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).
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.
