Wang DC, Bose P, Parmer R, Wiley RG, Thompson FJ (2001) Monoamine modulation of spinal reflex excitability of the lower limb in the rat: Intrathecal (i.t.) infusion of anti-DBH saporin toxin – time course for neurophysiology. Neuroscience 2001 Abstracts 771.5. Society for Neuroscience, San Diego, CA.
Summary: Progressive neurophysiological changes in the excitability of ankle extensor stretch reflex were identified following T8 spinal cord contusion injury (Thompson et. al., 1992). Previous study suggested that nonspecific monoamine depletion may be a significant contributor to the pathologic hyperreflexia associated with chronic spinal cord injury (Thompson et. al., 1999). To test a more specific hypothesis, a study was performed to evaluate the time course of changes in reflex excitability after i.t. injection of 250ng of anti-DBH saporin toxin to specifically lesion descending spinal noradrenergic neurons into the lumbar spinal cord of normal rats. Measures of H-reflex excitability were obtained prior to and at weekly intervals following toxin injection until a physiological plateau was observed. Significant decreases in rate-depression of H-reflexes were observed by the second week after toxin infusion and were maintained throughout the five weeks of testing. These studies indicate that selective lesioning of noradrenergic fibers produced specific changes in reflex excitability previously observed following midthoracic spinal cord contusion injury in the rat. The results of this study further implicate neurophysiological changes associated with monoamine loss as a contributing factor leading to hyperreflexia derived from chronic spinal cord injury. Correlated behavioral changes are reported in the companion poster, Bose et.al.
Related Products: Anti-DBH-SAP (Cat. #IT-03)