Chronic compression of mouse dorsal root ganglion alters voltage-gated sodium and potassium currents in medium-sized dorsal root ganglion neurons

被引:34
作者
Fan, Ni [1 ]
Donnelly, David F. [2 ]
LaMotte, Robert H. [1 ]
机构
[1] Yale Univ, Sch Med, Dept Anesthesiol, New Haven, CT 06520 USA
[2] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06520 USA
关键词
neuropathic pain; ion channels; whole-cell recordings; PRIMARY SENSORY NEURONS; ENHANCED EXCITABILITY; INFLAMMATORY PAIN; AFFERENT NEURONS; K+ CURRENTS; RAT MODEL; EXPRESSION; AXOTOMY; NA+; HYPERSENSITIVITY;
D O I
10.1152/jn.00752.2011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Fan N, Donnelly DF, LaMotte RH. Chronic compression of mouse dorsal root ganglion alters voltage-gated sodium and potassium currents in medium-sized dorsal root ganglion neurons. J Neurophysiol 106: 3067-3072, 2011. First published September 14, 2011; doi: 10.1152/jn.00752.2011.-Chronic compression (CCD) of the dorsal root ganglion (DRG) is a model of human radicular pain produced by intraforaminal stenosis and other disorders affecting the DRG, spinal nerve, or root. Previously, we examined electrophysiological changes in small-diameter lumbar level 3 (L3) and L4 DRG neurons treated with CCD; the present study extends these observations to medium-sized DRG neurons, which mediate additional sensory modalities, both nociceptive and non-nociceptive. Whole-cell patch-clamp recordings were obtained from medium-sized somata in the intact DRG in vitro. Compared with neurons from unoperated control animals, CCD neurons exhibited a decrease in the current threshold for action potential generation. In the CCD group, current densities of TTX-resistant and TTX-sensitive Na(+) current were increased, whereas the density of delayed rectifier voltage-dependent K(+) current was decreased. No change was observed in the transient or "A" current after CCD. We conclude that CCD in the mouse produces hyperexcitability in medium-sized DRG neurons, and the hyperexcitability is associated with an increased density of Na(+) current and a decreased density of delayed rectifier voltage-dependent K(+) current.
引用
收藏
页码:3067 / 3072
页数:6
相关论文
共 31 条
[11]   Strain differences in adrenergic sensitivity of neuropathic pain behaviors in an experimental rat model [J].
Lee, DH ;
Chung, KS ;
Chung, JM .
NEUROREPORT, 1997, 8 (16) :3453-3456
[12]   Sodium channel β2 subunits regulate tetrodotoxin-sensitive sodium channels in small dorsal root ganglion neurons and modulate the response to pain [J].
Lopez-Santiago, Luis F. ;
Pertin, Marie ;
Morisod, Xavier ;
Chen, Chunling ;
Hong, Shuangsong ;
Wiley, John ;
Decosterd, Isabelle ;
Isom, Lori L. .
JOURNAL OF NEUROSCIENCE, 2006, 26 (30) :7984-7994
[13]   Similar electrophysiological changes in axotomized and neighboring intact dorsal root ganglion neurons [J].
Ma, C ;
Shu, YS ;
Zheng, Z ;
Chen, Y ;
Yao, H ;
Greenquist, KW ;
White, FA ;
LaMotte, RH .
JOURNAL OF NEUROPHYSIOLOGY, 2003, 89 (03) :1588-1602
[14]   Multiple sites for generation of ectopic spontaneous activity in neurons of the chronically compressed dorsal root ganglion [J].
Ma, Chao ;
LaMotte, Robert H. .
JOURNAL OF NEUROSCIENCE, 2007, 27 (51) :14059-14068
[15]   Progressive tactile hypersensitivity: An inflammation-induced incremental increase in the excitability of the spinal cord [J].
Ma, QP ;
Woolf, CJ .
PAIN, 1996, 67 (01) :97-106
[16]   Inflammatory pain hypersensitivity mediated by phenotypic switch in myelinated primary sensory neurons [J].
Neumann, S ;
Doubell, TP ;
Leslie, T ;
Woolf, CJ .
NATURE, 1996, 384 (6607) :360-364
[17]  
NOGUCHI K, 1995, J NEUROSCI, V15, P7633
[18]  
Shir Y, 2001, ANESTH ANALG, V92, P1029, DOI 10.1097/00000539-200104000-00042
[19]   Mechanical and thermal hyperalgesia and ectopic neuronal discharge after chronic compression of dorsal root ganglia [J].
Song, XJ ;
Hu, SJ ;
Greenquist, KW ;
Zhang, JM ;
LaMotte, RH .
JOURNAL OF NEUROPHYSIOLOGY, 1999, 82 (06) :3347-3358
[20]   Ileitis modulates potassium and sodium currents in guinea pig dorsal root ganglia sensory neurons [J].
Stewart, T ;
Beyak, MJ ;
Vanner, S .
JOURNAL OF PHYSIOLOGY-LONDON, 2003, 552 (03) :797-807