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Hypothalamus catecholamine

Hi-receptors in the adrenal medulla stimulates the release of the two catecholamines noradrenaline and adrenaline as well as enkephalins. In the heart, histamine produces negative inotropic effects via Hr receptor stimulation, but these are normally masked by the positive effects of H2-receptor stimulation on heart rate and force of contraction. Histamine Hi-receptors are widely distributed in human brain and highest densities are found in neocortex, hippocampus, nucleus accumbens, thalamus and posterior hypothalamus where they predominantly excite neuronal activity. Histamine Hrreceptor stimulation can also activate peripheral sensory nerve endings leading to itching and a surrounding vasodilatation ( flare ) due to an axonal reflex and the consequent release of peptide neurotransmitters from collateral nerve endings. [Pg.589]

Pituitary Adenylyl Cyclase-activating Polypeptide (PACAP) is a 38-amino acid peptide (PACAP-38), which is widely expressed in the central nervous system. PACAP is most abundant in the hypothalamus. It is also found in the gastrointestinal tract, the adrenal gland and in testis. Its central nervous system functions are ill-defined. In the periphery, PACAP has been shown to stimulate catecholamine secretion from the adrenal medulla and to regulate secretion from the pancreas. Three G-protein coupled receptors have been shown to respond to PACAP, PAQ (PACAP type I) specifically binds PACAP, VPACi and VPAC2 also bind vasoactive intestinal peptide (VDP). Activation of PACAP receptors results in a Gs-mediated activation of adenylyl cyclase. [Pg.979]

Kirby LG, Chou-Green JM, Davis K, Lucki I (1997) The effects of different stressors on extracellular 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. Brain Res 760 218-230 Kirby LG, Rice KC, Valentino RJ (2000) Effects of corticotropin-releasing factor on neuronal activity in the serotonergic dorsal raphe nucleus. Neuropsychopharmacology 22 148-162 Kozicz T, Yanaihara H, Arimura A (1998) Distribution of urocortin-like immunoreactivity in the central nervous system of the rat. J Comp Neurol 391 1-10 Lavicky J, Dunn AJ (1993) Corticotropin-releasing factor stimulates catecholamine release in hypothalamus and prefrontal cortex in freely moving rats as assessedby microdialysis. J Neurochem 60 602-612... [Pg.201]

Phentermine (Adipex-P) b b 3.2 (0.1) An anorexiant that suppresses appetite by acting on the hypothalamus, leading to an increased release of catecholamines, ultimately reducing the appetite. [Pg.73]

Some information is available on the relationship between the CCK and the noradrenergic systems. In the lateral hypothalamus of satiated rats, perfused CCK-8S by push-pull perfusion enhanced the efflux of noradrenaline. However, in fasted animals, CCK-8S often suppressed the catecholamine s release. Perfused in the lateral hypothalamus, CCK exerted opposite effects. [Pg.430]

The effects of treatment with selegiline, an MAO-B inhibitor, on plasma levels of insulin-like growth factor I (IGF-I) (as indicator of GH secretion), levels of monoamines and their metabolites, and the activity and content of tyrosine hydroxylase — the rate-limiting enzyme in the biosynthesis of catecholamines — in the hypothalamus and hypophysis of old animals have been studied. It is believed that the antiaging effects of selegiline are due to restoration of hypothalamic hormones. [Pg.182]

Shekhar, A., Katner, J. S., Rusche, W. P., Sajdyk, T. J. Simon, J. R. (1994). Fear-potentiated startle elevates catecholamine levels in the dorsomedial hypothalamus of rats. [Pg.379]

Ajika K (1979) Simultaneous localization of LHRH and catecholamines in rat hypothalamus. J Anat 725 331-347. [Pg.497]

Fuxe K, Agnati LF, Andersson K, Eneroth P, Harfstrand A, Goldstein M, Zoli M (1984) Studies on neurotensin-catecholamine interactions in the hypothalamus and in the forebrain of the male rat. Neurochem Int 6 737-750. [Pg.505]

Kapoor V, Chalmers JP (1987) A simple, sensitive method for the determination of extracellular catecholamines in the rat hypothalamus using in vivo dialysis. J Neurosci Methods 79 173-182. [Pg.508]

Lavicky J, Dunn A (1993) Corticotropin-releasing factor stimulates catecholamine release in hypothalamus and prefrontal cortex in freely moving rats as assessed by microdialysis. J Neurochem 60 601-612. [Pg.510]

Leshin LS, Kraeling RR, Kiser TE (1995) Immunocytochemical localization of the catecholamine-synthesizing enzymes, tyrosine hydroxylase and dopamine-P-hydroxylase, in the hypothalamus of cattle. J Neurochem Anat 9 175-194. [Pg.510]

In its acute stages, benzene toxicity appears to be due primarily to the direct effects of benzene on the central nervous system, whereas the peripheral nervous system appears to be the target following chronic low-level exposures. In addition, because benzene may induce an increase in brain catecholamines, it may also have a secondary effect on the immune system via the hypothalamus-pituitary-adrenal axis (Hsieh et al. 1988b). Increased metabolism of catecholamines can result in increased adrenal corticosteroid levels, which are immunosuppressive (Hsieh et al. 1988b). [Pg.215]

It has been suggested that the vasodilation observed on stimulation of sympathetic fibers is a result of a sympathetic cholinergic innervation. In a recent study, Feigl stimulated the stellate ganglion and hypothalamus and found no evidence of cholinergic mediated coronary vasodilation. Information obtained by sympathetic stimulation of the coronary circulation has been recently criticized. The distribution of alpha and beta receptors within the coronary vasculature may vary with species and physiological state of the animal. Different experimental approaches may favor stimulation of either alpha or beta receptors. Other factors may be involved such as dose or time dependent actions of catecholamines on different receptors. [Pg.77]


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See also in sourсe #XX -- [ Pg.257 ]




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