NEUROCHEMICAL AND NEUROENDOCRINE CONTROL OF POST-EJACULATORY REFRACTORINESS IN THE MALE RAT

Central neural mechanisms play a functional role in the mediation of male copulatory behavior, including post-ejaculatory refractoriness. A series of experiments were designed to elucidate more clearly the neurochemical and neuroendocrine mechanisms responsible for the control of behavioral refractoriness. Electrolytic and neurochemical lesions were made in various areas of the Central Nervous System in order to disrupt monoaminergic neurotransmission. The results of Experiment 1 indicate that lesions in the rostral midbrain (1) lateral to the medial longitudinal fasciculus in the area of the dorsal noradrenergic bundle and (2) ventral to the medial lemniscus in the area of the ventral noradrenergic bundle cause a significant reduction in the length of the post-ejaculatory refractory period (RP). The possibility that dopaminergic cell bodies or serotonergic fibers of passage were also destroyed in this experiment led to a more careful examination of the relationship between central monoaminergic systems and behavioral refractoriness.

The results of Experiment 2 indicate that interference with serotonergic mechanisms, via electrolytic or chemical destruction of the dorsal raphe or administration of synthesis inhibitors will dramatically shorten the RP and curtail or abolish the accompanying post-ejaculatory ultrasonic vocalization. Conversely, in Experiment 3, electrolytic or neurochemical destruction of dopaminergic cell bodies within the substantia nigra or administration of dopamine receptor blockers caused a significant increase in the length of the RP as well as a significant increase in both mount and intromission latencies. The results of Experiment 4 suggest that, like dopamine, interference with noradrenergic systems will prolong the RP following ejaculation; electrolytic destruction of noradrenergic cell bodies in the locus coeruleus or administration of norepinephrine synthesis inhibitors caused a significant lengthening of the RP and a significant increase in mount and intromission latencies. The behavioral evidence obtained in these studies concerning the relationship between the monoamines and refractory behavior directly supports anatomical evidence indicating the existence of reciprocal facilitatory and inhibitory inter-connections among these systems. A specific hypothesis is forwarded concerning the functional relationship between these monoaminergic systems and the control of post-ejaculatory refractory behavior.

In the rat, the perinatal period of development is crucial with respect to sexual differentiation of neural tissues that eventually mediate copulatory behavior. In Experiment 5, neonatal hormonal manipulation, achieved through castration, administration of steroids or aromatase inhibitors (ATD) provide evidence that perinatal presence of androgens will masculinize an animal in a way that allows for the development of normal post-ejaculatory refractory behavior. The aromatization of androgens to estrogens which will "defeminize" an animal was found not be a necessary requirement for the development of post-ejaculatory refractoriness.

It appears likely that the endogenous opiates are involved in the modulation of neurotransmitter activity within the brain. Experiment 6 examined the relationship between endogenous and exogenous opiates and the control of masculine sexual behavior, including refractoriness. The results indicate that administration of the opiate antagonist naloxone (30mg/kg) has a dramatic facilitatory effect on male copulatory behavior, without influencing refractory behavior. Administration of morphine (6mg/kg) or the endogenous opiate B-endorphin (6ug) totally abolished copulatory behavior. The effects of naloxone, morphine and B-endorphin on male copulatory behavior are related to alterations in neurotransmitter levels within various Central Nervous System structures.