ArticleFrontiers in molecular neuroscience2012
Calcium-activated chloride current expression in axotomized sensory neurons: what for?
Article in Frontiers in molecular neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Glutamate-releasing BEST1 channel is a new target for neuroprotection against ischemic stroke with wide time window.Acta pharmaceutica Sinica. B · 2023Article
- Calcium in Neuronal and Glial Response to Axotomy.International journal of molecular sciences · 2021Review
- Computational Methods for Estimating Molecular System from Membrane Potential Recordings in Nerve Growth Cone.Scientific reports · 2018Article
- Distribution and Function of the Bestrophin-1 (Best1) Channel in the Brain.Experimental neurobiology · 2017Review
- Bestrophin 1 and retinal disease.Progress in retinal and eye research · 2017Review
- Activation of Ca(2+) -activated Cl(-) channel ANO1 by localized Ca(2+) signals.The Journal of physiology · 2016Review
- A novel computational biostatistics approach implies impaired dephosphorylation of growth factor receptors as associated with severity of autism.Translational psychiatry · 2014Article
- Activation of the Cl- channel ANO1 by localized calcium signals in nociceptive sensory neurons requires coupling with the IP3 receptor.Science signaling · 2013Article
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Authors and funding
2 authors.
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Abstract
Calcium-activated chloride currents (CaCCs) are activated by an increase in intracellular calcium concentration. Peripheral nerve injury induces the expression of CaCCs in a subset of adult sensory neurons in primary culture including mechano- and proprioceptors, though not nociceptors. Functional screenings of potential candidate genes established that Best1 is a molecular determinant for CaCC expression among axotomized sensory neurons, while Tmem16a is acutely activated by inflammatory mediators in nociceptors. In nociceptors, such CaCCs are preferentially activated under receptor-induced calcium mobilization contributing to cell excitability and pain. In axotomized mechano- and proprioceptors, CaCC activation does not promote electrical activity and prevents firing, a finding consistent with electrical silencing for growth competence of adult sensory neurons. In favor of a role in the process of neurite growth, CaCC expression is temporally correlated to neurons displaying a regenerative mode of growth. This perspective focuses on the molecular identity and role of CaCC in axotomized sensory neurons and the future directions to decipher the cellular mechanisms regulating CaCC during neurite (re)growth.
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