Autonomic dysreflexia AD is a potential life threatening condition characterized as 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 AD. In this study we tested this hypothesis by using both genetic modified mice lines 2-1 over-expressing and TSP KO and the drug, Gabapentin, which disrupting the binding of 2-1 with TSP, to block the formation of aberrant sympathetic nerve circuits and prevent occurring of AD. Current study suggested that mice carry an extra 2-1 gene developed more AD than WT littermates after T3 SCI. GBPs.c. 200mgkg TID treatment inhibits AD development in WT BL6 mice. Preliminary data from IHC study suggested GBP may promotes inhibitory synapse formation rather than reduce excitatory synapse formation. This study suggested that post-injury synaptogenesis is an important mechanism underlining the development of AD post T3 SCI.