Rapid Alterations of BDNF Protein Levels in the Rat Brain after Focal Ischemia: Evidence for Increased Synthesis and Anterograde Axonal Transport

Kokaia, Zaal; Andsberg, Gunnar; Qiao, Yan; Lindvall, Olle

doi:10.1006/exnr.1998.6888

Cited by 131 publications

(86 citation statements)

References 54 publications

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“…Increases in the neurotrophic factor BDNF occur after brain injury (Kokaia et al, 1998) and BDNF has also been shown to upregulate synapsin (Causing et al, 1997). The levels of synapsin we see in induced NSC transplanted mice significantly outstrip those seen in lesioned vehicleinjected controls at the CA1 region of the hippocampus, and are consistent with neurotrophin-induced sprouting.…”

Section: Discussionsupporting

confidence: 67%

Neural Stem Cells Improve Memory in an Inducible Mouse Model of Neuronal Loss

Yamasaki¹,

Blurton‐Jones²,

Morrissette³

et al. 2007

J. Neurosci.

146

124

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Neuronal loss is a major pathological outcome of many common neurological disorders, including ischemia, traumatic brain injury, and Alzheimer disease. Stem cell-based approaches have received considerable attention as a potential means of treatment, although it remains to be determined whether stem cells can ameliorate memory dysfunction, a devastating component of these disorders. We generated a transgenic mouse model in which the tetracycline-off system is used to regulate expression of diphtheria toxin A chain. After induction, we find progressive neuronal loss primarily within the hippocampus, leading to specific impairments in memory. We find that neural stem cells transplanted into the brain after neuronal ablation survive, migrate, differentiate and, most significantly, improve memory. These results show that stem cells may have therapeutic value in diseases and conditions that result in memory loss.

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Section: Discussionsupporting

confidence: 67%

Neural Stem Cells Improve Memory in an Inducible Mouse Model of Neuronal Loss

Yamasaki¹,

Blurton‐Jones²,

Morrissette³

et al. 2007

J. Neurosci.

146

124

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“…Increases in BDNF levels have been reported in pieces of tissue collected at the infarct or peri-infarct level (Kokaia et al, 1998;Madinier et al, 2009;Sulejczak et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Available studies support increased BDNF production after stroke as suggested by increased BDNF levels in areas collected either at the lesion site or around the lesion for at least one week following stroke (Kokaia et al, 1998;Madinier et al, 2009;Sulejczak et al, 2007). Because increased levels of BDNF mRNA were observed in degenerating and surviving neurons in the acute post-stroke period (Comelli et al, 1992;Kokaia et al, 1995;Rickhag et al, 2007;Zhao et al, 2000), it has been generally accepted that neurons are the predominant source of neosynthesized BDNF in the ischemic brain.…”

Section: Introductionmentioning

confidence: 96%

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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“…BDNF, on the other hand, is a key molecule of structural and functional integrity of the hippocampal formation (Thoenen 2000). Activity-dependent BDNF transcription and trafficking have been repeatedly linked to numerous physiological events and pathophysiological insults such as fear conditioning (Rattiner et al 2004), seizures (Lauterborn et al 1996;Chiaruttini et al 2008), ischemia (Kokaia et al 1998), as well as with consolidation of hippocampusdependent memory (Tyler et al 2002;Bramham and Messaoudi 2005). However, recent studies suggest that during prolonged periods of secretion, as observed in long-term potentiation, the endogenous activity-dependent pool of BDNF becomes rapidly depleted Santi et al 2006).…”

Section: Introductionmentioning

confidence: 99%

BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat

Perović

Tešić

Djordjevic

et al. 2012

AGE

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Neurotrophins are established molecular mediators of neuronal plasticity in the adult brain. We analyzed the impact of aging on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) protein isoforms, their receptors, and on the expression patterns of multiple 5′ exon-specific BDNF transcripts in the rat cortex and hippocampus throughout the life span of the rat (6, 12, 18, and 24 months of age). ProNGF was increased during aging in both structures. Mature NGF gradually decreased in the cortex, and, in 24-month-old animals, it was 30 % lower than that in adult 6-month-old rats. The BDNF expression did not change during aging, while proBDNF accumulated in the hippocampus of aged rats. Hippocampal total BDNF mRNA was lower in 12-month-old animals, mostly as a result of a decrease of BDNF transcripts 1 and 2. In contrast to the regionspecific regulation of specific exon-containing BDNF mRNAs in adult animals, the same BDNF RNA isoforms (containing exons III, IV, or VI) were present in both brain structures of aged animals. Deficits in neurotrophin signaling were supported by the observed decrease in Trk receptor expression which was accompanied by lower levels of the two main downstream effector kinases, pAkt and protein kinase C. The proteolytic processing of p75NTR observed in 12-monthold rats points to an additional regulatory mechanism in early aging. The changes described herein could contribute to reduced brain plasticity underlying the age-dependent decline in cognitive function.

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Rapid Alterations of BDNF Protein Levels in the Rat Brain after Focal Ischemia: Evidence for Increased Synthesis and Anterograde Axonal Transport

Cited by 131 publications

References 54 publications

Neural Stem Cells Improve Memory in an Inducible Mouse Model of Neuronal Loss

Neural Stem Cells Improve Memory in an Inducible Mouse Model of Neuronal Loss

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

BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat

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