PubMed · 12230737
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Mike Boggild, Helen Ford. 2002. Multiple sclerosis.. https://pubmed.ncbi.nlm.nih.gov/12230737/
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In experiment 1, nine light horse geldings (three 3 x 3 Latin squares) received dexamethasone (DEX; 125 microg/kg BW, i.m.), glucose (0.2 g/kg BW, i.v.), or nothing (control) once per day for 4 days. DEX increased (P < 0.001) glucose, insulin, and leptin concentrations and resulted in a delayed increase (P < 0.001) in IGF-I concentrations. In experiment 2, mares were similarly treated with DEX (n = 6) or vehicle (n = 6). DEX again increased (P < 0.01) glucose, insulin, and leptin concentrations; the delayed elevation in IGF-I concentrations occurred on day 10, 12, and 19, relative to the first day of treatment. In experiment 3, six light horse geldings received either 200 IU of adrenocorticotropin (ACTH) i.m. or vehicle twice daily for 4 days. ACTH increased (P < 0.001) cortisol concentrations. Further, ACTH resulted in increases (P < 0.01) glucose, insulin, and leptin concentrations. In experiment 4, plasma samples from four light horse stallions that were fed 6-n-propyl-2-thiouracil (PTU) at 6 mg/kg BW for 60 days to induce hypothyroidism were compared to samples from control stallions. On day 52, stallions receiving PTU had lower concentrations of thyroxine (P < 0.05) and triiodothyronine (P < 0.01) and higher (P < 0.01) concentrations of TSH. Leptin concentrations were higher (P < 0.01) in PTU-fed stallions from day 10 through 52. In conclusion, circulating concentrations of leptin in horses was increased by administering DEX. Treatment with ACTH increased cortisol and resulted in lesser increases in leptin, glucose, and insulin. In addition, PTU feeding results in lesser increases in leptin concentrations.
Morphine withdrawal is characterized by an increase in the hypothalamus-pituitary-adrenocortical (HPA) axis activity. Here, by means of in situ hybridization, the changes in CRH and vasopressin (AVP) mRNAs have been analysed within the rat hypothalamic paraventricular nucleus (PVN) during morphine dependence and after naloxone-precipitated morphine withdrawal. CRH and AVP mRNA expression were analysed 30 min following administration of saline or naloxone to control groups and to morphine dependent rats. The data for in situ hybridization analysis of PVN neurons show that there were no changes in the total size of labelled area for CRH or AVP mRNA during morphine withdrawal, indicating that dependence on morphine does not involve alterations in the number of neurons expressing CRH or AVP mRNA. However, levels of mRNA encoding for CRH were decreased in the PVN during morphine dependence and withdrawal. By contrast, injection of saline or naloxone to morphine dependent rats did not affect the intensity of AVM mRNA expression. All these findings are discussed in term of cellular events that couple morphine dependence-increased HPA axis activity with changes in gene expression in selective neurons of the PVN.
Central cholinergic systems differentially modulate hypothalamic-pituitary-adrenal (HPA) axis activity in female and male animals (sexual diergism). We previously reported that male rats had significantly greater HPA axis responses to stimulation by physostigmine (PHYSO), an acetylcholinesterase (AChE) inhibitor, compared to females. Females in defined estrous cycle stages, however, were not studied because of sample size limitations. We, therefore, determined HPA axis responses to stimulation by PHYSO in females during all estrous cycle stages (n = 78), and in male rats (n = 75). Plasma arginine vasopressin (AVP), adrenocorticotropic hormone (ACTH), and corticosterone (CORT) were measured. Estrous cycle stage was determined by light microscopy of vaginal smears. Proestrous and estrous females had higher ACTH and CORT responses compared to metestrous and diestrous females. Males had higher ACTH and AVP responses compared to females in all cycle stages. CORT responses followed the ACTH responses, except that females started from a higher baseline in all estrous stages, compared to males. These results suggest that cholinergic regulation of the HPA axis differs among females across stages of the estrous cycle, as well as between males and females. These effects are likely due to differences in circulating sex steroids and their actions within the brain.