Effects of venlafaxine and escitalopram treatments on NMDA receptors in the rat depression model

J Membr Biol. 2011 Aug;242(3):145-51. doi: 10.1007/s00232-011-9385-3. Epub 2011 Jul 14.


Depression may relate to neurocognitive impairment that results from alteration of N-methyl-D: -aspartate receptor (NMDAR) levels. Venlafaxine and escitalopram are two drugs commonly used to treat depression. The drugs may affect expression of NMDARs, which mediate learning and memory formation. The aim of the study was to examine whether the effects of venlafaxine and escitalopram treatments are associated with NMDARs in a rat model of depression. Forty male Wistar albino rats were randomly divided into four groups (n = 10) as follows: control group, chronic mild stress group (CMS), venlafaxine (20 mg/kg body weight per day) + CMS, and escitalopram (10 mg/kg body weight per day) + CMS. After induction of depression, a decrease in the concentration of NR2B was observed; venlafaxine treatment prevented the reduction of NR2B expression. Escitalopram treatment did not effect the reduced levels of NR2B resulting from depression. There was no significant difference in NR2A concentration among groups. The present data support the notion that venlafaxine plays a role in maintaining NR2B receptor in experimental depression. It may be possible that treatment with escitalopram has no effect on NMDARs in experimental depression.

MeSH terms

  • Animals
  • Antidepressive Agents, Second-Generation / pharmacology
  • Citalopram / pharmacology*
  • Cyclohexanols / pharmacology*
  • Depression / drug therapy*
  • Depression / metabolism
  • Disease Models, Animal
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Male
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Receptors, N-Methyl-D-Aspartate / metabolism*
  • Venlafaxine Hydrochloride


  • Antidepressive Agents, Second-Generation
  • Cyclohexanols
  • NR2A NMDA receptor
  • NR2B NMDA receptor
  • Receptors, N-Methyl-D-Aspartate
  • Citalopram
  • Venlafaxine Hydrochloride