Adaptation of Cortical NMDA Receptors by Chronic Treatment With Specific Serotonin Reuptake Inhibitors

Eur J Pharmacol. 1998 Jan 26;342(2-3):367-70. doi: 10.1016/s0014-2999(97)01589-6.

Abstract

Glycine displaces [3H]CGP-39653 ([3H]D,L-(E)-2-amino-4-propyl-5-phosphono-3-pentenoic acid) binding to the glutamate recognition site with both high and low affinity. We reported previously that chronic treatment with antidepressants reduced the proportion of high to low affinity sites, or, even eliminated the high affinity sites in case of citalopram. Here, we compared the effects of citalopram with another serotonin specific reuptake inhibitor, fluoxetine on this measure. Chronic administration of citalopram or fluoxetine eliminated high affinity glycine-displaceable [3H]CGP-39653 binding to the mouse cortex in 78 and 56% of animals, respectively, indicating that selective serotonin reuptake inhibitors produce qualitatively similar adaptive changes at NMDA receptors, that differ from other antidepressants in this neurochemical measure.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 2-Amino-5-phosphonovalerate / analogs & derivatives
  • 2-Amino-5-phosphonovalerate / metabolism
  • Adaptation, Physiological / drug effects*
  • Animals
  • Binding, Competitive / drug effects
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism*
  • Citalopram / pharmacology
  • Excitatory Amino Acid Antagonists / metabolism
  • Fluoxetine / pharmacology
  • Glycine / pharmacology
  • Male
  • Mice
  • Radioligand Assay
  • Receptors, N-Methyl-D-Aspartate / drug effects
  • Receptors, N-Methyl-D-Aspartate / metabolism*
  • Serotonin Uptake Inhibitors / pharmacology*

Substances

  • Excitatory Amino Acid Antagonists
  • Receptors, N-Methyl-D-Aspartate
  • Serotonin Uptake Inhibitors
  • Fluoxetine
  • Citalopram
  • CGP 39653
  • 2-Amino-5-phosphonovalerate
  • Glycine