In rats, probing against the vaginal cervix with a glass rod elevated the current threshold required to elicit vocalization in response to tail shock. This elevation in vocalization threshold was significantly attenuated by depletion of norepinephrine (NE) with synthesis inhibitors, blockade of alpha-NE receptors, and systemic or central administration of 6-hydroxydopamine. Furthermore, NE receptor stimulation significantly increased vocalization thresholds prior to and during vaginal stimulation. In contrast, dopamine (DA) receptor stimulation reduced, while DA receptor blockade enhanced, this antinociceptive effect of vaginal stimulation. Similarly, serotonin (5-HT) receptor stimulation reduced, and 5-HT depletion enhanced, this antinociceptive effect. Vaginal stimulation also induced an elevation in current threshold for leg withdrawal in response to foot shock. However, this threshold was completely unaffected by the monoamine synthesis inhibitors. In rats pretreated with a catecholamine synthesis inhibitor, two minutes of vaginal stimulation further reduced NE levels in the spinal cord, but did not affect telencephalon, hypothalamus, thalamus or midbrain. In addition, vaginal stimulation inpeded the depletion of striatal DA, with no effect on telencephalic DA. These findings suggest that vaginal stimulation activates NE neurons and decreases activity in DA neurons. At least part of this apparently analgesic effect of genital tract stimulation may be mediated by supraspinal monoaminergic mechanisms, some of which have a descending component that inhibits transmission in spinal pain pathways.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Clinical Neurology
- Developmental Biology