Biomedical subjects

J F Nelson

Publications and source records attributed to J F Nelson.

133 records · Page 8Linked to original sources

PubMedDate not supplied

Loss during aging of beta-endorphinergic neurons in the hypothalamus of female C57BL/6J mice.

Beta-endorphin (B-EP) content is often reduced in hypothalami of aging rodents. The objective of this study was to determine whether reduced B-EP content is associated with a reduced number of B-EP immunoreactive neurons. Serial coronal sections extending from the caudal hypothalamus through the retrochiasmatic area were examined by quantitative light microscopy in mature (5-6 month) and senescent (24-28 month) mice that had been ovariectomized 1 week earlier and injected with colchicine 24-48 h before sacrifice. Old mice were acyclic. As expected, B-EP immunoreactive cell bodies were restricted to the region of the arcuate nucleus. There was a 35% loss of B-EP immunopositive neurons in old, macroscopically disease-free animals. By contrast, some old animals with pituitary tumors had no loss of B-EP neurons. These results suggest that a subpopulation of B-EP neurons either die or stop synthesizing detectable concentrations of B-EP in aged mice. The basis for the absence of reduced B-EP neurons in some mice with pituitary tumors is unclear, but this observation underscores the importance of distinguishing age-related changes associated with diseases of aging from those that are independent of such diseases.

Aging↗

PubMedDate not supplied

Neuroendocrine involvement in aging: evidence from studies of reproductive aging and caloric restriction.

Neuroendocrine changes contribute to female reproductive aging, but changes in other tissues also play a role. In C57BL/6J mice, neuroendocrine changes contribute to estrous cycle lengthening and reduced plasma estradiol levels, but the midlife loss of cyclicity is mainly due to ovarian failure. Hypothalamic estrogen receptor dynamics and estrogenic modulation of gene expression are altered in middle-aged cycling mice. Although insufficient to arrest cyclicity, these neuroendocrine changes may contribute to other reproductive aging phenomena, such as altered gonadotropin secretion and lengthened estrous cycles. In women, the loss of ovarian oocytes, the cause of menopause, accelerates in the decade before menopause. Accelerated oocyte loss may in turn be caused by a selective elevation of plasma follicle stimulating hormone, and neuroendocrine involvement may thus be implicated in menopausal oocyte loss. Chronic calorie restriction retards both neural and ovarian reproductive aging processes, as well as age-related change in many other physiological systems. The diverse effects of food restriction raises the possibility of an underlying coordinated regulatory response of the organism to reduced caloric intake, possibly effected through alterations of neural and/or endocrine signalling. We are therefore attempting to identify neuroendocrine changes that may coordinate the life prolonging response of animals to food restriction. Our initial focus is on the glucocorticoid system. Food restricted rats exhibit daily periods of hyperadrenocorticism, manifest as elevated free corticosterone during the diurnal peak. We hypothesize that this hyperadrenocortical state potentiates cellular and organismic homeostasis throughout life in a manner similar to that achieved during acute stress, thereby retarding aging processes and extending life span.

Aging↗

PubMedDate not supplied

Food restriction delays the age-related increase in GFAP mRNA in rat hypothalamus.

Astrogliosis with advancing age is correlated with increased expression of glial fibrillary acidic protein (GFAP). Hypothalamic GFAP mRNA prevalence was determined in male F344 rats of different ages that were fed ad lib (AL) and compared with that of rats that were food-restricted (FR) to 60% of AL levels. Hypothalamic GFAP mRNA increased 3-fold at 24 to 25 months in AL rats compared with 3 and 6 month groups. There were no differences in GFAP mRNA levels between AL and FR rats from 3 to 18 months. However, GFAP mRNA was significantly lower in FR than in AL rats at 24 to 25 months; FR rats reached the level of GFAP mRNA in 24 to 25 months AL rats by 33 months. Hypothalamic glutamine synthetase mRNA also increased with age in both dietary groups but did not differ between dietary groups at any age. The observation that FR delays the increased expression of GFAP in the hypothalamus during aging lends support to the hypothesis that upregulation of GFAP mRNA is a biomarker of brain aging.

Aging↗

PubMedDate not supplied