Chronic haloperidol treatment impairs glutamate transport in the rat striatum

Eur J Pharmacol. 1999 Oct 8;382(2):139-42. doi: 10.1016/s0014-2999(99)00589-0.

Abstract

High-affinity, Na(+)-dependent transport of glutamate into neurons and glial cells maintains the extracellular concentration of this neurotransmitter at a sub-toxic level. Chronic blockade of dopamine D(2) receptors with haloperidol elevates extracellular glutamate levels in the striatum. The present study examines the effect of long-term haloperidol treatment on glutamate transporter activity using an assay based on measuring the uptake of D-[3H]aspartate in striatal synaptosomes prepared from male Wistar rats. The maximal rate of glutamate transport in the striatum is reduced by 63% following 27 weeks of haloperidol treatment. This impairment of glutamate transport may be important in chronic neuroleptic drug action.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aspartic Acid / pharmacokinetics
  • Biological Transport / drug effects
  • Corpus Striatum / drug effects*
  • Corpus Striatum / metabolism
  • Dopamine Antagonists / pharmacology*
  • Glutamic Acid / pharmacokinetics*
  • Haloperidol / pharmacology*
  • Male
  • Rats
  • Rats, Wistar
  • Synaptosomes / drug effects
  • Synaptosomes / metabolism
  • Tritium

Substances

  • Dopamine Antagonists
  • Tritium
  • Aspartic Acid
  • Glutamic Acid
  • Haloperidol