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Published in: Neurological Sciences 12/2014

01-12-2014 | Original Article

The responsiveness of TrkB to exogenous BDNF in frontal cortex during antibiotic treatment of Streptococcus pneumoniae meningitis

Authors: Xiaoqing Song, Di lian, Dake He, Jiaming Sun, MingJie Zhu, Ling Li

Published in: Neurological Sciences | Issue 12/2014

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Abstract

Our previous studies suggested that the expression of TrkB and BDNF decreased concomitantly in brain during Streptococcus pneumoniae meningitis after antibiotic treatment, and that adjuvant administration of exogenous BDNF could rescue neurons from S. pneumoniae meningitis. In this study, we investigated the responsiveness of TrkB to exogenous BDNF treatment in frontal cortex during antibiotic treatment of S. pneumoniae meningitis. We found that adjuvant administration of exogenous BDNF led to increased number of survived neurons, improved the conduction of central auditory pathway and neurological disfunction, and up-regulated TrkB expression at the mRNA level in the frontal cortex of rats under S. pneumonia meningitis (P < 0.01). When treated with placebo, on the contrary, neurons in the frontal cortex of control rats were seriously damaged and the TrkB expression was remarkably decreased. These findings indicated that exogenous BDNF could up-regulate TrkB expression and thus played a neuroprotective role in frontal cortex injury from S. pneumoniae meningitis. They further confirmed our previous report that the decrease of intrinsic BDNF and TrkB expression is involved in the pathogenesis of neurological brain damage during S. pneumoniae meningitis after antibiotic treatment.
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Metadata
Title
The responsiveness of TrkB to exogenous BDNF in frontal cortex during antibiotic treatment of Streptococcus pneumoniae meningitis
Authors
Xiaoqing Song
Di lian
Dake He
Jiaming Sun
MingJie Zhu
Ling Li
Publication date
01-12-2014
Publisher
Springer Milan
Published in
Neurological Sciences / Issue 12/2014
Print ISSN: 1590-1874
Electronic ISSN: 1590-3478
DOI
https://doi.org/10.1007/s10072-014-1862-x

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