Hypothalamic-pituitary regulatory system

All the hormones produced by the anterior pituitary except prolactin (PRL) are key participants in hormonal systems in which they regulate the production by peripheral tissues of hormones that perform the ultimate regulatory functions. In these systems, the secretion of the pituitary hormone is under the control of a hypothalamic hormone. Each hypothalamic-pituitary-endocrine gland system or axis provides multiple opportunities for complex neuroendocrine regulation of growth, development, and reproductive functions. 

GC exert their regulatory effects on the HPA system via two types of corticosteroid receptors the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR) (Reul and De Kloet 1985). GRs occur everywhere in the brain but are most abundant in hypothalamic CRH neurons and pituitary corticotropes. MRs, in contrast, are highly expressed in the hippocampus and, at lower expression levels, in hypothalamic sites involved in the regulation of salt appetite and autonomic outflow. The MR binds GC with a tenfold higher affinity than does the GR (Reul and De Kloet 1985). These findings on corticosteroid receptor diversity led to the working hypothesis that the tonic influences of corticosterone... 

One important neuronal TRH control center appears to be the paraventricular nucleus, but TRH Is widely distributed in the hypothalamus and highly concentrated in the median eminence (4). One important ipactor regulating TRH production is environmental temperature. Both peripheral thermal receptors and preoptic neuronal thermal receptors monitor environmental and central body temperature these receptors modulate preoptic neuronal outflow to the paraventricular nucleus and other TRH synthesizing neurons in the hypothalamus and median eminence which. In turn, modulate TRH secretion (4). Decreasing environmental and/or core body temperature Increase TRH output and increase the tonic level of TSH release. Somatostatin (SRIF) and dopamine can inhibit TSH release by actions at the pituitary level, and these inhibitory transmitters contribute to central nervous system modulation of TSH release (4). There is evidence that serotonin may be inhibitory in the adult rat, but this does not seem to be so in other species. Norepinephrine also may be inhibitory. Glucocorticoid can inhibit TSH release at the hypothalamic level, but the mechanism is not known. The exact roles of TRH and non-TRH regulatory factors in TSH control are not clear. Administration of somatostatin antiserum to adult rats increases basal TSH levels and potentiates the TSH response to cold (19). Inhibitory factors probably also play a role in the diurnal variation in TSH secretion, in the inhibitory reactions to stress, in the variation in thyroidal activity in psychosis, etc. 

Potential modes of action of lead reproductive toxicity include disraption of the hypothalamic-pituitaiy-gonadal axis through reduced luteinizing hormone secretion and reduction in the expression of the steroidogenic acute regulatory protein (Crain et al. 2008 EPA 2012). Lead may also interfere with cation-dependent secondary messenger systems that mediate pituitary hormone release... 

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