Overview
- Bettini, E. et al. (2010) J. Pharmacol. Exp. Ther. 335, 636.
Alomone Labs TCN 213 inhibits NMDA receptor channels expressed in Xenopus oocytes.A. Time course of NR1/NR2A currents, elicited by transient stimulations with 100 µM glutamate and 100 µM glycine every 100 sec, while membrane potential was held at -80 mV. 10 µM and 100 µM TCN 213 (#T-215) applied for 5 min (as indicated), inhibit current amplitude in a concentration-dependent manner. B. Superimposed current traces from the recording shown in A, upon application of control and of 10 µM and 100 µM TCN 213 (as indicated).
- Edman, S. et al. (2012) Neuropharmacology 63, 441.
- Black, S.A. et al. (2014) Front. Cell. Dev. Biol. 2, 45.
TCN 213 acts as a selective and potent NMDA (methyl-d-aspartate) receptor antagonist. This compound displays a high selectivity for GluN1/GluN2A-containing NMDAR receptors over GluN1GluN1/GluN2B containing NMDAR receptors. The degree of its antagonism is dependent on the concentration of the GluN1-site co-agonist, glycine or d-serine, and is independent of the glutamate concentration1. Relatively high concentrations of TCN 213 are required to achieve substantial block of GluN2A NMDAR-mediated responses.
NMDA receptors are heterotetrameric channels formed by the assembly of two obligatory GluN1 and two GluN2/GluN3 subunits. NMDAR plays an important role in a variety of cellular processes and brain functions such as, synaptic plasticity, addiction and stroke. NMDA receptors mediate physiological functions such as learning and memory formation. They play a role in glutamate excitotoxicity and are involved in many neurodegenerative conditions including Alzheimer’s disease2.
TCN 213 (#T-215) is a highly pure, synthetic, and biologically active compound.
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