The purpose of the present thesis is to ascertain that repeated vaginocervical stimulation (VS) promotes central nervous system (CNS) recovery in rats.; The first part of the research focused on whether VIP released into the spinal cord by vaginocervical stimulation produces analgesia. To determine the analgesic effect of selected VIP fragments, female rats received spinal surgery and were then treated with intrathecally administered VIP analogs. The VIP23-28 peptide fragment had an analgesic effect immediately after its direct administration to the spinal cord. The mechanism of action was investigated by injecting a VIP receptor antagonist, VIP-(7-28)/Neurotensin, directly to the lumbosacral spinal cord, or by intraperitoneal injection of the opioid antagonist, naloxone. To investigate whether VIP receptors mediate VS-induced analgesia (VSIA), a VIP antagonist was administered directly to the lumbosacral spinal cord. The tail flick latency (TFL) and vocalization threshold (VOCT) tests were used to measure pain thresholds in response to each treatment. The results indicate that spinal cord VIP receptors mediate the analgesia induced by VIP11-28, since the spinal cord-specific VIP antagonist reduced the VIP11-28-induced elevation of TFL (Chapter I). The opioid receptor antagonist naloxone did not block the VIP11-28-induced TFL elevation (Chapter II), indicating that VIP11-28-induced analgesia is independent of the endogenous opioid system. We also demonstrated that pre-treatment with a VIP antagonist did not block VS-induced analgesia on the TFL test (Chapter IV), indicating that VS-induced analgesia is independent of a VIP-ergic system.; The second part of this dissertation addresses the effect of repeat vaginocervical stimulation (VS) on VS-induced analgesia after unilateral denervation of the female rat reproductive tract. Female rats with unilateral genitospinal nerve transection received repeated VS. Unilateral genitospinal nerve transection attenuated VS-induced analgesia. In those rats, repetitive daily VS for one week increased VS-induced analgesia. This suggests that repeated stimulation enhances the recovery of a sensory response in the spinal cord after a peripheral nerve lesion.; We hypothesize that repeated VS stimulation enhances recovery of VS-induced analgesia by releasing VIP, which stimulates sprouting of pelvic nerve terminals in the spinal cord. To test this hypothesis, we labeled pelvic nerves with horseradish peroxidase (HRP) in animals that had been or were not subjected to repeated VS.; We observed increases in HRP particle density in both the deafferented side and the intact side of the spinal cord dorsal horn in VS-treated rats compared to rats that did not receive the repetitive daily VS treatment.; We conclude that one week of repetitive vaginocervical stimulation, in unilaterally-pelvic-neurectomized rats, enhances functional recovery of the remaining pelvic nerve, stimulating pelvic nerve terminal sprouting in the spinal cord probably due to a VS-induced VIP release from the remaining pelvic nerves. |