezole, a selective [[alpha].sub.2] AR antagonist. In addition, this effect was occluded by prior application of the opioid, [D-[Ala.sup.2]]-methionine-enkephalinamide (DALA), which hyperpolarizes interneurons, suggesting that the inhibition of the late IPSP by NE may result from the [[alpha].sub.2] AR-mediated hyperpolarization of interneurons located in stratum lacunosummoleculare.
The inhibition of the late IPSP by NE caused a time-dependent increase in the excitability of CA1 pyramidal neurons by reducing the amplitude of the after-hyperpolarization following afferent stimulation.
(1) Dwight E. Bergles and (2) Van A. Doze *
(1) Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, and
(2) Department of Pharmacology, Physiology & Therapeutics, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58202
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|Title Annotation:||COMMUNICATIONS: PROFESSIONAL|
|Author:||Bergles, Dwight E.; Doze, Van A.|
|Publication:||Proceedings of the North Dakota Academy of Science|
|Date:||Mar 1, 2003|
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