Premium
Effect of antipsychotic drugs on brain‐derived neurotrophic factor expression under reduced N‐methyl‐D‐aspartate receptor activity
Author(s) -
Fumagalli Fabio,
Molteni Raffaella,
Roceri Mila,
Bedogni Francesco,
Santero Raffaella,
Fossati Claudia,
Gennarelli Massimo,
Racagni Giorgio,
Riva Marco Andrea
Publication year - 2003
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10609
Subject(s) - nmda receptor , haloperidol , brain derived neurotrophic factor , typical antipsychotic , neurotrophic factors , olanzapine , neuroscience , neurotrophin , antipsychotic , pharmacology , psychology , schizophrenia (object oriented programming) , atypical antipsychotic , medicine , receptor , dopamine , psychiatry
Brain‐derived neurotrophic factor (BDNF) promotes a variety of neuromodulatory processes during development as well as in adulthood. This neurotrophin has been associated with synaptic plasticity, suggesting that its regulation may represent one of the mechanisms through which psychotropic drugs alter brain function. Because reduced glutamatergic function represents a major feature of schizophrenia, we investigated the effects of the concomitant administration of haloperidol or olanzapine with the N‐methyl‐D‐aspartate (NMDA) receptor antagonist MK‐801 on BDNF expression. MK‐801 reduces the hippocampal expression of the neurotrophin; this effect was exacerbated by haloperidol, but it was normalized by olanzapine. Our data reveal a fine tuning of BDNF biosynthesis and a differential modulation by antipsychotic drugs when NMDA‐mediated transmission is reduced, suggesting that haloperidol and olanzapine can produce different effects on brain plasticity through the modulation of BDNF expression. © 2003 Wiley‐Liss, Inc.