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The Journal of Neuroscience, March 15, 1998, 18(6):2174-2187
Distribution of the Tetrodotoxin-Resistant Sodium Channel PN3 in
Rat Sensory Neurons in Normal and Neuropathic Conditions
Sanja D.
Novakovic,
Elda
Tzoumaka,
Joseph G.
McGivern,
Miki
Haraguchi,
Lakshmi
Sangameswaran,
Kathleen R.
Gogas,
Richard M.
Eglen, and
John C.
Hunter
Center for Biological Research, Neurobiology Unit, Roche
Bioscience, Palo Alto, California 94304-1397
The novel sodium channel PN3/ -SNS, which was cloned from a rat
dorsal root ganglion (DRG) cDNA library, is expressed predominantly in
small sensory neurons and may contribute to the tetrodotoxin-resistant (TTXR) sodium current that is believed to be
associated with central sensitization in chronic neuropathic pain
states. To assess further the role of PN3, we have used
electrophysiological, in situ hybridization and
immunohistochemical methods to monitor changes in TTXR
sodium current and the distribution of PN3 in normal and peripheral
nerve-injured rats. (1) Whole-cell patch-clamp recordings showed that
there were no significant changes in the TTXR and
TTX-sensitive sodium current densities of small DRG neurons after
chronic constriction injury (CCI) of the sciatic nerve. (2)
Additionally, in situ hybridization showed that there
was no change in the expression of PN3 mRNA in the DRG up to 14 d
after CCI. PN3 mRNA was not detected in sections of brain and spinal
cord taken from either normal or nerve-injured rats. (3) In contrast,
immunohistochemical studies showed that major changes in the
subcellular distribution of PN3 protein were caused by either CCI or
complete transection of the sciatic nerve. The intensity of PN3
immunolabeling decreased in small DRG neurons and increased in sciatic
nerve axons at the site of injury. The alteration in immunolabeling was
attributed to translocation of presynthesized, intracellularly located
PN3 protein from neuronal somata to peripheral axons, with subsequent accumulation at the site of injury. The specific subcellular
redistribution of PN3 after peripheral nerve injury may be an important
factor in establishing peripheral nerve hyperexcitability and resultant neuropathic pain.
Key words:
PN3; sodium channel; tetrodotoxin-resistant; distribution; sensory neuron; neuropathic pain; chronic constriction
injury; neuroma; nociception
Copyright © 1998 Society for Neuroscience 0270-6474/98/1862174-14$05.00/0
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