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The Role of Acid Sensing Ion Channels in Spinal Cord Injury

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Final rept. 30 Sep 2010-29 Sep 2012

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Secondary neuronal damage occurs during the sub-acute phase of spinal cord injury SCI and is a major mechanism of permanent neurological dysfunction. The development of new hypotheses focusing on secondary damage is of paramount importance for devising new therapeutics to prevent the morbidity and mortality associated with spinal cord injury in humans. Recently, acidosis-evoked activation of the acid sensing ion channel 1a ASIC1a was determined to substantially contribute to secondary neuronal damage following cerebral ischemia. The purpose of this proposal is to determine how ASIC1a contributes to neuron death associated with SCI and whether administration of the ASIC1a inhibitor PcTx1 will significantly reduce neurological deficits following SCI. We will assess both immunohistochemical changes in the lesions as well as behavioral outcomes following injury. In the past year, we have determined that administration of the ASIC1a-inhibiting peptide PcTx1 1 hour after SCI results in an increased number of oligodendrocytes precursors in the injured spinal cord. The presence of the cells could afford better recovery from spinal cord contusion injury and indicates that further studies into the therapeutic potential of ASIC1 inhibitors to limit permanent damage following SCI are warranted. The completion of these aims will provide a foundation to promote further study on the role of acidosis in SCI and elucidate the therapeutic value of ASIC1a inhibition for SCI.

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  • Anatomy and Physiology
  • Medicine and Medical Research

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