Forebrain regulation of sexual response in male rats

Several experiments examined the effects of forebrain lesions on the sexual response of male rats, including copulation and noncontact erection (NCE). NCE is evoked by remote cues from inaccessible estrous females and is analogous to human psychogenic erection. Therefore, NCE may measure sexual arousal, even in males that can not copulate. The four brain nuclei selected for study were known to be involved in the neural regulation of copulation, but this is the first exploration of their role in NCE. Lesions in the medial preoptic area (MPOA) abolished copulation, but caused only small and transient impairment of NCE. These results suggest that males with MPOA lesions, though incapable of copulating, were sexually aroused by estrous females. In contrast, lesions in the bed nucleus of the stria terminalis (BST) caused severe deficits in the display of NCE, but had a much smaller effect on copulation, primarily longer interintromission intervals and ejaculatory latencies. After either radiofrequency (RF) or N-methyl-D-aspartic acid (NMDA) lesions of the paraventricular nucleus of the hypothalamus (PVH), lesioned males had moderate deficits in NCE, and all copulated to ejaculation. However, males with RF lesions of both parvocellular and magnocellular neurons had lower intromission ratios, indicating erectile deficit in copula, whereas NMDA-lesioned males, in which the magnocellular neurons were spared, copulated normally. Either RF lesions or 6-hydroxydopamine (6-OHDA) depletions of dopamine in nucleus accumbens (NAcc) caused longer NCE latencies, but there was little or no deficit in copulation. In these studies, the number of nose pokes during NCE tests was similar in the lesion and control groups, suggesting that any deficit in NCE was not due to reduced attention to the female. These results, in conjunction with previous reports, add to our understanding of the neural regulation of sexual responding. NCE and copulatory behavior clearly have different neural mediation. An intact medial amygdala (MeA; research of others) and BST are essential for inducing NCEs. Intact PVH and NAcc may facilitate expression of this behavior, whereas the MPOA is redundant or superfluous. Some MeA and BST neurons may exert their effect on NCE via an extra-MPOA pathway.