Abstract

Male rats exhibit maternal behavior prepuberally and in adulthood, but the neural mechanisms and the ability of males to respond to hormones that stimulate maternal aggression (following arousal of maternal behavior) in females have not been studied. In Experiment 1, males were exposed to pups to stimulate maternal behavior (sensitization) after either radiofrequency lesions of the MPOA or sham lesions with nonactivated electrodes that penetrated the MPOA. Nonsurgical males served as a CONTROL group. The LESION male group showed severe deficits in all components of maternal behavior compared to the latter two groups that showed no behavioral deficits. Females in the LESION group and those given SHAM 1 lesions (produced by electrodes without current introduced into the MPOA) also showed severe deficits in maternal behavior compared to SHAM 2 females (electrode lowered to above the MPOA without current) and nonsurgical CONTROL females. In Experiment 2, prolonged estradiol (E2), progesterone (P) treatment followed by an injection of either 20 μg or 100 μg/kg estradiol benzoate (EB) or oil in castrated males was effective in stimulating short-latency maternal behavior, mainly in the 100 μg/kg EB group. Males of this group also showed a high level of maternal aggression that was inversely correlated with their latencies for maternal behavior. All groups showed maternal aggression when maternal behavior was established. The results indicate the MPOA mediates maternal behavior in males as it does in females; maternal aggression in males accompanies the stimulation of maternal behavior and may be stimulated by the same hormones.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.