Expression of fos and in vivo median eminence release of LHRH identifies an active role for preoptic area kisspeptin neurons in synchronized surges of LH and LHRH in the ewe.

We tested the working hypothesis that Fos will identify the critical population of kisspeptin neurons that accompanies the LHRH surge using a synchronized follicular phase model in intact cycling ewes. The model generates an LH surge that starts within a defined 2-h window in a 20-d synchronized cycle. With a modified push-pull cannula in vivo LHRH release from the median eminence was sampled in luteal phase ewes, ewes undergoing an LH surge for 2-4 h, and postsurge animals whose LH surge peaked 10-12 h earlier.

Ethanol suppression of the hypothalamic proopiomelanocortin level and the splenic NK cell cytolytic activity is associated with a reduction in the expression of proinflammatory cytokines but not anti-inflammatory cytokines in neuroendocrine and immune cells.

Background: Immune signals activate a network of cytokines in the central nervous system (CNS) that in turn causes release of neurotransmitters and hormones to modulate immune cell functions. We have recently shown that hypothalamic beta-endorphin neurons, via inhibition of the sympathetic neuronal activity, activate natural killer (NK) cell function in the spleen, and this communication is disrupted following chronic ethanol administration. Beta-endorphin neuronal function is known to be regulated by various proinflammatory and anti-inflammatory cytokines.

Role of beta-endorphin, corticotropin-releasing hormone, and autonomic nervous system in mediation of the effect of chronic ethanol on natural killer cell cytolytic activity.

Background: We have recently shown that alcohol feeding suppresses natural killer (NK) cell cytolytic activity partly by decreasing the function of hypothalamic beta-endorphin (beta-EP) neurons. The neuronal mechanism by which hypothalamic beta-EP communicates with the spleen to regulate the action of ethanol on NK cells is not known. In the present study, we evaluated the roles of beta-EP neurons, corticotropin releasing hormone (CRH) neurons, and the autonomic nervous system (ANS) in regulation of the ethanol effect on splenic NK cell cytolytic function.

Prenatal ethanol exposure alters the expression of period genes governing the circadian function of beta-endorphin neurons in the hypothalamus.

Sleep-wake disturbances and stress hyper-responsiveness have been observed in human neonates, children and adolescents who were exposed to alcohol during the prenatal period. Using the laboratory rat as an animal model, we investigated whether fetal ethanol exposure during gestational days 10-21 affects the circadian function of the stress-axis regulatory beta-endorphin neurons in the hypothalamus. Fetal ethanol-exposed rats showed abnormality in the circadian expression of proopiomelanocortin (POMC) mRNA encoding the peptide beta-endorphin in the arcuate nucleus of the hypothalamus during the adult period.

Beta-endorphin modulation of interferon-gamma, perforin and granzyme B levels in splenic NK cells: effects of ethanol.

The effects of ethanol and beta-endorphin (beta-EP) on productions of cytolytic factors granzyme B, perforin and IFN-gamma in splenic rat NK cells were determined. Intracranial administration of beta-EP increased protein and mRNA levels of cytolytic factors in NK cells. Chronic ethanol feeding reduced the basal and beta-EP-induced levels of cytolytic factors in NK cells.