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

B. Stauch Slusher; K. C. Rissolo; P. F. Jackson; L. M. Pullan

doi:10.1007/BF02336139

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

B. Stauch Slusher, K. C. Rissolo, P. F. Jackson, L. M. Pullan

Research output: Contribution to journal › Article › peer-review

25 Scopus citations

Abstract

It was shown in the present study that several structurally diverse antagonists of the glycine site of the NMDA receptor, including (R)-HA-966, L 689,560, 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.

Original language	English (US)
Pages (from-to)	175-185
Number of pages	11
Journal	Journal of Neural Transmission
Volume	97
Issue number	3
DOIs	https://doi.org/10.1007/BF02336139
State	Published - Oct 1994
Externally published	Yes

Keywords

NMDA receptors
Parkinson's disease
Reserpine
alpha-methyl-para-tyrosine
dopamine
glutamate
glycine

ASJC Scopus subject areas

Neurology
Clinical Neurology
Psychiatry and Mental health
Biological Psychiatry

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10.1007/BF02336139

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title = "Centrally-administered glycine antagonists increase locomotion in monoamine-depleted mice",

abstract = "It was shown in the present study that several structurally diverse antagonists of the glycine site of the NMDA receptor, including (R)-HA-966, L 689,560, 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.",

keywords = "NMDA receptors, Parkinson's disease, Reserpine, alpha-methyl-para-tyrosine, dopamine, glutamate, glycine",

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AU - Stauch Slusher, B.

AU - Rissolo, K. C.

AU - Jackson, P. F.

AU - Pullan, L. M.

PY - 1994/10

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N2 - It was shown in the present study that several structurally diverse antagonists of the glycine site of the NMDA receptor, including (R)-HA-966, L 689,560, 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.

AB - It was shown in the present study that several structurally diverse antagonists of the glycine site of the NMDA receptor, including (R)-HA-966, L 689,560, 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.

KW - NMDA receptors

KW - Parkinson's disease

KW - Reserpine

KW - alpha-methyl-para-tyrosine

KW - dopamine

KW - glutamate

KW - glycine

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

Abstract

Keywords

ASJC Scopus subject areas

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