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Histamine excites neonatal rat sympathetic preganglionic neurons in vitro via activation of H-1 receptors

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UNSPECIFIED. (2006) Histamine excites neonatal rat sympathetic preganglionic neurons in vitro via activation of H-1 receptors. JOURNAL OF NEUROPHYSIOLOGY, 95 (4). pp. 2492-2500. ISSN 0022-3077

Full text not available from this repository.
Official URL: http://dx.doi.org/10.1152/jn.01135.2004

Abstract

The role of histamine in regulating excitability of sympathetic preganglionic neurons (SPNs) and the expression of histamine receptor mRNA in SPNs was investigated using whole-cell patch-clamp electrophysiological recording techniques combined with single-cell reverse transcriptase polymerase chain reaction (RT-PCR) in transverse neonatal rat spinal cord slices. Bath application of histamine (100 mu M) or the H-1 receptor agonist histamine trifluoromethyl toluidide dimaleate (HTMT; 10 mu M) induced membrane depolarization associated with a decrease in membrane conductance in the majority (70%) of SPNs tested, via activation of postsynaptic H-1 receptors negatively coupled to one or more unidentified K+ conductances. Histamine and HTMT application also induced or increased the amplitude and/or frequency of membrane potential oscillations in electrotonically coupled SPNs. The H-2 receptor agonist dimaprit (10 mu M) or the H-3 receptor agonist imetit (100 nM) were without significant effect on the membrane properties of SPNs. Histamine responses were sensitive to the H-1 receptor antagonist triprolidine (10 mu M) and the nonselective potassium channel blocker barium (1 mM) but were unaffected by the H-2 receptor antagonist tiotidine (10 mu M) and the H-3 receptor antagonist, clobenpropit (5 mu M). Single cell RT-PCR revealed mRNA expression for H-1 receptors in 75% of SPNs tested, with no expression of mRNA for H-2, H-3, or H-4 receptors. These data represent the first demonstration of H-1 receptor expression in SPNs and suggest that histamine acts to regulate excitability of these neurons via a direct postsynaptic effect on H-1 receptors.

Item Type: Journal Article
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Q Science > QP Physiology
Journal or Publication Title: JOURNAL OF NEUROPHYSIOLOGY
Publisher: AMER PHYSIOLOGICAL SOC
ISSN: 0022-3077
Date: April 2006
Volume: 95
Number: 4
Number of Pages: 9
Page Range: pp. 2492-2500
Identification Number: 10.1152/jn.01135.2004
Publication Status: Published
URI: http://wrap.warwick.ac.uk/id/eprint/33767

Data sourced from Thomson Reuters' Web of Knowledge

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