Store-Operated CRAC Channels Regulate Gene Expression and Proliferation in Neural Progenitor Cells DOI Open Access
A. Somasundaram,

Andrew Shum,

Helen J. McBride

et al.

Journal of Neuroscience, Journal Year: 2014, Volume and Issue: 34(27), P. 9107 - 9123

Published: July 2, 2014

Calcium signals regulate many critical processes during vertebrate brain development including neurogenesis, neurotransmitter specification, and axonal outgrowth. However, the identity of ion channels mediating Ca2+ signaling in developing nervous system is not well defined. Here, we report that embryonic adult mouse neural stem/progenitor cells (NSCs/NPCs) exhibit store-operated entry (SOCE) mediated by release-activated (CRAC) channels. SOCE NPCs was blocked CRAC channel inhibitors La3+, BTP2, 2-APB Western blots revealed presence canonical proteins STIM1 Orai1. Knock down or Orai1 significantly diminished NPCs, lost from transgenic mice lacking knock-in expressing loss-of-function mutant, R93W. Therefore, make essential contributions to NPCs. activated epidermal growth factor acetylcholine, latter occurring through muscarinic receptors. Activation stimulated gene transcription calcineurin/NFAT (nuclear T cells) a mechanism consistent with local microdomains near Importantly, suppression deletion expression attenuated proliferation cultured as neurospheres and, in vivo, subventricular zone mice. These findings show serve major route key effector functions proliferation, indicating are important regulators mammalian neurogenesis.

Language: Английский

Regulation of neurogenesis by calcium signaling DOI
Anna B. Toth,

Andrew Shum,

Murali Prakriya

et al.

Cell Calcium, Journal Year: 2016, Volume and Issue: 59(2-3), P. 124 - 134

Published: March 1, 2016

Language: Английский

Citations

141

Axon Initiation and Growth Cone Turning on Bound Protein Gradients DOI Open Access

Jianning Mai,

L. Fok,

Huijun Gao

et al.

Journal of Neuroscience, Journal Year: 2009, Volume and Issue: 29(23), P. 7450 - 7458

Published: June 10, 2009

Extracellular gradients of secreted guidance factors are known to guide axon pathfinding and neuronal migration. These likely bind cell surfaces or extracellular matrix, but whether how they may act in bound remains mostly unclear. In this study, we have developed a new technique for rapid production stable microscopic substrate-bound proteins by covalent bonding the with an epoxy-coated glass substrate while diffusing agarose gel. Using method, found that netrin-1 brain-derived neurotrophic factor (BDNF) can polarize initiation turning axons cultured hippocampal neurons. Furthermore, BDNF gradient caused attractive repulsive polarizing response on low- high-average density BDNF, respectively. This novel bidirectional depended basal level cAMP neuron. Finally, our data showed neuron9s absolute difference rather than relative across neuron, minimal effective 1–2 molecule/μm2 surface. Thus, highly growth, diffusive printing is useful studying responses induced protein gradients.

Language: Английский

Citations

133

Control of cortical neuronal migration by glutamate and GABA DOI Creative Commons
Heiko J. Luhmann, Atsuo Fukuda, Werner Kilb

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2015, Volume and Issue: 9

Published: Jan. 30, 2015

Neuronal migration in the cortex is controlled by paracrine action of classical neurotransmitters glutamate and GABA. Glutamate controls radial pyramidal neurons acting primarily on NMDA receptors regulates tangential inhibitory interneurons activating non-NMDA receptors. GABA, ionotropic GABAA-rho GABAA receptors, has a dichotomic radially migrating as GO signal lower layers STOP upper cortical plate (CP), respectively. Metabotropic GABAB promote into CP interneurons. Besides endogenous GABAergic agonist taurine relevant controlling migration. To smaller extent glycine receptor activation can also influence Activation GABA causes increases intracellular Ca2+ transients, which neuronal cytoskeleton. Pharmacological or genetic manipulation during early corticogenesis induce heterotopic cell clusters loss lamination, i.e. disorders be associated with neurological neuropsychiatric diseases. The pivotal role major clinical relevance, since number drugs these (e.g. anti-epileptics, anesthetics, alcohol) may disturb normal pattern when present corticogenesis.

Language: Английский

Citations

131

5-HT7R/G12Signaling Regulates Neuronal Morphology and Function in an Age-Dependent Manner DOI Creative Commons

Fritz Kobe,

Daria Guseva, Thomas P. Jensen

et al.

Journal of Neuroscience, Journal Year: 2012, Volume and Issue: 32(9), P. 2915 - 2930

Published: Feb. 29, 2012

The common neurotransmitter serotonin controls different aspects of early neuronal differentiation, although the underlying mechanisms are poorly understood. Here we report that activation 5-HT 7 receptor promotes synaptogenesis and enhances synaptic activity in hippocampal neurons at postnatal stages. An analysis Gα 12 -deficient mice reveals a critical role G -protein for receptor-mediated effects neurons. In organotypic preparations from hippocampus juvenile mice, stimulation R/G signaling potentiates formation dendritic spines, increases excitability, modulates plasticity. contrast, older preparations, morphogenetic synaptogenic /G abolished. Moreover, inhibition had no effect on plasticity adult animals. Expression production -proteins undergoes strong regulation with pronounced transient increase during Thus, regulated expression may represent molecular mechanism by which specifically initial networks development.

Language: Английский

Citations

122

Store-Operated CRAC Channels Regulate Gene Expression and Proliferation in Neural Progenitor Cells DOI Open Access
A. Somasundaram,

Andrew Shum,

Helen J. McBride

et al.

Journal of Neuroscience, Journal Year: 2014, Volume and Issue: 34(27), P. 9107 - 9123

Published: July 2, 2014

Calcium signals regulate many critical processes during vertebrate brain development including neurogenesis, neurotransmitter specification, and axonal outgrowth. However, the identity of ion channels mediating Ca2+ signaling in developing nervous system is not well defined. Here, we report that embryonic adult mouse neural stem/progenitor cells (NSCs/NPCs) exhibit store-operated entry (SOCE) mediated by release-activated (CRAC) channels. SOCE NPCs was blocked CRAC channel inhibitors La3+, BTP2, 2-APB Western blots revealed presence canonical proteins STIM1 Orai1. Knock down or Orai1 significantly diminished NPCs, lost from transgenic mice lacking knock-in expressing loss-of-function mutant, R93W. Therefore, make essential contributions to NPCs. activated epidermal growth factor acetylcholine, latter occurring through muscarinic receptors. Activation stimulated gene transcription calcineurin/NFAT (nuclear T cells) a mechanism consistent with local microdomains near Importantly, suppression deletion expression attenuated proliferation cultured as neurospheres and, in vivo, subventricular zone mice. These findings show serve major route key effector functions proliferation, indicating are important regulators mammalian neurogenesis.

Language: Английский

Citations

121