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Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8
Mohammed A Nassar1, Alessandra Levato, L Caroline Stirling
1Department of Biology, University College London, WC1E 6BT, London, UK. M.nassar@ucl.ac.uk
Molecular Pain
|August 23, 2005
Summary
Nav1.7 and Nav1.8 sodium channels are crucial for inflammatory pain but not neuropathic pain. Deleting these channels in mice did not affect neuropathic pain development, showing they are not required for this condition.
Area of Science:
- Neuroscience
- Pain Research
- Molecular Biology
Background:
- Voltage-gated sodium channels Nav1.7 and Nav1.8 are highly expressed in nociceptors.
- These channels are implicated in inflammatory pain.
- Their role in neuropathic pain is uncertain, though channel mis-expression by damaged neurons is implicated.
Purpose of the Study:
- To investigate the role of Nav1.7 and Nav1.8 in the development of neuropathic pain.
- To determine if Nav1.7 or Nav1.8 are necessary for neuropathic pain in mouse models.
Main Methods:
- Generation of Nav1.7 knockout mice.
- Generation of Nav1.7 and Nav1.8 double knockout mice.
- Assessment of neuropathic pain development using behavioral tests.
- Evaluation of inflammatory pain symptoms and acute pain thresholds.
Main Results:
- Deletion of Nav1.7 alone did not affect neuropathic pain development.
- Double knockout mice lacking both Nav1.7 and Nav1.8 developed normal levels of neuropathic pain.
- These double knockout mice showed no inflammatory pain symptoms and had altered acute pain thresholds.
Conclusions:
- Nav1.7 plays a significant role in inflammatory pain.
- Neither Nav1.7 nor Nav1.8, alone or in combination, are required for the development of neuropathic pain.
- These findings differentiate the roles of Nav1.7 and Nav1.8 in inflammatory versus neuropathic pain states.