Alterations in BDNF and synapsin I within the occipital cortex and hippocampus after mild traumatic brain injury in the developing rat: reflections of injury-induced neuroplasticity
Articolo
Data di Pubblicazione:
2002
Citazione:
Alterations in BDNF and synapsin I within the occipital cortex and hippocampus after mild traumatic brain injury in the developing rat: reflections of injury-induced neuroplasticity / G. S. Griesbach, D. A. Hovda, R. Molteni, F. Gomez-Pinilla. - In: JOURNAL OF NEUROTRAUMA. - ISSN 0897-7151. - 19:7(2002 Jul), pp. 803-814. [10.1089/08977150260190401]
Abstract:
Brain-derived neurotrophic factor (BDNF), its signal transduction receptor trkB, and its downstream effector, synapsin I, were measured in the hippocampus and occipital cortex of young animals after fluid-percussion brain injury (FPI). Isofluorane anaesthetized postnatal day 19 rats were subjected to a mild lateral FPI or sham injury. Rats were sacrificed at 24 h, 7 days, or 14 days after injury in order to determine mRNA expression. Additional animals were sacrificed at 7 and 14 days after injury for protein analysis. Only FPI animals exhibited hemispheric differences in BDNF levels. These animals exhibited a contralateral increase, ranging from 40% to 75%, in BDNF mRNA within both the hippocampus and occipital cortex at 24 h and 7 days after injury. The increase in message within the occipital cortex was accompanied by an increase in BDNF protein at 7 and 14 days after injury. However, hippocampal BDNF protein increased in both hemispheres at postinjury day 7 and was restricted to the ipsilateral hippocampus at postinjury day 14. At postinjury day 7, both trkB and synapsin I mRNA expression increased ipsilaterally and decreased contralaterally in the occipital cortex. In addition, synapsin I phosphorylation was increased by 20% in the ipsilateral cortex and by 30% in the hippocampus on this day. These results indicate that the developing brain responds to a mild injury by modifying factors related to synaptic plasticity and suggest that regions remote from the site of injury express neurotrophic signals potentially needed for compensatory responses.
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
Animals ; Brain-Derived Neurotrophic Factor ; Hippocampus ; Synapsins ; Messenger RNA ; Rats; Receptor trkB ; Neuronal Plasticity ; Brain Injuries ; Gene Expression Regulation ; Occipital Lobe
Elenco autori:
G.S. Griesbach, D.A. Hovda, R. Molteni, F. Gomez Pinilla
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