Sachs B D, Bitran D
Department of Psychology, University of Connecticut, Storrs 06269-1020.
Brain Res. 1990 Sep 24;528(1):99-108. doi: 10.1016/0006-8993(90)90200-u.
Five experiments were addressed at two questions: (1) is the influence of the brain on spinal control of reflexive erection exclusively inhibitory; and (2) are the effects of copulation on erectile potential mediated by the brain, the spinal cord, or both? After various amounts of antecedent copulation, spinal anesthesia was induced in male rats by tetracaine (TET) injected through chronically implanted cannulae into the thoracic or lumbar spinal subarachnoid space, and the animals were then tested for reflexive penile erections (supine position, penile sheath retracted, no phasic stimulation applied). In sexually rested rats, TET injected at either T4 or T10 reduced reflex latency but also reduced the number and intensity of responses. Penile erection was inhibited by TET injected at L5, the region of the cord receiving sensory and motor projections from the genitalia. In previous studies surgical transection of the thoracic cord facilitated erection latency and production. In the present experiments the divergent effects of intrathecal TET on these variables suggested that they are controlled by separate systems within the spinal cord and that in the sexually rested rat the net influence of the brain is to inhibit the latency system and excite the production system. After rats copulated to sexual satiety, thoracic spinal block did not reverse the complete abolition of reflexive erections, establishing for the first time that copulation has direct inhibitory effects on the spinal cord's intrinsic system. Fewer antecedent ejaculations had less inhibitory effects on reflexive erection, and TET then acted, as in rested males, to reduce the erection latency and the number of erections, indicating that copulation may act on the brain's descending influences on spinal systems. The overall pattern of results suggested that the brain exerts both excitatory and inhibitory influences on separate, interacting spinal mechanisms that regulate the latency to reflexive erection and the number and intensity of erections displayed.
