Induction of brain-derived neurotrophic factor (BDNF) and the receptor trk B mRNA following middle cerebral artery occlusion in rat

Arai, Shouichi; Kinouchi, Hiroyuki; Akabane, Atsuya; Owada, Yuji; Kamii, Hideyuki; Kawase, Makoto; Yoshimoto, Takashi

doi:10.1016/0304-3940(96)12720-8

Cited by 49 publications

(19 citation statements)

References 23 publications

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“…Contralateral changes in BDNF synthesize have been poorly investigated after stroke as compared to ipsilateral changes. However, consistent with enhanced BDNF production in areas opposite to the lesion site, increased BDNF mRNA has been reported in the contralateral hippocampus after focal brain ischemia (Arai et al, 1996;Kokaia et al, 1995).…”

Section: Discussionsupporting

confidence: 61%

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

Béjot

Prigent‐Tessier

Cachia

et al. 2011

Neurochemistry International

124

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Although brain-derived neurotrophic factor (BDNF) plays a central role in recovery after cerebral ischemia, little is known about cells involved in BDNF production after stroke.The present study testes the hypothesis that neurons are not the unique source of neosynthesized BDNF after stroke and that non neuronal-BDNF producing cells differ according to the delay after stroke induction. For this purpose, cellular localization of BDNF and BDNF content of each hemisphere were analysed in parallel before and after (4h, 24h and 8d) ischemic stroke in rats. Stroke of different severities was induced by embolization of the brain with variable number of calibrated microspheres allowing us to explore the association between BDNF production and neuronal death severity. The main results are that a) unilateral stroke increased BDNF production in both hemispheres with a more intense and long-lasting effect in the lesioned hemisphere, b) BDNF levels either of the lesioned or unlesioned hemispheres were not inversely correlated to neuronal death severity whatever the delay after stroke onset, c) in the unlesioned hemisphere, stroke resulted in increased BDNF staining in neurons and ependymal cells (at 4h and 24h), d) in the lesioned hemisphere, beside neurons and ependymal cells, microglial cells (at 24h), endothelial cells of cerebral arterioles (at 4h and 24h) and astrocytes (at 8d) exhibited a robust BDNF staining as well. Taken together, overall data suggest that non neuronal cells are able to produce substantial amount of BDNF after ischemic stroke and that more attention should be given to these cells in the design of strategies aimed at improving stroke recovery through BDNFrelated mechanisms.

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Section: Discussionsupporting

confidence: 61%

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

Béjot

Prigent‐Tessier

Cachia

et al. 2011

Neurochemistry International

124

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“…The role of neurotrophins in ischemia induced cell death is less clean Several studies have suggested that neurotrophins may play a role in the recovery from ischemic brain lesions (Arai et al, 1996;Kokaia et al, 1995;Lindvall et al, 1992;Merlio et al, 1993;Tsukahara et al, 1994). In vitro, BDNF and NT-3 can protect neurons from death (Korsching, 1993;Nakao et al, 1995) and cerebellar granule neurons from glutamateinduced toxicity (Lindholm et al, 1993).…”

Section: Neurotrophic Factorsmentioning

confidence: 98%

Death and neuroprotection of retinal ganglion cells after different types of injury

et al. 2000

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In adult Sprague-Dawley rats, retinal ganglion cell survival was investigated after intraorbital optic nerve section and after transient ischemia of the retina induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The thickness of the inner nuclear and inner plexiform layers was also assessed after transient periods (120 min) of retinal ischemia induced by selective ligature of the ophthalmic vessels. In addition, we have also investigated the neuroprotective effects of different substances in these paradigms. The intraocular injection of brain-derived neurotrophic factor increased RGC survival after retinal ischemia induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The caspase-inhibitor Z-DEVD increased retinal ganglion cell survival after optic nerve section and also after 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. The peptide Bcl-2 did not increase retinal ganglion cell survival after optic nerve section but increased retinal ganglion cell survival after 60 or 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. Finally, BDNF, nifedipine, naloxone and bcl-2 prevented in part the decrease in thickness of the inner nuclear layer and inner plexiform layer induced by selective ligature of the ophthalmic vessels. Our results suggest that retinal ganglion cell loss induced by different types of injury, may be prevented by substances with neuroprotective effects, by altering steps of the cascade of events leading to cell death.

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“…Previous studies have suggested that BDNF and trkB are upregulated in the ischemic brain (Arai et al, 1996;Schmidt-Kastner et al, 2001). We therefore investigated whether FGF-2 was required for mediating ischemia-related Quantitative evaluation of optical densities (Figs.…”

Section: Induction Of Hippocampal Bdnf and Trkb Mrna Expression Aftermentioning

confidence: 99%

Enlarged infarct volume and loss of BDNF mRNA induction following brain ischemia in mice lacking FGF-2

Kiprianova

Schindowski

Halbach

et al. 2004

Experimental Neurology

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Induction of brain-derived neurotrophic factor (BDNF) and the receptor trk B mRNA following middle cerebral artery occlusion in rat

Cited by 49 publications

References 23 publications

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats

Death and neuroprotection of retinal ganglion cells after different types of injury

Enlarged infarct volume and loss of BDNF mRNA induction following brain ischemia in mice lacking FGF-2

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