Na_v1.8-null mice show stimulus-dependent deficits in spinal neuronal activity

• Main Authors: Wood John N, Matthews Elizabeth A, Dickenson Anthony H
• Format: Article
• Language: English
• Published: SAGE Publishing 2006-02-01
• Series: Molecular Pain
• Online Access: http://www.molecularpain.com/content/2/1/5

<p>Abstract</p> <p>Background</p> <p>The voltage gated sodium channel Na_v1.8 has a highly restricted expression pattern to predominantly nociceptive peripheral sensory neurones. Behaviourally Na_v1.8-null mice show an increased acute pain threshold to noxious mechanical pressure and also deficits in inflammatory and visceral, but not neuropathic pain. Here we have made in vivo electrophysiology recordings of dorsal horn neurones in intact anaesthetised Na_v1.8-null mice, in response to a wide range of stimuli to further the understanding of the functional roles of Na_v1.8 in pain transmission from the periphery to the spinal cord.</p> <p>Results</p> <p>Na_v1.8-null mice showed marked deficits in the coding by dorsal horn neurones to mechanical, but not thermal, -evoked responses over the non-noxious and noxious range compared to littermate controls. Additionally, responses evoked to other stimulus modalities were also significantly reduced in Na_v1.8-null mice where the reduction observed to pinch > brush. The occurrence of ongoing spontaneous neuronal activity was significantly less in mice lacking Na_v1.8 compared to control. No difference was observed between groups in the evoked activity to electrical activity of the peripheral receptive field.</p> <p>Conclusion</p> <p>This study demonstrates that deletion of the sodium channel Na_v1.8 results in stimulus-dependent deficits in the dorsal horn neuronal coding to mechanical, but not thermal stimuli applied to the neuronal peripheral receptive field. This implies that Na_v1.8 is either responsible for, or associated with proteins involved in mechanosensation.</p>