Rapid communicationIfenprodil and SL 82.0715 are antagonists at the polyamine site of the N-methyl-D-aspartate (NMDA) receptor
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Cited by (143)
NMDA receptor binding is reduced within mesocorticolimbic regions following chronic inhalation of toluene in adolescent rats
2015, Brain ResearchCitation Excerpt :Sections were collected in a 1: 3 series with a total of two sections per slide separated by ~500 μm. Receptor binding of [3H]-ifenprodil, a high affinity non-competitive NMDA receptor antagonist selective for the GluN2B subunit (Carter et al., 1989; Williams, 1993; Williams et al., 1993) and [3H]-epibatidine, which binds to the α2−4, β2, β4 nACh receptor subunits (Marks et al., 1998; Jensen et al., 2005; Duncan et al., 2009) was investigated within regions of the mesocorticolimbic system via in vitro autoradiography. All ligands were purchased from Perkin Elmer (Waltham, MA, USA).
Ifenprodil, a NR2B-selective antagonist of NMDA receptor, inhibits reverse Na<sup>+</sup>/Ca<sup>2+</sup> exchanger in neurons
2012, NeuropharmacologyCitation Excerpt :The NR2 subunit that contains the glutamate binding site has four different isoforms, encoded by different genes NR2A–NR2D (Cull-Candy et al., 2001). Ifenprodil was found to be the first neuroprotective agent selective for NR2B-containing NMDARs (NR2B-NMDARs) (Carter et al., 1988, 1989; Williams, 1993). Importantly, ifenprodil increases the potency of protons to block the NMDAR (Mott et al., 1998) and protects neurons against glutamate excitotoxicity in an activity-dependent manner (Kew et al., 1996).
Pharmacological modulation of NMDA receptor activity and the advent of negative and positive allosteric modulators
2012, Neurochemistry InternationalCitation Excerpt :In this context it was tested in animal models as an anti-stroke agent and found to have some therapeutic benefit. Further studies showed that this agent was an NMDA receptor blocker with an unusual mechanism of action (Carter et al., 1989, 1990; Legendre and Westbrook, 1991). The blockade is neither use-dependent nor voltage-dependent and is selective for GluN1/GluN2B receptors (Hess et al., 1996; Legendre and Westbrook, 1991; Williams, 1993).
The improvement of the anti-hyperalgesic effect of ketamine and of its isomers by the administration of ifenprodil
2010, European Journal of PharmacologyCitation Excerpt :Ifenprodil is also used to control moderate to severe pain and its analgesic effect has been demonstrated in several models of inflammatory and neuropathic pain (Chizh et al., 2001; Sakurada et al., 1998; Xu and Yang, 2006). The mechanism of action of ifenprodil seems to involve the interaction with the polyamine site (Christopher et al., 1989) increasing NR2B sensitivity to the ion channel blockage by protons and forcing the agonist-bound state of the NMDA receptor into a conformation with low open probability (Mott et al., 1998). Besides its action mechanism competing with polyamine site of NMDA receptor, Ifenprodil exclusively blocks the NMDA receptor by binding to the inactivated form of the ion channel coupled to NMDA receptor, increasing its probability to keep it on inactivated (Reynolds and Miller, 1989).