NMDARN-Methyl-D-Aspartate Receptor
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The combination of increased postsynaptic NMDAR function and elevated glutamate levels in the synapse found after ethanol withdrawal creates a "hyperglutamatergic" state associated with seizure activity and neuronal injury (see figure 2C).
The N-methyl-Daspartate receptor (NMDAR) is one of the main excitatory amino acid receptors.
The immunochemical identification of NMDAR was performed by use of commercial antibodies and antibodies kindly supplied by Dr.
Proper functioning of NMDAr in the brain is critical for learning, memory and the ability to form new neuronal connections (neuroplasticity).
Most patients with anti-NMDAR encephalitis have intrathecal synthesis of NMDAR antibodies.[2],[6],[7] Compelling clinical and laboratory evidence exists that anti-NMDAR antibodies are pathogenic.
[28] had reported that there were several waves of NMDAR subunit rises, after LTP induction by high-frequency stimulation (HFS).
On the other hand, some patients with teratoma developed several kinds of encephalitis without NMDAR antibodies.
The activation of iNOS by inflammatory processes and of nNOS by [Ca.sup.2+] influx through NMDAR leads to an increase in intracellular levels of RNS.
Retrospective testing of specimens from case-patients with undiagnosed disease in the California Encephalitis Project identified a newly described autoimmune syndrome, termed anti-N-methyl-D-asparate receptor (NMDAR) encephalitis, as the leading cause of encephalitis among patients [less than or equal to] 30 years of age (19).
The high calcium amplitude that leads to LTP is thought to be generated by calcium influx through the NMDAR. The low calcium leading to LTD has more diverse sources.
It was unclear whether the NMDA-type glutamate receptor (NMDAR), another major route of [Ca.sup.2+] influx into neurons, can contribute to endocannabinoid release.