| Brain derived neurotrophic factor (BDNF), which is the second member of neurotrophin family and widely distributed throughout the central nervous system, activates various signal transduction pathways in cells and exerts its biological function by binding with the high-affinity TrkB receptor to activate Protein Tyrosine Kinase. BDNF not only plays an important role in regulating neuronal survival, differentiation, proliferation, maturation and outgrowth during the development of the central nervous system (CNS), but also is essential in retaining the survival and normal physiologic function of mature neurons. There have been a large number of results of investigations on the structure, signal transduction and molecular cloning of BDNF and its receptor, TrkB, as well as the expression and control of BDNF gene under physiologic situation and its biologic role in nervous system. In order to develop the application of BDNF in the treatment of brain damage and optical and auditory impediment, recently, the expressions and effects of BDNF and TrkB have been investigated under the situation ofhypoglyceraia, ischemia, traumatic brain damage and noxious stimulation, in particular, the effects of BDNF on protecting and regrowing optical and auditory neurons after some injury have been studied. A lot of experiments have shown that the expression of BDNF and its receptor in extensive region of brain is obviously elevated in response to ischemic and hypoxic brain damages, the administration of exogenous BDNF can increase the population of survival brain neurons and recover memory function after ischemic and hypoxic brain damage, especially, it has more potent neuroprotective action on in ischemic-hypoxic brain injury in the developing brain. Some studies have shown that BDNF can enhance and protect survival of spiral ganglion cells and induce them regrowth, when exogenous BDNF was applied in cochlea after deafness.Latest, reports have released that human immune cells activated by specific antigen in vitro can secrete BDNF which can support neuronal survival, BDNF immunoreactivity is demonstrable in inflammatory infiltrates in the brain of patients with acute disseminated leukoencephalopathy or multiple sclerosis. The expression and effects of BDNF and TrkB in the inflammatory tissue infected by bacteria, however, aren' t clear. Although it has been reported that glucocorticoid can stimulate the expression of BDNF in cerebral cortex and hippocampus under normal physiology situation, the expression of BDNF in various brain injury is still unclear.Bacterial meningitis is the most common serious infection of the central nervous system. Though newer and more potent antibiotics are continually developed and applied, and there are more and more advanced nurse, the mortality and permanent neurologic deficits still high occur following bacterial meningitis inchildren. Once bacteria have gained access to the central nervous system, their multiplication triggers a complex host response. Alteration of the cerebral vasculature, with disruption of the blood brain barrier and global and focal ischemia, ultimately lead to functional and structural brain damage. Inflammation also often affect cochlear inner hair cells and cranial nerve, which leads to many sequelaes involving in deafness, blindness, facial paralysis and retardation in serious patients. It is essential to emphasize possible therapeutic strategies to prevent its harmful consequences. We infer that the expressions of BDNF, BDNF mRNA and TrkB mRNA in CNS may enhance in bacterial meningitis, and exogenous BDNF may have neuroprotective effect in bacterial meningitis.Part I The dynamic change of expressions of BDNF and its receptor in experimental bacterial meningitisObjectiveTo investigate the expressions of BDNF, BDNF mRNA and TrkB mRNA in brain after bacterial meningitis and their changes after antibiotic and dexamethasone used, in order to discuss the possible mechanisms of mortality and high occuring neurologic deficits following bacterial meningi...
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