Binge-level doses of ethanol have been demonstrated to severely disrupt the cerebellum and cerebellar-dependent tasks when administered to rodent subjects during the early postnatal period. NMDA receptor-mediated excitotoxicity associated with ethanol withdrawal has been implicated as a significant component contributing to neurotoxic effects resulting from early ethanol exposure, and studies using MK-801 have reported protection from ethanol-induced damage. The present study examined whether the administration of MK-801 during ethanol withdrawal would ameliorate ethanol-associated cell death in the interpositus nucleus of the cerebellum, as well as behavioral deficits in a cerebellar dependent task. Long Evans rat pups were treated with ethanol (5.25 g/kg) in a binge-like manner on postnatal day 6 using intragastric intubation. Subjects then received an injection of MK-801 (0.5 mg/kg) or vehicle during withdrawal, 30 hours after ethanol exposure. Rats were then trained on an eyeblink classical conditioning task as juveniles (40 days of age) and cerebellar interpositus nucleus numbers were assessed following conditioning. Ethanol-exposed subjects exhibited reductions in neuronal populations as well as behavioral deficits during eyeblink conditioning. However, MK-801 administration significantly attenuated observed deficiencies, suggesting a protective effect resulting from MK-801 treatment during ethanol withdrawal. These results support the role of NMDA receptor-mediated excitotoxicity as a component mechanism by which ethanol produces teratogenicity. Additionally, our findings support previous reports which have shown correlations between dependent measures of eyeblink classical conditioning behavior and unbiased cell counts in the interpositus nucleus.
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Introduction
Delineation of the underlying neurophysiological mechanisms of ejaculatory behavior is crucial for the treatment of male sexual dysfunction, including premature ejaculation. Recent studies provide compelling evidence that a population of lumbar spinothalamic (LSt) cells may play a role in the regulation of the ejaculatory response. Subsequent to ejaculation, LSt cells exhibit markers of activation that are not only highly correlated with ejaculatory behavior, but are also absent following the expression of other components of sexual behavior, such as mounts or intromissions. Similarly, targeted chemical lesion of LSt cells using substance P-saporin abolishes ejaculatory behavior explicitly. Early evidence suggests that pharmacological manipulation of LSt cells may offer additional evidence of crucial LSt cell involvement in the generation of ejaculation.
Aim
This review is intended to summarize what has currently been revealed regarding the role of LSt cells in the regulation and generation of ejaculatory behavior, and also to discuss the direction of future behavioral investigations.
Methods
Information presented in this discussion was derived from analysis of numerous recent articles detailing the delineation of anatomical and physiological correlates of sexual behavior, as well as numerous literature searches using the National Library of Medicine PubMed Services.
Results
A great deal of the work that has led to the implication of LSt cells in ejaculatory behavior is reviewed in the present article, including clinical data, as well as anatomical, physiological, and behavioral examinations. The rationale for ongoing pharmacological studies is also discussed.
Conclusion
LSt cells appear to play a vital role in the generation and regulation of ejaculatory behavior. Additional elucidation of this “ejaculation generator” could prove invaluable for the future treatment of male sexual dysfunction. Studies are currently in progress to further reveal the precise function of these cells and mechanisms of action through which they operate.
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