PubMed · 5696962
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A Moxham, J D Nabarro. 1968. Urinary testosterone excretion.. https://doi.org/10.1016/0009-8981(68)90040-5
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The hippocampus is involved in learning, affect, and the neurobiology of stress. After recording individual emotional reactivity (ER) during handling for vaginal smear screening (VSS), serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA), in the hypothalamus-preoptic area (HY-PA) and hippocampus were studied in two rat lines with different susceptibility to Freund's adjuvant arthritis (FAA), in relation to active avoidance behavior (AB), and under basal conditions in the FAA susceptible strain, in relation to ER, cycle stage and 20 h prior surgical stress. FAA susceptible rats compared to non-susceptible under equally low ER, showed higher AB, but lower 5-HIAA and 5-HIAA/5-HT ratio, under basal conditions, and upon termination of avoidance assay, only in hippocampus. In rats with different ER after prolonged VSS, high ER paralleled on diestrus-2 (DE-2), increased 5-HIAA and 5-HIAA/5-HT in the hippocampus and HY-PA, and adrenal weight, but decreased thymus and hippocampal weight. Under equal ER 5-HIAA and 5-HIAA/5-HT in the hippocampus and 5-HIAA/5-HT in the HY-PA were diminished on proestrus vs DE-2 but not estrus. Under equal distribution of proestrus and estrus higher ER paralleled higher hippocampal 5-HIAA. After equally high ER, combined with 20 h prior surgical stress, diminished hippocampal 5-HIAA/5-HT ratio, paralleled pronounced increase in adrenal weight compared to controls. Results suggest: negative association of hippocampal 5-HT to avoidance learning, a positive one to ER, modulated by cycle stage, and a role of differentiated 5-HT in homeostasis of HPA system.
Corticotropin-releasing factor (CRF) and its family of peptides are critical coordinators of homeostasis whose actions are mediated through their receptors, CRF receptor 1 (CRFR1) and CRFR2, found throughout the CNS and periphery. The phenotypes of mice deficient in either CRFR1 or CRFR2 demonstrate the critical role these receptors play. CRFR1-mutant mice have an impaired stress response and display decreased anxiety-like behavior, whereas CRFR2-mutant mice are hypersensitive to stress and display increased anxiety-like behavior. To further elucidate the roles of both CRF receptors and determine their interaction in behaviors, we have generated mice deficient in both CRFR1 and CRFR2. The behavioral phenotype of these mice demonstrates a novel role of the mother's genotype on development of pup anxiety. We have found that although the female double-mutant mice display anxiolytic-like behavior, the male double-mutant mice show significantly more anxiety-like behavior compared with the females. We have also determined that the dam's CRFR2 genotype affects the anxiety-like behavior of the male mice, such that a pup born to a heterozygous or mutant dam displays significantly more anxiety-like behavior regardless of that pup's genotype. Double-mutant mice also display an even greater impairment of their hypothalamic-pituitary-adrenal axis response to stress than that of the CRFR1-mutant mice. CRF mRNA levels are elevated in CRFR1- and double-mutant mice, and urocortin III and vasopressin mRNA levels are increased in CRFR2- and double-mutant mice. These results indicate that both CRFR1 and CRFR2 have critical roles in gene regulation and the maintenance of homeostasis in response to stress.
Several studies have demonstrated that opioids regulate a number of immune cell functions either through direct mechanisms or through the modulation of central nervous system outputs. It has been previously shown that morphine increases serum interleukin-6 (IL-6) levels; however, the mechanism by which this effect is produced is unknown. In the present study, experiments were designed to address the potential role of central opioid receptors, peripheral autonomic ganglia, and activation of the adrenals in the elevation of plasma IL-6 after morphine administration. A rapid and significant (2-fold) increase in plasma IL-6 was observed after morphine administration (10 mg/kg s.c.) to rats. This effect of morphine peaked within 30 min and remained elevated for at least 2 h. Central microinjection of morphine (10 microg/2 microl i.c.v.) mimicked the effects of peripherally administered morphine and was completely blocked by naltrexone (10 mg/kg s.c.) pretreatment. Pretreatment with a ganglionic blocker, chlorisondamine (0.5 mg/kg i.p.), also blocked the elevation of IL-6 by morphine, suggesting a role of the autonomic nervous system. In adrenalectomized animals, morphine administration did not increase IL-6 levels, whereas in adrenal demedullated animals, the effect of morphine remained intact. Thus, the adrenal cortex may be a potential source of IL-6, because IL-6 mRNA has been localized in the adrenal gland. Collectively, these data suggest a unique mechanism by which stimulation of central opioid receptors results in the elevation of plasma IL-6 through autonomic activation specifically of the adrenal cortex.