Journal
PHARMACOLOGICAL RESEARCH
Volume 62, Issue 6, Pages 523-529Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.phrs.2010.07.009
Keywords
Attention-Deficit/Hyperactivity Disorder; Brain derived neurotrophic factor; Methylphenidate; Atomoxetine
Categories
Funding
- Fondazione Mariani [R-06-52]
- Ministry of University and Research [2005059982, 2007STRNHK]
- Compagnia di San Paolo Torino Italy [3940IT/PF pratica 2008 2177]
Ask authors/readers for more resources
The stimulant methylphenidate and the non-stimulant atomoxetine are widely used for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD) but the molecular mechanisms of their therapeutic action are not fully understood The aim of our study was to investigate in adolescent rats the subchronic effect of these two drugs on neuronal plasticity through a detailed analysis of BDNF expression and signalling in order to establish the contribution of these mechanisms in the pharmacotherapy of ADHD Atomoxetine (ATX) up-regulated BDNF mRNA levels in the hippocampus whereas methylphenidate (MPH) Increased BDNF gene expression in the nucleus accumbens and caudate-putamen Opposite effects were seen in the prefrontal cortex a critical region in attention disorders where ATX increased while MPH reduced total and exon IV BDNF mRNA levels Analysis of BDNF-mediated signalling in the prefrontal cortex revealed that ATX enhanced AKT and GSK3 beta phosphorylation whereas MPH reduced the synaptic levels of trkB the high-affinity BDNF receptor and ERK1/2 activation Our findings show that ATX and MPH exert an opposite modulation of the BDNF system primarily in prefrontal cortex that independently from the behavioral control exerted by the two drugs may be Important for long-term consequences on cognitive function (C) 2010 Elsevier Ltd All rights reserved
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available