NaV1.8 channels are expressed in large, as well as small, diameter sensory afferent neurons

被引:25
|
作者
Ramachandra, Renuka [1 ]
McGrew, Stephanie Y. [1 ]
Baxter, James C. [1 ]
Howard, Jason R. [1 ]
Elmslie, Keith S. [1 ]
机构
[1] AT Still Univ Hlth Sci, Kirksville Coll Osteopath Med, Dept Pharmacol, Baker Lab Pharmacol, Kirksville, MO 63501 USA
基金
美国国家卫生研究院;
关键词
cutaneous afferents; muscle afferents; dorsal root ganglia neurons; tetrodotoxin-resistant (TTX-R); SODIUM-CHANNELS; PAIN STATES; DRG NEURONS; RAT; ELECTROGENESIS; ROLES; AXONS;
D O I
10.4161/chan.22445
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Sensory neurons in the dorsal root ganglia (DRG) express a subset of voltage dependent sodium channels (Na-V) including Na(V)1.1, 1.6, 1.7, 1.8 and 1.9. Previous work supported preferential localization of Na(V)1.8 channels to small-medium diameter, nociceptive afferent neurons. However, we recently published evidence that Na(V)1.8 was the dominant Na-V channel expressed in the somas of small, medium and large diameter muscle afferent neurons, which is consistent with other reports. Here, we extend those results to show that Na(V)1.8 expression is not correlated with afferent neuron diameter. Using immunocytochemistry, we found Na(V)1.8 expression in similar to 50% of sensory afferent neurons with diameters ranging from 20 to 70 mu m. In addition, electrophysiological analysis shows that the kinetic and inactivation properties of Na(V)1.8 current are invariant with neuron size. These data add further support to the idea that Na(V)1.8 contributes to the electrical excitability of both nociceptive and non-nociceptive sensory neurons.
引用
收藏
页码:34 / 37
页数:4
相关论文
共 50 条
  • [1] GTPγs increases Nav1.8 current in small-diameter dorsal root ganglia neurons
    Saab, CY
    Cummins, TR
    Waxman, SG
    EXPERIMENTAL BRAIN RESEARCH, 2003, 152 (04) : 415 - 419
  • [2] GTPγS increases Nav1.8 current in small-diameter dorsal root ganglia neurons
    Carl Y. Saab
    Theodore R. Cummins
    Stephen G. Waxman
    Experimental Brain Research, 2003, 152 : 415 - 419
  • [3] Contribution of Nav1.8 sodium channels to action potential electrogenesis in DRG neurons
    Renganathan, M
    Cummins, TR
    Waxman, SG
    JOURNAL OF NEUROPHYSIOLOGY, 2001, 86 (02) : 629 - 640
  • [4] Nav1.7 and Nav1.8: Diabetes-induced Changes in Primary Sensory Neurons in Rats
    Lv, Jianlin
    Wang, Mingjie
    Xia, Meng
    JOURNAL OF NEUROGASTROENTEROLOGY AND MOTILITY, 2016, 22 (04) : 707 - 708
  • [5] Cyclosporin A and deltamethrin block the downregulation of Nav1.8 sodium channels expressed in Xenopus oocytes
    Choi, JS
    Soderlund, DM
    NEUROSCIENCE LETTERS, 2004, 367 (03) : 389 - 393
  • [6] Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice
    Yu, Jie
    Fang, Qi
    Lou, Guo-Dong
    Shou, Wen-Ting
    Yue, Jia-Xing
    Tang, Ying-Ying
    Hou, Wei-Wei
    Xu, Tian-Le
    Ohtsu, Hiroshi
    Zhang, Shi-Hong
    Chen, Zhong
    CNS NEUROSCIENCE & THERAPEUTICS, 2013, 19 (09) : 649 - 658
  • [7] TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons
    Gasperini, Robert J.
    Hou, Xu
    Parkington, Helena
    Coleman, Harry
    Klaver, David W.
    Vincent, Adele J.
    Foa, Lisa C.
    Small, David H.
    MOLECULAR NEURODEGENERATION, 2011, 6
  • [8] Histamine modulation of acute nociception involves regulation of Nav1.8 in primary afferent neurons in mice
    于捷
    Hiroshi Ohtsu
    中国药理学与毒理学杂志, 2012, 26 (03) : 432 - 433
  • [9] TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons
    Robert J Gasperini
    Xu Hou
    Helena Parkington
    Harry Coleman
    David W Klaver
    Adele J Vincent
    Lisa C Foa
    David H Small
    Molecular Neurodegeneration, 6
  • [10] NaV1.8 channels are prime targets of oxidative stress in dorsal root ganglia neurons
    Schink, M.
    Schirmeyer, J.
    Schoenherr, R.
    Leipold, E.
    Heinemann, S. H.
    ACTA PHYSIOLOGICA, 2015, 213 : 138 - 139