Glycine modulates [3H]MK-801 binding to the NMDA receptor in rat brain

Wong, Erik H. F.; Knight, Anthony; Ransom, Richard W.

doi:10.1016/0014-2999(87)90095-1

Cited by 162 publications

(61 citation statements)

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“…This is in accordance with electrophysiological and receptor-binding studies showing an increase in binding of channel blockers -such as dizocilpine -when the glycine binding site is stimulated (Wong et al, 1987). However, CGP 37849, which per se has anticataleptic potency, loses its potency when combined with D-cycloserine (Table 3).…”

Section: Osupporting

confidence: 85%

Anticataleptic potencies of glutamate-antagonists

et al. 1991

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Summary.The anticataleptic effects of non-competitive and competitive NMDA antagonists as well as those of an agonist at the allosteric glycine binding site of the NMDA receptor were tested in the catalepsy model. Some of these drugs were further tested in a reaction time task demanding rapid locomotor initiation. The results show that the non-competitive NMDA antagonists dizocilpine and memantine as well as the competitive antagonists CGP 39551, CGP 37849 and CPPene antagonized dopamine D2 receptor mediated catalepsy induced by haloperidol. D-cycloserine, a partial glycine agonist per se had no effects, but it enhanced the anticataleptic effects of dizocilpine when coadministered. However, the effects of CGP 37849 were abolished. Dopamine D1 receptor mediated catalepsy induced by SCH 23390 was antagonized by dizocilpine, memantine, CPPene, but not by CGP 37849. In the reaction time task dizocilpine, memantine and CGP 37849 were tested for their anti-akinetic and anti-bradykinetic potencies. All these compounds improved haloperidolinduced slowing of reaction time. However, they acted differentially on haloperidol-induced slowing of movement execution and decreased initial acceleration. Thus, antagonists at the NMDA receptor may have a therapeutic potential in the treatment of Parkinson's disease. Their potency can be manipulated specifically at the glycine binding site.

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Section: Osupporting

confidence: 85%

Anticataleptic potencies of glutamate-antagonists

et al. 1991

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“…Electrophysiological experiments using isolated outside-out membrane patches (1) and radioligand binding studies (2)(3)(4) indicate an allosteric interaction through a strychnineinsensitive glycine recognition site that is part of the N-Me-D-Asp receptor/ion channel complex.…”

mentioning

confidence: 99%

7-Chlorokynurenic acid is a selective antagonist at the glycine modulatory site of the N-methyl-D-aspartate receptor complex.

Kemp¹,

Foster²,

Leeson³

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

397

245

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“…Glycine is also able to enhance the specific binding of radioligands interacting with the ion channel of the NMDA receptor complex (3)(4)(5). Despite the high concentrations of glycine in body fluids, this glycine modulatory site may not be maximally stimulated in vivo (6,7), and selective glycine receptor antagonists such as 7-chlorokynurenic acid are effective anticonvulsants and protect against NMDA receptor-induced excitotoxicity (7,8).…”

mentioning

confidence: 99%