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 journalArticlepeer-review

25 Scopus citations


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 languageEnglish (US)
Pages (from-to)175-185
Number of pages11
JournalJournal of Neural Transmission
Issue number3
StatePublished - Oct 1994
Externally publishedYes


  • 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


Dive into the research topics of 'Centrally-administered glycine antagonists increase locomotion in monoamine-depleted mice'. Together they form a unique fingerprint.

Cite this