Search PubMed⌕ Search

Biomedical subjects

L C Krey

Publications and source records attributed to L C Krey.

83 records · Page 5Linked to original sources
PubMed1975

Surgical disconnection of the medial basal hypothalamus and pituitary function in the rhesus monkey. II. GH and cortisol secretion.

Eighteen female rhesus monkeys subjected to complete or anterior disconnection of the medial basal hypothalamus (MBH) were studied to assess the effects of these deafferentation procedures on GH and cortisol secretion. Basal serum levels of GH were not disturbed or were slightly elevated following complete or anterior MBH disconnection. GH secretion in response to vasopressin administration or insulin hypoglycemia, however, was abolished by complete isolation of the MBH. In contrast, the elevations in serum cortisol concentrations observed in response to these noxious stimuli were not noticeably affected. The normal diurnal rhythm in cortisol secretion remained fully evident following anterior deafferentation, but was severely attenuated or abolished when all neuronal inputs to the MBH were transected. Such observations suggest that the central components of the neuroendocrine systems which regulate basal GH secretion and which subserve stress-induced elevations in cortisol secretion are resident within the MBH-hypophysial unit. In addition, these data indicate that the mechanisms underlying the diurnal rhythm in cortisol secretion, as well as those mediating the discharges of GH in response to vasopressin administration and insulin hypoglycemia, are dependent on the integrity of neuronal connections between the MBH and other hypothalamic and/or extrahypothalamic areas.

Animals↗
PubMed1975

Surgical disconnection of the medial basal hypothalamus and pituitary function in the rhesus monkey. III. Thyroxine secretion.

The effects of complete and anterior disconnection of the medial basal hypothalamus (MBH( on TSH secretion in the rhesus monkey were assessed by measuring serum thyroxine concentrations. Following complete MBH disconnection, serum thyroxine concentrations declined to 50% of preoperative control levels within 7 days. In 6 of 10 animals, thyroxine levels remained depressed throughout the postoperative observation period of 60 to 150 days. In the remainder, serum thyroxine concentrations returned to control levels after 3 weeks. Anterior disconnection of the MBH had variable effects on thyroid function. In 4 of 7 animals, serum thyroxine concentrations declined for 5 days following the operation but returned to preoperative levels within the next 3 weeks. In 2 others, serum thyroxine levels did not change while in the remaining animal thyroxine concentrations increased transiently to twice preoperative levels before returning to normal values. Thus, in the monkey, as in the rat, anterior MBH disconnection has little consistent effect on thyroid function, while complete isolation of the MBH causes a moderate decline which is most readily attributable to a decrease in thyrotropin secretion. The variations in the effects of anterior and complete MBH disconnection on thyroid function could not be confidently correlated with variations in the placement of the cuts.

Animals↗
PubMed1975

Surgical disconnection of the medial basal hypothalamus and pituitary function in the rhesus monkey. IV. Prolactin secretion.

The effects of anterior and complete hypothalamic deafferentation on prolactin secretion in the rhesus monkey have been assessed. Complete disconnection ofthe medial basal hypothalamus (MBH) had no apparent effect on serum prolactin concentrations, in either intact or ovariectomized monkeys, nor did it diminish the stimulation of prolactin secretion induced by sodium pentobarbital anesthesia. Anterior disconnection of the MBH in intact females was also without effect on prolactin secretion. When the MBH was inadvertently damaged during the complete disconnection procedure, serum prolactin levels increased approximately 5-fold in otherwise intact animals while remaining unchanged in ovariectomized monkeys, thereby suggesting that ovarian hormones may modulate the secretion of prolactin in response to a reduction of hypothalamic inhibitory influences. In contrast, basal serum prolactin concentrations were not notably influenced by ovariectomy or estrogen administration nor were the patterns of prolactin secretion related to the phases of the menstrual cycle. The results of these studies suggest that the consequences of complete MBH disconnection on prolactin secretion are essentially the same in the rhesus monkey and in the rat, although major differences exist between these species with regard to the influence of estrogen on the production of this hormone.

Animals↗
PubMedDate not supplied

The adrenocortical axis in the aged rat: impaired sensitivity to both fast and delayed feedback inhibition.

Aged rats secrete excessive amounts of the species-typical glucocorticoid, corticosterone, under basal conditions, following the end of stress and during habituation to mild stressors. Furthermore, the aged rat is resistant to the inhibitory effects of the synthetic glucocorticoid dexamethasone upon subsequent corticosterone secretion. These observations have led to the hypothesis that the aged adrenocortical axis is desensitized to the inhibitory effects of glucocorticoids. In the present study, we have defined this negative-feedback deficit more precisely. The aged adrenocortical axis is subject to both rate-sensitive fast feedback regulation by corticosterone and to level-sensitive delayed feedback. Moreover, there is no age difference in the maximal extent of feedback inhibition which can be attained. However, the sensitivity to both forms of feedback regulation is diminished in aged rats, in that the aged adrenocortical axes are responsive under feedback conditions which completely inhibit corticosterone secretion in young animals. Such insensitivity is likely to underlie the incidences of hyperadrenocorticism apparent in the aged rat; we speculate that progressive degeneration in the aged hippocampus might be the cause of this dampened sensitivity to feedback inhibition.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Intracellular receptors mediate gonadal steroid modulation of LHRH-induced LH release.

Primary cultures of enzymatically dispersed rat pituitary cells were used to study the role of intracellular receptors in gonadal steroid modulation of LHRH-induced LH release. Nuclear receptors for both testosterone (T) and 17 beta-estradiol (E) were observed, with KD values of 6.3 and 0.1 nM respectively. Occupation of these receptors was correlated with modulation of LH secretion. The relationship between these two parameters was nonlinear, so that steroid effects on LH secretion were maximal when fewer than 50% of the receptors were occupied. The androgen antagonist cyproterone blocked both T binding to nuclear receptors and T inhibition of LH secretion. Similarly, the estrogen antagonist CI-628 blocked both E binding and E stimulation of LH secretion. In cultures derived from pseudohermaphrodite rats. T did not bind to nuclear receptors, nor did it inhibit LH secretion. These results, showing a relationship between occupation of nuclear receptors and modulation of LH secretion, suggest that steroid effects on LH secretion are mediated by these receptors.

Animals↗