title: The responsiveness of TrkB to exogenous BDNF in frontal cortex during antibiotic treatment of Streptococcus pneumoniae meningitis.
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.
authors.affiliation: Department of Pediatric Neurology, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200092, China.
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Song
authors.forename: Di
authors.initials: D
authors.lastname: Lian
authors.forename: Dake
authors.initials: D
authors.lastname: He
authors.forename: Jiaming
authors.initials: J
authors.lastname: Sun
authors.forename: MingJie
authors.initials: M
authors.lastname: Zhu
authors.forename: Ling
authors.initials: L
authors.lastname: Li
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001933:Brain Stem / Q000187:drug effects / Q000503:physiopathology; D019208:Brain-Derived Neurotrophic Factor / Q000627:therapeutic use*; D004195:Disease Models, Animal; D016057:Evoked Potentials, Auditory, Brain Stem / Q000187:drug effects; D005625:Frontal Lobe / Q000187:drug effects* / Q000378:metabolism*; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects*; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism*; D008586:Meningitis, Pneumococcal / Q000188:drug therapy / Q000473:pathology*; D011505:Protein-Tyrosine Kinases / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D020813:Receptor, trkB; D013997:Time Factors
chemical_list: D000900:Anti-Bacterial Agents; D019208:Brain-Derived Neurotrophic Factor; D008562:Membrane Glycoproteins; D011505:Protein-Tyrosine Kinases; D020813:Receptor, trkB; C000591259:tropomyosin-related kinase-B, human