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: Autonomic dysreflexia (AD) is a potential life threatening condition characterized by episodic vascular hypertension (often with bradycardia) that develops in most people with a spinal cord injury (SCI) above thoracic spinal level T5. Using telemetric recording we were able to detect biphasic spontaneous AD developed in mice with T3 SCI; the early phase of AD occurs within first week which is likely due to loss of descending control of sympathetic outflow and the late phase occurs weeks post injury which is likely caused by the formation of aberrant sympathetic neural circuits at the site of injury. We proposed that post- injury inhibition of reactive synaptogenesis would block the onset or reduce the severity of delayed onset AD. Experiments funded by this grant will test this hypothesis using both genetically modified mice (a2d-1 KO, a2d-1 over- expressing and TSP KO) and wild- type mice receiving chronic infusions of Gabapentin (GBP) a drug that inhibits binding of neuronal a2d-1 receptors with glial thrombospondins (TSP). We predict that chronic GBP will block the formation of aberrant sympathetic nerve circuits and prevent the onset of AD. Similar results are predicted using mice deficient in either the a2d-1 receptor or TSP. Conversely, transgenic overexpression ofa2d-1 is expected to accelerate the onset of AD or exacerbate severity of dysreflexia. Preliminary data generated in Year 1 show that the frequency of AD increases early after SCI in mice engineered to overexpressa2d-1; however, these effects are transient-- late phase AD does not develop in transgenic mice or in mice with the genetic background on which these transgenics were created. Future studies will determine AD frequency in the knockout mice (see above) or C57BL/6 mice treated with GBP.

Reversing Maladaptive Plasticity to Cure Autonomic Dysreflexia after Spinal Cord Injury