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Kainate receptor neurotransmitter release

EVIDENCE FOR PRESYNAPTIC KAINATE RECEPTORS AS MODULATORS OF NEUROTRANSMITTER RELEASE... [Pg.34]

Kerchner, G. A., Wilding, T. J., Huettner, J. E and Zhuo, M. (2002) Kainate receptor subunits underlying presynaptic regulation of neurotransmitter release in the dorsal horn. J. [Pg.45]

The excitatoiy amino acids (EAA), glutamate and aspartate, are the principal excitatory neurotransmitters in the brain. They are released by neurons in several distinct anatomical pathways, such as corticofugal projections, but their distribution is practically ubiquitous in the central nervous system. There are both metabotropic and ionotropic EAA receptors. The metabotropic receptors bind glutamate and are labeled mGluRl to mGluRB. They are coupled via G-proteins to phosphoinositide hydrolysis, phospholipase D, and cAMP production. Ionotropic EAA receptors have been divided into three subtypes /V-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole-proprionic acid (AMPA), and kainate receptors (Nakanishi 1992). [Pg.53]

Several neurotransmitter and receptor changes are observed in Alzheimer s disease (Nordberg 1992). Losses occur in nicotinic receptors, but muscarinic receptors are relatively preserved. Reductions are also seen in serotonin 5-HTl and 5-HT2 receptors. Glutamate NMDA receptors decrease, while kainate receptors increase. j8-adrenergic and dopamine receptors are preserved. Decreases occur in receptors for somatostatin and neuropeptide Y, but corticotrophin-releasing factor receptors increase. Across all receptor subtypes for which there is a loss, the number of receptors decrease but the affinity constant remains unchanged. [Pg.148]


See other pages where Kainate receptor neurotransmitter release is mentioned: [Pg.928]    [Pg.226]    [Pg.255]    [Pg.520]    [Pg.928]    [Pg.134]    [Pg.60]    [Pg.19]    [Pg.351]    [Pg.408]    [Pg.508]    [Pg.157]    [Pg.157]   


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