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Vitamin brain receptors

Eyles DW, Smith S, Kinobe R, Hewison M, McGrath JJ. 2005. Distribution of the vitamin D receptor and 1 alpha-hydroxylase in human brain. J Chem Neuroanat 29 21-30. [Pg.83]

J. J. and Mackay-Sim, A. (2006) Swimming behaviour and post-swimming activity in Vitamin D receptor knockout mice. Brain Res Bull 69, 74-78. [Pg.281]

Durk MR, Chan GN, Campos CR, Peart JC, Chow EC, Lee E et al (2012) la,25-Dihydroxyvitamin D3-liganded vitamin D receptor increases expression and transport activity of P-glycoprotein in isolated rat brain capillaries and human and rat brain microves-sel endothelial cells. J Neurochem 123 944-953... [Pg.553]

Deficiencies of most of the vitamins have been found in one or another group of elderly individuals. Studies have demonstrated poor intake, low serum levels and, less often, decreased tissue stores in the elderly. Of the fat soluble vitamins, deficiency of vitamin D seems most common. We have found that despite exposure to strong sun, serum 25-hydroxy-vitamin D levels were lower in healthy, active, elderly individuals than in young controls (Omdahl et al., 1982). The most active of the vitamin D metabolites, 1,25-dihydroxy-vitamin D, also falls with age (Slo-vik et al., 1981). Recently, brain receptors for 1,25-dihydroxy-vitamin D3 have been demonstrated in rats (Stumpf et al, 1982). The role of such receptors is not clear, but their presence suggests a central modulation of calcium homeostasis, conceivably important for the maintenance of normal mental status. [Pg.78]

Particular attention is given to the development of new mechanistic biomarker assays and bioassays that can be used as indices of the toxicity of mixtures. These biomarker assays are typically based on toxic mechanisms such as brain acetylcholinesterase inhibition, vitamin K antagonism, thyroxin antagonism, Ah-receptor-mediated toxicity, and interaction with the estrogenic receptor. They can give integrative measures of the toxicity of mixtures of compounds where the components of the mixture share the same mode of action. They can also give evidence of potentiation as well as additive toxicity. [Pg.254]

Sunderland T, Tariot PN, Newhouse PA. (1988). Differential responsivity of mood, behavior, and cognition to cholinergic agents in elderly neuropsychiatric populations. Brain Res. 472 4y. 371-89. Tachikawa E, Kudo K, Flarada K, Kashimoto T, Miyate Y, Kakizaki A, Takahashi E. (1999). Effects of ginseng saponins on responses induced by various receptor stimuli. EurJ Pharmacol 369(1) 23-32. Tagami M, Ikeda K, Yamagata K, Nara Y, Fujino FI, Kubota A, Numano F, Yamori Y. (1999). Vitamin E prevents apoptosis in hippocampal neurons caused by cerebral ischemia and reperfusion in stroke-prone spontaneously hypertensive rats. Lab Invest. 79(5) 609-15. [Pg.490]

Correct answer = D. Carbidopa inhibits the peripheral decarboxylation of levodopa, permitting lower dosage. Chlorpromazine blocks the dopamine receptor site in the brain and therefore blocks the beneficial effects of levodopa. Vitamin B6 enhances the peripheral decarboxylation of levodopa. Dopamine does not itself cross the blood-brain barrier. Phenelzine inhibits the metabolism of norepinephrine and serotonin and may produce a hypertensive crisis. [Pg.99]

There is a great deal of evidence that deficiency of serotonin (5-hydroxytryptamine) is a factor in depressive illness, and many antidepressant drugs act to decrease its catabolism or enhance its interaction with receptors. A key enzyme involved in the synthesis of serotonin (and the catecholamines) is aromatic amino acid decarboxylase, which is pyridoxal phosphate-dependent. Therefore, it has been suggested that vitamin Be deficiency may result in reduced formation of the neurotransmitters and thus be a factor in the etiology of depression. Conversely, it has been suggested that supplements of vitamin Be may increase aromatic amino acid decarboxylase activity, and increase amine synthesis and have a mood-elevating or antidepressant effect. There is little evidence that vitamin Be deficiency affects the activity of aromatic amino acid decarboxylase. In patients with kidney failure, undergoing renal dialysis, the brain concentration of pyridoxal phosphate falls to about 50% of normal, with no effect on serotonin, catecholamines, or their metabolites (Perry etal., 1985). [Pg.264]

Goti D, Hrzenjak A, Levak-Frank S, Frank S, van der Westhyzen DR, et al. 2001. Scavenger receptor class B, type I is expressed in porcine brain capillary endothelial cells and contributes to selective uptake of HDL-associated vitamin E. J. Neurochem. 76(2) 498-508... [Pg.655]

Phospholipids and glycosphingolipids are amphipathic lipid constituents of membranes (Chapter 10). They play an essential role in the synthesis of plasma lipoproteins (Chapter 20) and eicosanoids (Chapter 18). They function in transduction of messages from cell surface receptors to second messengers that control cellular processes (Chapter 30) and as surfactants. Cholesterol is mainly of animal origin and is an essential constituent of biomembranes (Chapter 10). In plasma, cholesterol is associated with lipoproteins (Chapter 20). Cholesterol is a precursor of bile acids formed in the liver of steroid hormones secreted by adrenals, gonads, and placenta and 7-dehydrocholesterol of vitamin D formed in the skin. In tissues, cholesterol exists primarily in the unesterified form (e.g., brain and erythrocytes), although appreciable quantities are esterified with fatty acids in liver, skin, adrenal cortex, and plasma lipoproteins. [Pg.401]


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See also in sourсe #XX -- [ Pg.852 ]




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