Biological Effects

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The primary physiological effect of TRH is to stimulate secretion of the thyroid-stimulating hormone (TSH). Secretion of TRH, however, is under control of the thyroid hormones T3 and thyroxin (T4). These hormones exert negative feedback control on thyreotropic cells of the pituitary.

TRH also stimulates the release of prolactin, but this is not regarded as the main stimulatory pathway for prolactin release. TRH release is also subject to control through neurotransmitters. Among these are norepinephrine (which stimulates TRH secretion) and dopamine (which inhibits the release of TRH).

TRH has been reported to reduce stress- and deprivation-induced eating, hy-pothetically by induction of satiation. Early work demonstrated thyroid extracts reduced alcohol intake; and recent research shows a TRH analog specifically inhibits alcohol preference. It seems likely that TRH is one of several functional elements in the integrative neuropeptide control of alcohol consumption via short-term satiation (Kulkowsky et al. 2000).

TRH levels seem to affect motor behavior. Peripherally or locally administered TRH stimulates motor activity, an effect which involves enhanced turnover of the mesolimbic dopaminergic system and of the noradrenergic system. TRH also affects spinal cord motor activity since TRH, as well as serotonin, facilitates the discharge of motoneurons. Tissue culture experiments show a direct involvement of TRH in the development and activity of spinal motoneurons. TRH induces trophic effects, stimulates axonal outgrowth and the activity of choline actyltransferases.

TRH is also a mediator of peripheral effects. Intravenously applied TRH can alter blood circulation. In the periphery of the body, TRH application induces vasoconstriction, whereas in the brain vasodilatatory effects predominate.

TRH also induces gastro-intestinal effects, since it stimulates secretion of pepsin. However, these effects are variable, depending on the species and the manner in which TRH is administered. Gastrointestinal effects of TRH include an involvement in the pathogenesis of ulcer. The formation of a gastric ulcer can be experimentally induced by intracisternal injection of TRH, which mediates an increase in peripheral vagal activity through an enhancement of discharge from vagal nuclei. Curiously, this effect is accompanied by a reduction of the secretion of gastric acids.

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Beat The Battle With The Bottle

Beat The Battle With The Bottle

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