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References in periodicals archive ?
Based on the wealth of data generated over the past 2 decades regarding the central role of GLU receptors (NMDA, AMPA, kainate, and others) in brain health and disease, modulating GLU pathways is rapidly emerging as a key target for drug development for neuropsychiatric disorders.
Our previous study showed that GluR5-containing kainate receptors (non-NMDA glutamate receptor) regulate the inhibitory synaptic transmission through endogenous glutamate; therefore, we tested how neonatal propofol and etomidate exposure affect endogenous glutamatergic tonic regulation to inhibitory synaptic transmission in P90 approximately rats.
Its possible mechanisms of action are hypothesized to be related to its ability to facilitate GABAergic transmission and antagonize AMPA and kainate glutamate receptor subtypes (De Sousa, 2010).
Topiramate inhibits voltage-dependent sodium and L-type calcium channels, potentiates GABA-mediated inhibitory neurotransmission through binding to a novel site on the GABAA-receptor complex and reduces excitatory neurotransmission by blocking a-amino-3-hydroxy-5methyl-4-isoxazolepropionic acid (AMPA) and kainate subtypes of glutamate receptors.
In the present work it is shown that phosphorylation of kainate receptors on its own promotes their activity.
Heat shock protein 27 shows a distinctive widespread and temporal pattern of induction in CNS glial and neuronal cells compared to heat shock protein 70 and caspase-3 following kainate administration.
iGluR-NMDA belongs to the ionotropic receptors family that has three functionally different types: a-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPA), high-affinity kainate receptors and N-Methyl-D-Aspartate (iGluR-NMDA) receptors.
The protein's attachment or withdrawal helps control the ability of kainate receptors to regulate signals passed along synapses linking the brain's millions of nerve cells.
Neurotoxic effect of domoic acid: mediation by kainate receptor electrophysiological studies in the rat.
Domoic acid, the alleged "mussel neurotoxin" might produce its neurotoxic effect through Kainate receptor activation: an electrophysiological study in rat dorsal hippocampus.
Excitotoxicity appears to be primarily dependent on NMDA and kainate receptor activation.
There also were reductions in muscarinic and kainate binding, but the differences were smaller.