Abstract:
:Neuropathic pain may be produced, at least in part, by the increased activity of primary afferent neurons. Studies have suggested that an accumulation of voltage-gated sodium channels at the site of peripheral nerve injury is a primary precursory event for subsequent afferent hyperexcitability. In this study, a human sodium channel (hPN3, SCN10A) has been cloned from the lumbar 4/5 dorsal root ganglia (DRG). Expression of hPN3 in Xenopus oocytes showed that this clone is a functional voltage-gated sodium channel. The amino acid sequence of hPN3 is most closely related to the rat PN3/SNS sodium channels which are expressed primarily in the small neurons of rat DRGs. The homologous relationship between rPN3 and hPN3 is defined by (i) a high level of sequence identity (ii) sodium currents that are highly resistant to tetrodotoxin (TTX) (iii) similar tissue distribution profiles and (iv) orthologous chromosomal map positions. Since rPN3/SNS has been implicated in nociceptive transmission, hPN3 may prove to be a valuable target for therapeutic agents against neuropathic pain.
journal_name
Painjournal_title
Painauthors
Rabert DK,Koch BD,Ilnicka M,Obernolte RA,Naylor SL,Herman RC,Eglen RM,Hunter JC,Sangameswaran Ldoi
10.1016/S0304-3959(98)00120-1subject
Has Abstractpub_date
1998-11-01 00:00:00pages
107-114issue
2eissn
0304-3959issn
1872-6623pii
00006396-199811010-00003journal_volume
78pub_type
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