Changes to Kv3.1, Kv3.1b, Kv4.3, SK3, HCN1, HCN2, and HCN4 Ion Channels in Dorsal Root Ganglion Following Peripheral Nervous System Injury

Abstract

<p>Peripheral nerve injury causes significant alterations in spinal sensory and motor circuits, including alterations of neuron excitability and synaptic function. Despite reinnveration of peripheral target tissues, e.g. skin or muscle, by both sensory and motor axons following injury, seldom is there complete functional recovery. Sensory information is communicated from the periphery to the central nervous system (CNS) by way of afferent neurons whose cell bodies are located in the dorsal root ganglia (DRG), accessory structures that lie adjacent to the spinal cord. The DRG neurons relay peripheral sensory information such as muscle proprioception to the CNS and can play a regulatory role in motor control. Thus any changes to the structure of the neurons within the DRG would likely affect multiple functions. Their ability to faithfully transmit information is dependent on the complement of ion channels they express. Indeed, DRG neurons have previously been shown to exhibit abnormal firing properties and an increased sensitivity to excitability by neighboring neurons following injury (Ishikawa 1999), which partly accounts for the irregular sensations following nerve damage. We hypothesize that after peripheral nerve injury there will be a change in expression of ion channels of the DRG neurons whose axons have been damaged. To confirm this hypothesis tibial nerve crush and cut injury models were used. The crush model will allow peripheral reinnervation of the target muscle, but the cut and ligation model would prevent peripheral reinnervation from occurring, allowing us to distinguish between mechanisms that mayor may not be dependent on signals from the periphery. DRG tissue was analyzed using immunofluorescent techniques that detected the presence of candidate ion channels: Kv3.1, Kv3.1b, Kv4.3, SK3, HCN1, HCN2, and HCN4. The data suggests that following injury there is a change in the proportion of DRG neurons that express imunoreactivity for these ion channels.</p><p>This presentation occurred at the Wright State University Campus-Wide Celebration of Research, Scholarship and Creative Activities on April 8, 2011</p>