Beta3, a novel auxiliary subunit for the voltage gated sodium channel is upregulated in sensory neurones following streptozocin induced diabetic neuropathy in rat.

摘要

In the present study we have used in situ hybridization to examine the changes in mRNA expression of the voltage gated sodium channel subunits beta1 and beta3, which occur in response to streptozocin induced diabetic neuropathy. Under control conditions beta1 mRNA was detected throughout the spinal cord and in large dorsal root ganglion (DRG) Abeta fibres whilst beta3 mRNA was expressed exclusively in the layers I/II and X of the spinal cord and in small DRG c-fibres. Following streptozocin treatment, the expression of beta1 mRNA remained unchanged in both the spinal cord and DRG whilst beta3 message was significantly increased in both the spinal cord and in medium diameter Adelta type DRG neurones. In conclusion, the present study illustrates that the development of the neuropathic pain state is associated with distinct changes in the pattern of beta3 subunit expression and that these changes appear to be specific to the neuropathic pain state induced.