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Excitatory amino acid

Compounds that have agonistic properties at glutamate or aspartate receptors are also CNS stimulants, readily cause convulsions, and presumably could also be employed as analeptics. Three separate excitatory amino acid receptor subtypes have been characterized pharmacologically, based on the relative potency of synthetic agonists. These three receptors are named for their respective prototypical agonists A/-methyl-D-aspartate [6384-92-5]... [Pg.463]

Within the nervous system, ChEs were shown to be involved in membrane conductance and transmission of excitatory amino acids, learning and memory, neurite growth, neuritic translocation and acute stress reactions. Recent findings propose AChE s involvement in apoptosome formation [2]. [Pg.358]

Glutamate is a small amino acid which constitutes the most important neurotransmitter at excitatory synapses in the mammalian brain. Glutamate can act on several different types of receptors including cation channels and G-protein-coupled receptors. [Pg.552]

Most neurons in the central nervous system are stimulated by L- glutamate, the major excitatory amino acid in the brain. The postsynaptic actions of... [Pg.657]

Orexin neurons, likely to be glutamatergic themselves, express the excitatory amino acid transporter EAAT3, vesicular glutamate transporters VGLUT1 and VGLUT2, secretogranin II, ionotropic (NMDAR,... [Pg.911]

Acamprosate. Acamprosate (calcium acetylhomotaurinate), an amino acid derivative, affects both GABA and excitatory amino acid (i.e., glutamate) neurotransmission (the latter effect most likely being the one that is important for its therapeutic effects in alcoholism). Initially evaluated in a singlecenter trial in France, acamprosate was shown to be twice as effective as placebo in reducing the rate at which alcoholic patients returned to drinking (Lhuin-tre et al. 1985). The safety and efficacy of the medication have been studied most widely in Europe, and three of these studies provided the basis for the recent approval of acamprosate by the FDA for clinical use in the United States. As with naltrexone, there exist a number of meta-analytic studies that provide consistent evidence of the efficacy of the medication in the treatment of alcohol dependence. [Pg.28]

Lynch DR, Guttmann RP (2002) Excitotoxicity perspectives based on N-methyl-D-aspartate receptor subtypes. J Pharmacol Exp Ther 300(3) 717-723 Magnuson DS, Knudsen BE, Geiger JD, Brownstone RM, Nath A (1995) Human immunodeficiency virus type 1 tat activates non-N-methyl-D-aspartate excitatory amino acid receptors and causes neurotoxicity. Ann Neurol 37(3) 373-380 Mamdouh Z, Chen X, Kerini LM, Maxfield FR, Muller WA (2003) Targeted recycling of PECAM from endothelial surface-connected compartments during diapedesis. Nature 421(6924) 748-753... [Pg.27]

Rothman S (1984) Synaptic release of excitatory amino acid neurotransmitter mediates anoxic neuronal death. J Neurosci 4(7) 1884-1891... [Pg.30]

HIV proteins can also disrupt ion homeostasis in astrocytes, which compromises neuronal function (Pulliam et al. 1993 Benos et al. 1994a, b Holden et al. 1999). Intact HIV-1 virions or gpl20 also markedly inhibit glutamate uptake by astrocytes and cause reductions in excitatory amino acid transporter-2 (EAAT2) mRNA and protein levels (Wang et al. 2003). The inability of astrocytes to buffer extracellular glutamate is likely to decrease the excitotoxic threshold of bystander neurons. [Pg.362]

Excellent biological arguments exist for a direct impact of fever specifically on neurological outcome. On a local level, fever produces increased levels of excitatory amino acids (e.g., glutamate and dopamine), free radicals, lactic acid, and pyr-uvate. There is an increase in cell depolarizations and BBB breakdown. Enzymatic function is impaired and cytoskeletal stability reduced. These events lead to increased cerebral edema, with a possible reduction in CPP as well as larger volumes of ischemic injury. " ... [Pg.168]

The excitatory amino acids are found in most sensory fibres of both large- and small-diameter fibres and, in the latter, they are co-localised with peptides such as substance P. The co-existence of these two transmitters suggests that they are released together in... [Pg.218]

Colingridge, G and Singer, W (1990) Excitatory amino acid receptors and synaptic plasticity. Trends Pharm. Sci. 11 290-296. [Pg.224]


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See also in sourсe #XX -- [ Pg.158 ]




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