PubMed · 14931738
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G OLSEN. 1952-03-20. [Plastic surgery].. https://pubmed.ncbi.nlm.nih.gov/14931738/
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The role of alcohol consumption and alcoholism as an addiction in regulating the chemistry of the brain and its physiology has gained a backlog of interest over the past few decades. Besides the notion that alcohol acts as a brain depressant, the molecular mechanisms and neuronal interactions are not well understood. Emerging evidence implicates alcohol as a neurochemical messenger that influences a cross talk amongst the nervous, immune, and endocrine systems. Specifically, alcohol acts as a crucial regulator of the hypothalamic-pituitary-adrenal (HPA) axis, thereby modulating the release of hormones, particularly adrenocorticotropic hormone (ACTH) and corticosterone (CORT). It is the aim of this review, therefore, to investigate current concepts on how alcohol, particularly ethanol, and alcoholism affect neuro-immune-endocrine neurochemical interactions via the regulation of the HPA axis, taking into consideration bio-behavioral and physiochemical aspects.
Hypothalamic neuromedin U (NMU) appears to have a role in the regulation of appetite and the hypothalamo-pituitary-adrenal (HPA) axis. Acute administration of NMU into the paraventricular nuclei (iPVN) increases plasma adrenocorticotrophic hormone and corticosterone, and inhibits food intake in fasted rats. No studies have as yet investigated the chronic effects of centrally administered NMU. We investigated the effect of twice-daily iPVN injections of 0.3 nmol NMU for 7 days on food intake, body weight, the HPA axis, and behavior in freely fed rats. Chronic iPVN NMU was not associated with a decrease in food intake or body weight. Chronic iPVN NMU produced a typical behavioral response on day 1 and day 4 of the study, and resulted in the elevation of plasma corticosterone present 18 h after the final injection. These results suggest NMU may have a role in the regulation of the HPA axis and behavior.
We have previously observed that a single exposure to immobilization (IMO), a severe stressor, caused long-term (days to weeks) desensitization of the response of the hypothalamic-pituitary-adrenal (HPA) axis to the homotypic stressor, with no changes in behavioral reactivity to novel environments. In contrast, other laboratories have reported that a single exposure to footshock induced a long-term sensitization of both HPA and behavioral responses to novel environments. To test whether these apparent discrepancies can be explained by the use of different stressors or different strains of rats, we studied in the present work the long-term effects of a single exposure to two different stressors (footshock or IMO) in two different strains of rats (Sprague-Dawley from Iffa-Credo and Wistar rats from Harlan). We found that both strains showed desensitization of the HPA response to the same (homotypic) stressor after a previous exposure to either shock or IMO. The long-term effects were higher after IMO than shock. No major changes in behavior in two novel environments (circular corridor, CC and elevated plus-maze, EPM) were observed after a single exposure to shock or IMO in neither strain, despite the fact that shocked rats showed a conditioned freezing response to the shock boxes. The present results demonstrate that long-term stress-induced desensitization of the HPA axis is a reliable phenomenon that can be observed with different stressors and strains. However, only behavioral changes related to shock-induced conditioned fear were found, which suggests that so far poorly characterized factors are determining the long-term behavioral consequences of a single exposure to stress.