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Related Experiment Videos

Glycine and D-serine decrease MK-801-induced hyperactivity in mice

M Nilsson1, A Carlsson, M L Carlsson

  • 1Department of Pharmacology, University of Göteborg, Sweden.

Journal of Neural Transmission (Vienna, Austria : 1996)
|January 1, 1997
PubMed
Summary
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Glycine agonists like D-serine may help treat schizophrenia by strengthening N-methyl-D-aspartate (NMDA) receptor function. This study suggests the glycine site on NMDA receptors is not fully saturated in vivo.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Pharmacology

Background:

  • Schizophrenia symptoms can be mimicked by phencyclidine, an N-methyl-D-aspartate (NMDA) receptor antagonist.
  • This suggests a potential hypofunction in central glutamate systems in schizophrenia.
  • Glycine agonists are explored for schizophrenia treatment by enhancing glutamatergic transmission.

Purpose of the Study:

  • To investigate if NMDA receptor-mediated neurotransmission can be enhanced by modulating the associated glycine site.
  • To determine if the glycine site on NMDA receptors is saturated in vivo.

Main Methods:

  • Testing the effects of systemic and intraventricular glycine, D-serine, and L-serine.
  • Administering these substances to mice exhibiting hyperactivity induced by the NMDA receptor antagonist MK-801.

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Main Results:

  • Systemic glycine and D-serine reduced MK-801-induced hyperactivity.
  • Intraventricular D-serine decreased MK-801-induced hyperactivity, while L-serine did not.
  • These effects were observed during specific time intervals post-administration.

Conclusions:

  • The NMDA receptor-associated glycine site may not be saturated in vivo.
  • D-serine shows potential as a therapeutic agent for conditions involving NMDA receptor hypofunction, possibly schizophrenia.
  • Modulating the glycine site offers a potential strategy for enhancing glutamatergic neurotransmission.