Stroke-Induced Neurogenesis: Physiopathology and Mechanisms

Taupin, Philippe

doi:10.2174/156720206775541769

Cited by 25 publications

(12 citation statements)

References 68 publications

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“…This indicates that the pathology referred to in the present study is not influenced by chronic ischaemia, a condition that has been described in brains of human drug abusers, for review, see Buttner (2011). In contrast, ischaemic brain injury is considered to induce hippocampal neurogenesis (Merson and Bourne, 2014;Taupin, 2006). Thus, mixed influences on adult neurogenesis should be assumed when studying adult neurogenesis in drug addicts.…”

Section: Discussionmentioning

confidence: 61%

Alterations of neuronal precursor cells in stages of human adult neurogenesis in heroin addicts

Bayer

Franke

Ficker

et al. 2015

Drug and Alcohol Dependence

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Section: Discussionmentioning

confidence: 61%

Alterations of neuronal precursor cells in stages of human adult neurogenesis in heroin addicts

Bayer

Franke

Ficker

et al. 2015

Drug and Alcohol Dependence

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“…Thus, it is conceivable that the alteration in tau isoform ratio, as well as the increase in tau hyperphosphorylation, after brain ischemic insult may provide the pathological basis for the prevalence of AD in stroke patients (Tatemichi et al 1992;Guglielmotto et al 2009). However, the possibility that induction of 3R tau plays a role in axonal outgrowth during regeneration after ischemic brain injury cannot be excluded (Hoffman and Cleveland 1988;Taupin 2006).…”

Section: Discussionmentioning

confidence: 99%

Hypoxic ischemia and proteasome dysfunction alter tau isoform ratio by inhibiting exon 10 splicing

Suh¹,

Im²,

Moon³

et al. 2010

Journal of Neurochemistry

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J. Neurochem. (2010) 114, 160–170. Abstract Alternative splicing of tau exon 10 influences microtubule assembly and stability during development and in pathological processes of the central nervous system. However, the cellular events that underlie this pre‐mRNA splicing remain to be delineated. In this study, we examined the possibility that ischemic injury, known to change the cellular distribution and expression of several RNA splicing factors, alters the splicing of tau exon 10. Transient occlusion of the middle cerebral artery reduced tau exon 10 inclusion in the ischemic cortical area within 12 h, resulting in the induction of three‐repeat (3R) tau in cortical neurons. Ubiquitinated protein aggregates and reduced proteasome activity were also observed. Administration of proteasome inhibitors such as MG132, proteasome inhibitor I and lactacystin reduced tau exon 10 splicing in cortical cell cultures. Decreased levels of Tra2β, an RNA splicing factor responsible for tau exon 10 inclusion, were detected both in cortical cell cultures exposed to MG132 and in cerebral cortex after ischemic injury. Taken together, these findings suggest that transient focal cerebral ischemia reduces tau exon 10 splicing through a mechanism involving proteasome‐ubiquitin dysfunction and down‐regulation of Tra2β.

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“…Neurogenesis is upregulated by environmental enrichment, learning, exercise and brain injury, and may play a role in central plasticity and recovery of function (Kempermann et al, 1997, Jin et al, 2001, Brown et al, 2003a, Prickaerts et al, 2004, Ernst et al, 2006, Olson et al, 2006, Taupin, 2006, Uda et al, 2006, Brene et al, 2007, Ploughman, 2008). In contrast, anti-cancer drugs, irradiation and alcohol suppress neurogenesis (Crews et al, 2006, Dietrich et al, 2006, Duffner, 2006, Nixon, 2006).…”

mentioning

confidence: 99%

Noise trauma impairs neurogenesis in the rat hippocampus

et al. 2010

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The hippocampus, a major site of neurogenesis in the adult brain, plays an important role in memory. Based on earlier observations where exposure to high-intensity noise not only caused hearing loss but also impaired memory function, it is conceivably that noise exposure may suppress hippocampal neurogenesis. To evaluate this possibility, nine rats were unilaterally exposed for 2 h to a high-intensity, narrow band of noise centered at 12 kHz at 126 dB SPL. The rats were also screened for noise-induced tinnitus, a potential stressor which may suppress neurogenesis. Five rats developed persistent tinnitus-like behavior while the other four rats showed no signs of tinnitus. Age-matched sham controls showed no signs of hearing loss or tinnitus. The inner ear and hippocampus were evaluated for sensory hair cell loss and neurogenesis 10 weeks post-exposure. All noise exposed rats showed severe loss of sensory hair cells in the noise-exposed ear, but essentially no damage in the unexposed ear. Frontal sections from the hippocampus were immunolabeled for doublecortin to identify neuronal precursor cells, or Ki67 to label proliferating cells. Noise-exposed rats showed a significant reduction of neuronal precursors and fewer dividing cells as compared to sham controls. However, we could not detect any difference between rats with behavioral evidence of tinnitus versus rats without tinnitus. These results show for the first time that high intensity noise exposure not only damages the cochlea but also causes a significant and persistent decrease in hippocampal neurogenesis that may contribute to functional deficits in memory.

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Stroke-Induced Neurogenesis: Physiopathology and Mechanisms

Cited by 25 publications

References 68 publications

Alterations of neuronal precursor cells in stages of human adult neurogenesis in heroin addicts

Alterations of neuronal precursor cells in stages of human adult neurogenesis in heroin addicts

Hypoxic ischemia and proteasome dysfunction alter tau isoform ratio by inhibiting exon 10 splicing

Noise trauma impairs neurogenesis in the rat hippocampus

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