Centrally-administered glycine antagonists increase locomotion in monoamine-depleted mice

It was shown in the present study that several structurally diverse antagonists of the glycine site of the NMDA receptor, including (R)-HA-966, L689,560, 5,7-dichlorokynurenic acid, 7-chlorokynurenic acid, and two of ZENECA's novel pyridazinoindole glycine antagonists, caused marked reversal of...

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Veröffentlicht in:	Journal of Neural Transmission 1994-01, Vol.97 (3), p.175-185
Hauptverfasser:	SLUSHER, B. S, RISSOLO, K. C, JACKSON, P. F, PULLAN, L. M
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Anticonvulsants. Antiepileptics. Antiparkinson agents Behavior, Animal - drug effects Biogenic Monoamines - physiology Biological and medical sciences glycine Glycine - antagonists & inhibitors Male Medical sciences Mice Motor Activity - drug effects Neuropharmacology Pharmacology. Drug treatments Pyrrolidinones - pharmacology Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors Serine - pharmacology Stimulation, Chemical
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Zusammenfassung:	It was shown in the present study that several structurally diverse antagonists of the glycine site of the NMDA receptor, including (R)-HA-966, L689,560, 5,7-dichlorokynurenic acid, 7-chlorokynurenic acid, and two of ZENECA's novel pyridazinoindole glycine antagonists, caused marked reversal of akinesia when administered intrastriatally to monoamine depleted mice. Coinjection of the glycine agonist D-serine antagonized this locomotor stimulation. In addition, all glycine antagonists tested did not cause significant locomotor stimulation when intrastriatally administered to normal mice. These data suggest that glycine antagonists may offer therapeutic utility in the treatment of idiopathic Parkinson's disease.
ISSN:	0300-9564 1435-1463
DOI:	10.1007/BF02336139