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Immunolocalisation of sodium channel NaG in the intact and injured human peripheral nervous system

Published online by Cambridge University Press:  26 March 2001

K. COWARD
Affiliation:
Peripheral Neuropathy Unit, Imperial College School of Medicine, Hammersmith Hospital Campus, London
A. MOSAHEBI
Affiliation:
Blond McIndoe Laboratories, University Department of Surgery, Royal Free and University College Medical School, Royal Free Campus, London
C. PLUMPTON
Affiliation:
Molecular Pharmacology, GlaxoWellcome Research & Development, Medicines Research Centre, Stevenage, Hertfordshire
P. FACER
Affiliation:
Peripheral Neuropathy Unit, Imperial College School of Medicine, Hammersmith Hospital Campus, London
R. BIRCH
Affiliation:
Peripheral Nerve Injury Unit, Royal National Orthopaedic Hospital, Stanmore, Middlesex, UK
S. TATE
Affiliation:
Molecular Pharmacology, GlaxoWellcome Research & Development, Medicines Research Centre, Stevenage, Hertfordshire
C. BOUNTRA
Affiliation:
Neurosciences Unit, GlaxoWellcome Research & Development, Medicines Research Centre, Stevenage, Hertfordshire
G. TERENGHI
Affiliation:
Blond McIndoe Laboratories, University Department of Surgery, Royal Free and University College Medical School, Royal Free Campus, London
P. ANAND
Affiliation:
Peripheral Neuropathy Unit, Imperial College School of Medicine, Hammersmith Hospital Campus, London
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Abstract

The voltage-gated ‘glial’ sodium channel NaG belongs to a distinct molecular class within the multi-gene family of mammalian sodium channels. Originally found in central and peripheral glia, NaG has since been detected in neurons in rat dorsal root ganglia (DRG) and may play a role in Schwann cell-axon interactions. We have studied the presence of NaG-like immunoreactivity in the intact and injured human peripheral nervous system using a specific affinity-purified antibody. Nerve fibres in normal and injured peripheral nerves and normal skin exhibited intense NaG-immunoreactivity. Numerous NaG-immunoreactive nerve fibres surrounded neuronal cell bodies within postmortem control DRG, and in DRG avulsed from the spinal cord (i.e. after traumatic central axotomy). There were no significant differences in the pattern of NaG immunostaining between control and avulsed DRG, or with delay after injury. Generally, the neuronal cell bodies were only very weakly immunoreactive to NaG, indicating that the NaG immunoreactivity was predominantly in Schwann cells/myelin. In accord, we demonstrated NaG immunostaining in cultured human and rat Schwann cells, and in distal nerve after wallerian degeneration. NaG thus appears to be a useful new marker for Schwann cells in the human PNS, and a role in neuropathy deserves investigation.

Type
Research Article
Copyright
© Anatomical Society of Great Britain and Ireland 2001

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