Elsevier

Physiology & Behavior

Volume 86, Issue 3, 15 October 2005, Pages 356-368
Physiology & Behavior

Dopamine, the medial preoptic area, and male sexual behavior

https://doi.org/10.1016/j.physbeh.2005.08.006Get rights and content

Abstract

The medial preoptic area (MPOA), at the rostral end of the hypothalamus, is important for the regulation of male sexual behavior. Results showing that male sexual behavior is impaired following MPOA lesions and enhanced with MPOA stimulation support this conclusion. The neurotransmitter dopamine (DA) facilitates male sexual behavior in all studied species, including rodents and humans. Here, we review data indicating that the MPOA is one site where DA may act to regulate male sexual behavior. DA agonists microinjected into the MPOA facilitate sexual behavior, whereas DA antagonists impair copulation, genital reflexes, and sexual motivation. Moreover, microdialysis experiments showed increased release of DA in the MPOA as a result of precopulatory exposure to an estrous female and during copulation. DA may remove tonic inhibition in the MPOA, thereby enhancing sensorimotor integration, and also coordinate autonomic influences on genital reflexes. In addition to sensory stimulation, other factors influence the release of DA in the MPOA, including testosterone, nitric oxide, and glutamate. Here we summarize and interpret these data.

Introduction

The neurotransmitter dopamine (DA) is important for male sexual behavior. One region where DA may act to facilitate male sexual behavior is the medial preoptic area (MPOA), a region at the rostral end of the hypothalamus, which is important for endocrine activity and essential for the expression of male sexual behavior. In this review we summarize and interpret data that indicate that DA in the MPOA facilitates male sexual behavior; also, we describe sensory and hormonal factors that might regulate release of DA in the MPOA.

Section snippets

Dopamine agonists and antagonists

Evidence supporting the hypothesis that dopamine enhances male sexual behavior comes from studies of drugs that relieve symptoms of Parkinson's disease or schizophrenia. DA-mediated enhancement of sexual behavior was first recognized when administration of l-dopa (3,4-dihydroxy-l-phenylalanine), the precursor to DA, to men suffering from Parkinson's disease resulted in increased libido and sexual potency [1], [2], [3], [4]; this increase was not related to improvements in locomotor function [5]

Ablation of the MPOA

The MPOA is perhaps the most important site for the regulation of male sexual behavior in all vertebrate species. It receives indirect input from every sensory modality [31] and sends projections to structures that are critical for the initiation and patterning of copulation [32]. The MPOA's role as a central integrative site for the regulation of male sexual behavior is confirmed by ablation studies, in which damage to the MPOA impaired male sexual behavior; this effect is observed in all

Dopamine input to the MPOA

DA-containing cell bodies are concentrated in two major dopaminergic cell groups, the substantia nigra (A9), which sends axons to the caudate-putamen and comprises the nigrostriatal dopamine pathway, and the ventral tegmental area (A10), which sends axons to the nucleus accumbens septi and several other areas and comprises the mesolimbic dopamine pathway (reviewed in e.g. Ref. [67]). A9 cells play a major role in the regulation of motor functions, whereas A10 cells are important for motivation

Summary

In summary, both systemically administered and intra-MPOA DA agonists facilitate copulation, genital reflexes, and sexual motivation, whereas DA antagonists impair those measures. Small increases in DA in the MPOA may disinhibit genital reflexes via D2-like receptors, and slightly larger increases may promote parasympathetically mediated erection and the early stages of copulation, via D1-like receptors. Larger amounts of DA or of D2 agonists in the MPOA may shift the autonomic balance to favor

Acknowledgements

This research was supported by NIH grants R01 MH40826 and K02 MH01714 to EMH.

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