No abstract

The amplitude of the H-reflex increases chronically after incomplete SCI and is associated with the development of exaggerated hindlimb reflexes. Although the mechanism for this increased H-reflex is not clear, previous studies have shown that pharmacological activation of the 5-HT 2 receptors (5-HT 2 R) can potentiate the monosynaptic reflex. This study tested the hypothesis that increased expression of 5-HT 2 R on motoneurons is involved in increased H-reflex amplitude after a standardized clinically-relevant contusive SCI. Adult female rats were subjected to contusion, complete surgical transection, or a T8 laminectomy only. At 4wks after surgery, H-reflex recordings from the hindpaw plantar muscles of contused rats showed twice the amplitude of that in laminectomy controls or transected rats. To probe the role of 5-HT 2 R in this increased amplitude, dose response studies were done with the selective antagonists, mianserin or LY53857, and the 5-HT 2 R agonist, (±)-1-(2,5-Dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI). The drugs were intrathecally infused into the lumbar cord while recording the H-reflex. Mianserin did not have any significant effects on the H-reflex after transection, consistent with the loss of distal serotonergic innervation. After contusion, both 5-HT 2 R antagonists reduced the H-reflex reflex amplitude with a significantly higher ID 50 compared to the uninjured controls. The 5-HT 2 R agonist, DOI, significantly increased reflex amplitude in contused but not control rats. Furthermore, while 5-HT immunoreactivity was similar, contused rats displayed increased 5-HT 2A R immunoreactivity in plantar muscle motoneurons compared to uninjured controls. We conclude that increased expression of 5-HT 2 R is likely to be involved in the enhanced H-reflex that develops after contusive SCI.