Molecular mechanisms regulating the retrograde axonal transport of neurotrophins

Reynolds, Anna; Bartlett, Selena E.; Hendry, Ian A.

doi:10.1016/s0165-0173(00)00028-x

Cited by 81 publications

(53 citation statements)

References 98 publications

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“…Excess BDNF vesicles transported to the neurite terminal that are not captured by stimulation would then be expected to return to the cell body for degradation, or perhaps even reuse, to maintain homeostasis. While retrograde transport of BDNF from the postsynaptic terminal has been reported (Bhattacharyya et al, 2002;Curtis et al, 1995;DiStefano et al, 1992;Reynolds et al, 2000;Yano and Chao, 2004), it is unlikely that the BDNF-GFP vesicles we observed moving in the retrograde direction in hippocampal neurons represent vesicles that was released and endocytosed, since we were studying unstimulated neurons. Besides, the BDNF-GFP signal in such putative vesicles, if generated, would be far too weak to be detected.…”

Section: Discussionmentioning

confidence: 79%

A bi-directional carboxypeptidase E-driven transport mechanism controls BDNF vesicle homeostasis in hippocampal neurons

Park

Cawley

Loh

2008

Molecular and Cellular Neuroscience

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Anterograde transport of brain-derived neurotrophic factor (BDNF) vesicles from the soma to neurite terminals is necessary for activity-dependent secretion of BDNF to mediate synaptic plasticity, memory and learning, and retrograde BDNF transport back to the soma for recycling. In our study, overexpression of the cytoplasmic tail of the carboxypeptidase E (CPE) found in BDNF vesicles significantly reduced localization of BDNF in neurites of hippocampal neurons. Live-cell imaging showed that the velocity and distance of movement of fluorescent protein-tagged CPE-or BDNFcontaining vesicles were reduced in both directions. In pull-down assays, the CPE tail interacted with dynactin along with kinesin-2 and kinesin-3, and cytoplasmic dynein. Competition assays using a CPE tail peptide verified specific interaction between the CPE tail and dynactin. Thus, the CPE cytoplasmic tail binds dynactin that recruits kinesins or dynein for driving bi-directional transport of BDNF vesicle to maintain vesicle homeostasis and secretion in hippocampal neurons.

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Section: Discussionmentioning

confidence: 79%

A bi-directional carboxypeptidase E-driven transport mechanism controls BDNF vesicle homeostasis in hippocampal neurons

Park

Cawley

Loh

2008

Molecular and Cellular Neuroscience

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“…The CH1 domain of p52ShcA might be responsible for these interactions since this domain was tyrosine-phosphorylated upon engagement with different cell surface receptors (12). Another study showed IL-2 induced phosphorylation of p52shcA on both tyrosine and serine residues, and maximum phosphorylation was observed within 5 min after IL-2 stimulation of T-lymphocytes (41). In contrast, we showed that IL-2-stimulated tyrosine phosphorylation of p52ShcA in IEC peaked at ϳ120 min and was sustained up to 360 min.…”

Section: Discussionmentioning

confidence: 99%

Molecular mechanism of interleukin-2-induced mucosal homeostasis

Mishra

Waters

Kumar

2012

American Journal of Physiology-Cell Physiology

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“…However, as BDNF can be transported in the axon in both anterograde or retrograde direction (DiStefano et al, 1992;Reynolds et al, 2000;von Bartheld et al, 1996), changes in BDNF levels in a specific brain area does not necessarily mean changes in BDNF production in that area. For instance, BDNF proteins have been detected in the adult rodent striatum despite the absence of BDNF mRNA (von Bartheld et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

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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Molecular mechanisms regulating the retrograde axonal transport of neurotrophins

Cited by 81 publications

References 98 publications

A bi-directional carboxypeptidase E-driven transport mechanism controls BDNF vesicle homeostasis in hippocampal neurons

A bi-directional carboxypeptidase E-driven transport mechanism controls BDNF vesicle homeostasis in hippocampal neurons

Molecular mechanism of interleukin-2-induced mucosal homeostasis

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

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