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Titolo:
Norepinephrine modulates single hypothalamic arcuate neurons via alpha(1) and beta adrenergic receptors
Autore:
Kang, YM; Ouyang, W; Chen, JY; Qiao, JT; Dafny, N;
Indirizzi:
Univ Texas, Sch Med, Dept Neurobiol & Anat, Houston, TX 77225 USA Univ Texas Houston TX USA 77225 t Neurobiol & Anat, Houston, TX 77225 USA Shanxi Med Univ, Dept Neurobiol, Taiyuan 030001, Shanxi, Peoples R China Shanxi Med Univ Taiyuan Shanxi Peoples R China 030001 xi, Peoples R China
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 869, anno: 2000,
pagine: 146 - 157
SICI:
0006-8993(20000630)869:1-2<146:NMSHAN>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
SENSITIVE POTASSIUM CHANNELS; INDUCED ANTINOCICEPTION; ENDOGENOUS OPIOIDS; PAIN MODULATION; LOCUS COERULEUS; DORSAL RAPHE; SPINAL LEVEL; GUINEA-PIG; RAT-BRAIN; NUCLEUS;
Keywords:
arcuate neurons; norepinephrine; phentolamine; prazosin; yohimbine; propranolol; naloxone; morphine; glibenclamide; cromakalim; brain slice; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Dafny, N Univ Texas, Sch Med, Dept Neurobiol & Anat, Houston, TX 77225 USAUniv Texas Houston TX USA 77225 ol & Anat, Houston, TX 77225 USA
Citazione:
Y.M. Kang et al., "Norepinephrine modulates single hypothalamic arcuate neurons via alpha(1) and beta adrenergic receptors", BRAIN RES, 869(1-2), 2000, pp. 146-157

Abstract

The effects of norepinephrine (NE) on the electrophysiological activities of single hypothalamic arcuate neurons were studied using extracellular recording of 385 neurons from 169 brain slices in rats. The results showed that: (1) of 236 neurons selected randomly and tested with NE application, 137(58.0%) were excited, 67 (28.4%) were inhibited, and 32 (13.6%) failed to respond; (2) substitution of low Ca2+-high Mg2+ artificial cerebrospinal fluid (ACSF) for normal ACSF abolished the NE-induced inhibitory effect but failed to abolish the excitatory effect; (3) both the NE-induced excitatory and inhibitory effects were antagonized partly by phentolamine, prazosin, and propranolol but not by yohimbine; (4) naloxone and glibenclamide, a blocker of adenosine triphosphate-sensitive (K-ATP) channels, blocked the NE-induced inhibitory effect; and (5) neurons that were inhibited by NE were also inhibited by morphine and cromakalim, an agonist of K-ATP channels, and moreover, the morphine-induced inhibitory effect could be blocked by glibenclamide, while the cromakalim-induced inhibitory effect was not blocked by naloxone. These results imply that: (a) NE excites arcuate neurons through amechanism that is insensitive to lowering the extracellular Ca2+ suggesting a direct postsynaptic response through alpha(1)- and beta-adrenergic receptors, while NE inhibits cells through at least an inhibitory interneuron in arcuate and so is dependent on a Ca2+-sensitive presynaptic release mechanism; and (b) the inhibitory interneuron may be opioidergic, being excited first through alpha(1)- and beta-adrenergic receptors, after which the released opioids inhibit the neurons being recorded with an involvement of activation of K-ATP channels. This possibility needs to be substantiated in much more detail. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 10:01:47