cAMP-Dependent Co-Stabilization of Axonal Arbors from Adjacent Developing Neurons

Faculty Opinions recommendation of cAMP-Dependent Co-stabilization of Axonal Arbors from Adjacent Developing Neurons.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.738792789.793580569 ◽

2020 ◽

Author(s):

Patricia Gaspar

Keyword(s):

Developing Neurons ◽

Axonal Arbors

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cAMP-Dependent Co-stabilization of Axonal Arbors from Adjacent Developing Neurons

Cell Reports ◽

10.1016/j.celrep.2020.108220 ◽

2020 ◽

Vol 33 (1) ◽

pp. 108220 ◽

Cited By ~ 1

Author(s):

Alice Louail ◽

Martijn C. Sierksma ◽

Antoine Chaffiol ◽

Sarah Baudet ◽

Ahlem Assali ◽

...

Keyword(s):

Developing Neurons ◽

Axonal Arbors

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Mercury Toxicity and Neurogenesis in the Mammalian Brain

International Journal of Molecular Sciences ◽

10.3390/ijms22147520 ◽

2021 ◽

Vol 22 (14) ◽

pp. 7520

Author(s):

Louise C. Abbott ◽

Fikru Nigussie

Keyword(s):

Neural Networks ◽

Progenitor Cells ◽

Adult Neurogenesis ◽

Neural Progenitor Cells ◽

Mammalian Brain ◽

Mercury Toxicity ◽

Embryonic Neurogenesis ◽

Programmed Death ◽

Final Integration ◽

Developing Neurons

The mammalian brain is formed from billions of cells that include a wide array of neuronal and glial subtypes. Neural progenitor cells give rise to the vast majority of these cells during embryonic, fetal, and early postnatal developmental periods. The process of embryonic neurogenesis includes proliferation, differentiation, migration, the programmed death of some newly formed cells, and the final integration of differentiated neurons into neural networks. Adult neurogenesis also occurs in the mammalian brain, but adult neurogenesis is beyond the scope of this review. Developing embryonic neurons are particularly susceptible to neurotoxicants and especially mercury toxicity. This review focused on observations concerning how mercury, and in particular, methylmercury, affects neurogenesis in the developing mammalian brain. We summarized information on models used to study developmental mercury toxicity, theories of pathogenesis, and treatments that could be used to reduce the toxic effects of mercury on developing neurons.

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Pink1 attenuates propofol-induced apoptosis and oxidative stress in developing neurons

Journal of Anesthesia ◽

10.1007/s00540-017-2431-2 ◽

2017 ◽

Vol 32 (1) ◽

pp. 62-69 ◽

Cited By ~ 5

Author(s):

Chao Liang ◽

Fang Du ◽

Jing Cang ◽

Zhanggang Xue

Keyword(s):

Oxidative Stress ◽

Induced Apoptosis ◽

Developing Neurons ◽

And Oxidative Stress

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Reelin promotes microtubule dynamics in processes of developing neurons

Histochemistry and Cell Biology ◽

10.1007/s00418-012-1025-1 ◽

2012 ◽

Vol 139 (2) ◽

pp. 283-297 ◽

Cited By ~ 17

Author(s):

Maurice Meseke ◽

Ersin Cavus ◽

Eckart Förster

Keyword(s):

Microtubule Dynamics ◽

Developing Neurons

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Assessment of Connectivity in Neuronal Cultures by Recording from Axonal Arbors

Frontiers in Neuroscience ◽

10.3389/conf.fnins.2016.93.00077 ◽

2016 ◽

Vol 10 ◽

Author(s):

Huber Stefan ◽

Bullmann Torsten ◽

Deligkaris Kosmas ◽

Hierlemann Andreas ◽

Frey Urs

Keyword(s):

Neuronal Cultures ◽

Axonal Arbors

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Isoflurane Neurotoxicity Is Mediated by p75NTR-RhoA Activation and Actin Depolymerization

Anesthesiology ◽

10.1097/aln.0b013e318201dcb3 ◽

2011 ◽

Vol 114 (1) ◽

pp. 49-57 ◽

Cited By ~ 89

Author(s):

Brian P. Lemkuil ◽

Brian P. Head ◽

Matthew L. Pearn ◽

Hemal H. Patel ◽

John C. Drummond ◽

...

Keyword(s):

Caspase 3 ◽

Hippocampal Slice ◽

Hippocampal Slices ◽

Neurotrophin Receptor ◽

P75 Neurotrophin Receptor ◽

Actin Depolymerization ◽

Rhoa Activation ◽

Hippocampal Slice Cultures ◽

Developing Neurons

Background The mechanisms by which isoflurane injured the developing brain are not clear. Recent work has demonstrated that it is mediated in part by activation of p75 neurotrophin receptor. This receptor activates RhoA, a small guanosine triphosphatase that can depolymerize actin. It is therefore conceivable that inhibition of RhoA or prevention of cytoskeletal depolymerization might attenuate isoflurane neurotoxicity. This study was conducted to test these hypotheses using primary cultured neurons and hippocampal slice cultures from neonatal mouse pups. Methods Primary neuron cultures (days in vitro, 4-7) and hippocampal slice cultures from postnatal day 4-7 mice were exposed to 1.4% isoflurane (4 h). Neurons were pretreated with TAT-Pep5, an intracellular inhibitor of p75 neurotrophin receptor, the cytoskeletal stabilizer jasplakinolide, or their corresponding vehicles. Hippocampal slice cultures were pretreated with TAT-Pep5 before isoflurane exposure. RhoA activation was evaluated by immunoblot. Cytoskeletal depolymerization and apoptosis were evaluated with immunofluorescence microscopy using drebrin and cleaved caspase-3 staining, respectively. Results RhoA activation was increased after 30 and 120 min of isoflurane exposure in neurons; TAT-Pep5 (10 μm) decreased isoflurane-mediated RhoA activation at both time intervals. Isoflurane decreased drebrin immunofluorescence and enhanced cleaved caspase-3 in neurons, effects that were attenuated by pretreatment with either jasplakinolide (1 μm) or TAT-Pep5. TAT-Pep5 attenuated the isoflurane-mediated decrease in phalloidin immunofluorescence. TAT-Pep5 significantly attenuated isoflurane-mediated loss of drebrin immunofluorescence in hippocampal slices. Conclusions Isoflurane results in RhoA activation, cytoskeletal depolymerization, and apoptosis. Inhibition of RhoA activation or prevention of downstream actin depolymerization significantly attenuated isoflurane-mediated neurotoxicity in developing neurons.

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Frizzled3 controls axonal development in distinct populations of cranial and spinal motor neurons

eLife ◽

10.7554/elife.01482 ◽

2013 ◽

Vol 2 ◽

Cited By ~ 28

Author(s):

Zhong L Hua ◽

Philip M Smallwood ◽

Jeremy Nathans

Keyword(s):

Cell Death ◽

Motor Neurons ◽

Planar Cell Polarity ◽

Motor Nerve ◽

Normal Wave ◽

Axon Growth ◽

Axonal Growth ◽

Cell Complexes ◽

Developing Neurons

Disruption of the Frizzled3 (Fz3) gene leads to defects in axonal growth in the VIIth and XIIth cranial motor nerves, the phrenic nerve, and the dorsal motor nerve in fore- and hindlimbs. In Fz3−/− limbs, dorsal axons stall at a precise location in the nerve plexus, and, in contrast to the phenotypes of several other axon path-finding mutants, Fz3−/− dorsal axons do not reroute to other trajectories. Affected motor neurons undergo cell death 2 days prior to the normal wave of developmental cell death that coincides with innervation of muscle targets, providing in vivo evidence for the idea that developing neurons with long-range axons are programmed to die unless their axons arrive at intermediate targets on schedule. These experiments implicate planar cell polarity (PCP) signaling in motor axon growth and they highlight the question of how PCP proteins, which form cell–cell complexes in epithelia, function in the dynamic context of axonal growth.

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