Histamine excites neonatal rat sympathetic preganglionic neurons in vitro via activation of H-1 receptors
Whyment, Andrew D., Blanks, Andrew M., Lee, Kevin, Renaud, L. P. and Spanswick, David. (2006) Histamine excites neonatal rat sympathetic preganglionic neurons in vitro via activation of H-1 receptors. Journal of Neurophysiology, Volume 95 (Number 4). pp. 2492-2500. ISSN 0022-3077Full text not available from this repository.
Official URL: http://dx.doi.org/10.1152/jn.01135.2004
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.
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