A NEURAL MODEL OF SLEEP-RELATED ERECTILE MECHANISMS

Markus H. Schmidt (1), P. Luppi, P. Fort, J.L. Valatx and Michel Jouvet

Cleveland Clinic Foundation, Department of Neurology, 9500 Euclid Ave.

Cleveland, Ohio 44195 U.S.A.

University of Claude Bernard, Dept. of Experimental Medicine,
 8, Ave. Rockefeller

Lyon, France

Introduction: Penile erections are a characteristic phenomenon of paradoxical sleep (PS). Our previous data demonstrate that neurotoxic lesions of the lateral preoptic area (LPOA) severely disrupt PS-related erections, whereas similar lesions of the medial preoptic area have minimal effects on erectile activity (Schmidt et al., 1998). Although these data clearly demonstrate an essential role of the LPOA in PS erectile mechanisms, it remains to be determined how the LPOA modulates the spinal generator controlling erections since the LPOA does not project to the spinal cord. Recent advances in erectile neurophysiology have elucidated a potential "final common path" from brain to spinal cord. These data suggest that penile erections involve a descending oxytocinergic excitation from the paraventricular nucleus (PVN) (Melis et al., 1994) and the removal of a descending serotonergic inhibition from the nucleus paragigantocellularis (nPGi) (Marson and McKenna, 1992). We injected the anterograde tracer phaseolus vulgaris leukoagglutinin (PHAL) into the LPOA to determine if it projects to known relay structures, i.e., the PVN and nPGi, which directly modulate the spinal erection generator.

Methods: PHAL was injected iontophoretically into the LPOA of two male Sprague-Dawley rats with the "target injection site" corresponding to the region of the LPOA in which bilateral lesions disrupted PS-related erections in previous experiments (Schmidt et al., 1998). The standard methods of iontophoretic injections, fixation techniques, and immunohistochemistry were performed as previously described (Luppi et al., 1995).

Results: A strong projection from the LPOA was observed to the PVN as seen by the large number of stained axonal fibers and terminal dot-like endings within the parvocellular and magnocellular divisions of the PVN. A significant number of stained fibers also were observed in the juxtafacial nPGi. A similar microinjection of PHAL 0.5 mm lateral to the "target injection site" failed to demonstrate stained axonal fibers within these structures.

Conclusions: These data demonstrate a strong projection from the LPOA to both the PVN and juxtafacial nPGi. The LPOA plays an essential role in PS-related erections. Although it does not project to the spinal cord, we hypothesize that the LPOA may modulate the spinal erection generator during PS through its relay connections with the PVN and nPGi, structures that contribute to a "final common path" from brain to spinal cord in erectile mechanisms (see figure). Afferent control of the LPOA from brainstem PS executive structures remains to be clarified. Moreover, the neurotransmitter within the LPOA involved in the efferent control of PS-related erections remains to be explored. These neuroanatomical results, together with our previous neurophysiological data, provide the first working neural model regarding PS-related erectile control.

Figure: Neural model of sleep related erectile mechanisms. See text for detail. Abbr.: LPOA, lateral preoptic area; PVN, paraventricular nucleus; nPGi, nucleus paragigantocellularis; OXY, oxytocin; 5-HT, serotonin; +, excitatory; -, inhibitory.

 

References: 
Luppi PH, Aston-Jones G, Akaoka H, Chouvet G and Jouvet M: Neuroscience 65:119-160, 1995.

Marson L and McKenna KE: Exp. Brain Res. 88:313-320, 1992.

Melis MR, Stancampiano R and Argiolas A: Pharmacol. Biochem. Behav. 48:203-207, 1994.

Schmidt MH, Valatx JL, Sakai K, Fort P, Luppi PH and Jouvet M: Sleep 21 (suppl):182.A, 1998.

Research supported by INSERM U52, CNRS URA 1195, and the Ohio Sleep Medicine Institute.

Abstracts - Listings: