BACKGROUND AMPA receptors are members of the ionotropic class of glutamate receptors, which also includes NMDA and kainate receptors. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. AMPA receptors mediate fast excitatory synaptic transmission in the CNS and play a key role in hippocampal synaptic long-term potentiation (LTP) and depression (LTD), which are two well established cellular models of learning and memory. AMPA receptors consist of GluR1-4 subunits which assemble as homomers or heteromers to form functional AMPA receptors. Each subunit possesses transmembrane regions, and all arranged to form a ligand-gated ion channel. The subunit composition determines the physiological properties of AMPA receptors: those containing the GluR2 subunit show low permeability to Ca2+ whereas those lacking this subunit show high Ca2+ permeability.1 L-glutamate acts as an excitatory neurotransmitter at many synapses in the central nervous system. Binding of the excitatory neurotransmitter L-glutamate induces a conformation change, leading to the opening of the cation channel, and thereby converts the chemical signal to an electrical impulse. The receptor then desensitizes rapidly and enters a transient inactive state. The functional role of GluR3 has remained elusive. In vitro studies of genetic knockout mice have not yielded significant alterations in synaptic communication. However, behavioral approaches utilizing knockout mice have shown that the subunit may be involved in exploration and motor coordination, suggesting that in vivo methodologies may be more forthcoming. It was suggested that GluR3 subunits are involved in the modulation of neural network activity. It was demonstrated that GluR3 subunits have diverse neurophysiological impact, modulating oscillatory networks for sleep, breathing and seizure generation.2 In addition; GluR3 can be an autoantigen to induce autoantibodies in patients, resulting in development of Rasmussen's encephalitis (RE), a childhood disease characterized by epileptic seizures associated with progressive destruction of a single cerebral hemisphere.3 RECENT PUBLICATIONS Hausknecht, K., S. Haj-Dahmane, Y. Shen, P. Vezina, C. Dlugos, and R. Shen. 2014. Excitatory Synaptic Function and Plasticity is Persistently Altered in Ventral Tegmental Area Dopamine Neurons after Prenatal Ethanol Exposure. Neuropsychopharmacology, 6 October.
REFERENCES 1. Mayer, M.L.: Curr. Opin. Neurobiol. 15:282-8, 2005 Products are for research use only. They are not intended for human, animal, or diagnostic applications. ПараметрыContact us regarding this antibody
*Optimal working dilutions must be determined by end user. Публикации
2014
Hausknecht, K., S. Haj-Dahmane, Y. Shen, P. Vezina, C. Dlugos, and R. Shen. 2014. Excitatory Synaptic Function and Plasticity is Persistently Altered in Ventral Tegmental Area Dopamine Neurons after Prenatal Ethanol Exposure. Neuropsychopharmacology, 6 October.
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