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Modulation of N-type Ca²⁺ currents by moxonidine via imidazoline I₁ receptor activation in rat superior cervical ganglion neurons.

Title
 Modulation of N-type Ca²⁺ currents by moxonidine via imidazoline I₁ receptor activation in rat superior cervical ganglion neurons. 
Authors
 Young-Hwan Kim ; Taick-Sang Nam ; Seungsoo Chung ; Duck-Sun Ahn 
Issue Date
2011
Journal Title
 Biochemical and Biophysicial Research Communications 
ISSN
 0006-291X 
Citation
 Biochemical and Biophysicial Research Communications, Vol.409(4) : 645~650, 2011 
Abstract
Moxonidine, an imidazoline deriviatives, suppress the vasopressor sympathetic outflow to produce hypotension. This effect has been known to be mediated in part by suppressing sympathetic outflow via acting imidazoline I(1) receptors (IR(1)) at postganglionic sympathetic neurons. But, the cellular mechanism of IR(1)-induced inhibition of noradrenaline (NA) release is still unknown. We therefore, investigated the effect of IR(1) activation on voltage-dependent Ca(2+) channels which is known to play an pivotal role in regulating NA in rat superior cervical ganglion (SCG) neurons, using the conventional whole-cell patch-clamp method. In the presence of rauwolscine (3 μΜ), which blocks α(2)-adrenoceptor (R(α2)), moxonidine inhibited voltage-dependent Ca(2+) current (I(Ca)) by about 30%. This moxonidine-induced inhibition was almost completely prevented by efaroxan (10 μΜ) which blocks IR(1) as well as R(α2). In addition, ω-conotoxin (CgTx) GVIA (1 μΜ) occluded moxonidine-induced inhibition of I(Ca), but, moxonidine-induced I(Ca) inhibition was not affected by pertussis toxin (PTX) nor shows any characteristics of voltage-dependent inhibition. These data suggest that moxonidine inhibit voltage-dependent N-type Ca(2+) current (I(Ca-N)) via activating IR(1). Finally, moxonidine significantly decreased the frequency of AP firing in a partially reversible manner. This inhibition of AP firing was almost completely occluded in the presence of ω-CgTx. Taken together, our results suggest that activation of IR(1) in SCG neurons reduced I(Ca-N) in a PTX-and voltage-insensitive pathway, and this inhibition attenuated repetitive AP firing in SCG neurons.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/93181
DOI
10.1016/j.bbrc.2011.05.058
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Physiology
Yonsei Authors
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Link
 http://www.sciencedirect.com/science/article/pii/S0006291X11008254
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