Abstract

Gentle probing against the cervix via the vagina (vaginocervical stimulation, VCS) increases tail flick latency (TFL) to radiant heat; greater force abolishes the tail flick response and other withdrawal responses. This effect occurs in spinal cord-transected rats and in intact rats. On the basis of our earlier finding that VCS releases vasoactive intestinal peptide (VIP) into the spinal cord, and others’ reports of neurotrophic effects of VIP in vitro, we hypothesized that repeated VCS would stimulate sprouting and sensorimotor function of terminals of genital nerve primary afferents in the sacral spinal cord. To test this hypothesis, in the present study, we denervated the genital tract only unilaterally, which significantly reduced the TFL-elevating effect of VCS. Then we applied repeated daily VCS for 1 week and compared the subsequent effectiveness of acute VCS in elevating TFL. The rats that received the repeated daily VCS showed a significantly greater elevation in TFL in response to acute VCS than control rats that did not receive the repeated stimulation. Then, to test whether daily repeated VCS stimulates sprouting of genital primary afferents in such unilaterally genital tract-denervated rats, we transected the contralateral remaining intact pelvic nerve, applied horseradish peroxidase (HRP) to its proximal cut end for 1–2 h, and 2–3 days later counted HRP particles in its terminal zone (L6–S1) in the spinal cord. There were significantly more HRP particles in the rats that received the daily repeated VCS than in the control rats. In the context of these findings, we conclude that VCS in rats can produce a functional sensorimotor recovery via a neurotrophic effect on compromised primary afferents in the spinal cord.

Highlights

  • Vaginocervical stimulation (VCS) in rats acts at the spinal cord to block withdrawal reflexes to noxious stimulation

  • The unilateral neurectomy significantly reduced the ability of VCS to inhibit the tail flick response

  • The tail flick latency (TFL) elevation to 300 g VCS was significantly higher in the unilateral neurectomy + daily VCS group (GenX + VCS) than in the unilateral neurectomy group that did not receive daily VCS (GenX)

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Summary

Introduction

Vaginocervical stimulation (VCS) in rats acts at the spinal cord to block withdrawal reflexes to noxious stimulation. A possible mechanism for this effect is that foot-shock-induced release of substance P into spinal cord superfusate is inhibited by concurrent VCS (Steinman et al, 1994). The pelvic nerves, which provide sensory innervation of the vagina and cervix (Komisaruk et al, 1972; Peters et al, 1987; Berkley et al, 1990, 1993) are the main mediator of this VCS-induced reflex inhibition, for transection of the pelvic nerves almost completely abolishes the ability of VCS to block withdrawal reflexes (Cunningham et al, 1991). Vasoactive intestinal peptide (VIP) is a possible mediator of this effect of VCS, for pelvic nerve contains VIP (Basbaum and Glazer, 1983), VCS releases VIP into spinal cord superfusates (Komisaruk et al, 1989 ), and VIP and certain of its fragments administered directly to the spinal cord, intrathecally, mimic the analgesia-producing effects of VCS (Komisaruk and Jordan, 1995). In a different context, VIP exerts neurotrophic effects (Brenneman and Eiden, 1986; Gozes et al, 1991; Gressens et al, 1993; Brenneman et al, 1999)

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