Hypothalamic

The posterior lobe of the pituitary, ie, the neurohypophysis, is under direct nervous control (1), unlike most other endocrine organs. The hormones stored in this gland are formed in hypothalamic nerve cells but pass through nerve stalks into the posterior pituitary. As early as 1895 it was found that pituitrin [50-57-7] an extract of the posterior lobe, raises blood pressure when injected (2), and that Pitocin [50-56-6] (Parke-Davis) causes contractions of smooth muscle, especially in the utems (3). Isolation of the active materials involved in these extracts is the result of work from several laboratories. Several highly active posterior pituitary extracts have been discovered (4), and it has been deterrnined that their biological activities result from peptide hormones, ie, low molecular weight substances not covalendy linked to proteins (qv) (5). 

In humans, the hypothalamic-derived protein and the hormone noncovalent complexes are packaged in neurosecretory granules, then migrate along axons at a rate of 1 4 mm/h until they reach the posterior pituitary where they are stored prior to release into the bloodstream by exocytosis (67). Considerable evidence suggests that posterior pituitary hormones function as neurotransmitters (68) vasopressin acts on the anterior pituitary to release adrenocorticotropic hormone [9002-60-2] (ACTH) (69) as well as on traditional target tissues such as kidneys. Both hormones promote other important central nervous system (CNS) effects (9,70). 

Alternative nomenclature for hypothalamic releasiag factors are iadicated. 

Intracerebroventricular injection of sulfolane in dosages of 300, 1000, and 3000 p.g caused the preoptic/anterior hypothalamic area temperature to rise 0.23, 0.47, and 0.56%, respectively. This hyperthermia was considered significant at the 3000-p.g dosage (30). 

Xenobiotic induced disruption of female fertility follows essentially the same pattern as that of the male and can be caused by changes in pituitary-hypothalamic function, primary disruption of ovarian structure or hormone secretion, or changes in the rate of hormone deactivation. In addition, there may be changes in the synthesis of estrogen induced production of the yolk protein by the liver (vitellogenesis), which in turn can lead to failure to lay down sufficient yolk in the developing oocytes. Vitellogenesis provides a valuable biomarker for endocrine dysfunction in both sexes,but is more properly considered as part of the liver function. 

Second-Order Hypothalamic Targets in Adiposity Signalling... 

Lesions of the lateral hypothalamic area (LHA) cause anorexia, whereas ablation of the paraventricular nucleus (PVN) cause a hyperphagic obesity syndrome. Consistent with these results, LHA neurons express the orexigenic neuropeptides MCH and orexin. PVN neurons produce several neuropeptides that are anorex-igenic when administered directly into the brain (CRH, TRH, oxytocin), in addition to their better known roles as endocrine regulators. LHA and PVN receive rich inputs from axons of NPY/AgRP and aMSH/CART-producing neurons in the arcuate nucleus. 

CART (cocaine- and amphetamine-regulated transcript) is a hypothalamic peptide that inhibits both normal and starvation-induced feeding when injected into cerebral ventricles of rats. CART is co-localized with the anorexigenic peptide a-melanocyte-stimulating hormone in neurons of the arcuate nucleus. Secretion of CART is stimulated by leptin and CART may be an endogenous inhibitor of food intake. 

Contraceptives. Figure 1 Regulation of hypothalamic and pituitary function by ovarian steroid hormones. 

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