Neuropeptide Y actions and the distribution of Ca2+-dependent Cl- conductance in rat dorsal root ganglion neurons

被引:17
作者
Abdulla, FA
Smith, PA
机构
[1] Univ Alberta, Dept Pharmacol, Edmonton, AB T6G 2H7, Canada
[2] Univ Alberta, Div Neurosci, Edmonton, AB T6G 2H7, Canada
[3] Tennessee State Univ, Sch Allied Hlth Sci, Dept Phys Therapy, Nashville, TN 37909 USA
来源
JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM | 1999年 / 78卷 / 01期
基金
英国医学研究理事会;
关键词
primary afferent; nodose ganglion; axotomy; trigeminal ganglion; chronic constriction injury; sensory neuron; sympathetically maintained pain; sympathetic ganglion;
D O I
10.1016/S0165-1838(99)00058-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neuropeptide Y (NPY) increases the excitability of 'small', nociceptive, dorsal root ganglion (DRG) neurons. This effect, which may contribute to the etiology of 'neuropathic' pain, has been attributed to attenuation of Ca2+-sensitive K+ conductance(s) (g(K,Ca)) following suppression of Ca2+ entry via N-type Ca2+ channels. A problem arises with this conclusion because rat DRG neurons normally contain high intracellular Cl- and some of them express a Ca2+-dependent Cl- conductance (g(Cl,Ca)). In this study, we find that in rat DRG neurons increasing intracellular Cl- does not attenuate the effect of 1 mu M NPY because g(Cl,Ca) is not found in 'small' DRG cells and the peptide failed to affect the g(Cl,Ca) found in 'large' cells. Thus, the presence of g(Cl,Ca) in a subpopulation of 'large' DRG neurons does not alter the conclusion that excitatory effects of NPY result from attenuation of g(K,Ca). (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:24 / 29
页数:6
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