2017
DOI: 10.1152/jn.00511.2017
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A role for the cystic fibrosis transmembrane conductance regulator in the nitric oxide-dependent release of Cl from acidic organelles in amacrine cells

Abstract: γ-Amino butyric acid (GABA) and glycine typically mediate synaptic inhibition because their ligand-gated ion channels support the influx of Cl However, the electrochemical gradient for Cl across the postsynaptic plasma membrane determines the voltage response of the postsynaptic cell. Typically, low cytosolic Cl levels support inhibition, whereas higher levels of cytosolic Cl can suppress inhibition or promote depolarization. We previously reported that nitric oxide (NO) releases Cl from acidic organelles and … Show more

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Cited by 8 publications
(13 citation statements)
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“…We have demonstrated that CFTR expression and function is required for the NOdrCl [ 7 ]. We began here by testing whether the CFTR protein was localized to the same regions of the cell as SV2, a synaptic vesicle marker protein.…”
Section: Resultsmentioning
confidence: 99%
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“…We have demonstrated that CFTR expression and function is required for the NOdrCl [ 7 ]. We began here by testing whether the CFTR protein was localized to the same regions of the cell as SV2, a synaptic vesicle marker protein.…”
Section: Resultsmentioning
confidence: 99%
“…ab131553; Abcam). We have previously characterized this antibody with a western blot showing a single band at the appropriate molecular weight [ 7 ]. Antibodies were diluted at 1:1000 in dilution solution and applied to cells at 4°C overnight then washed with PBS.…”
Section: Methodsmentioning
confidence: 99%
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“…These isogenic controls could be differentiated into neuronal cells and compared side-by-side with affected (i.e., uncorrected) cells for rigorous disease modeling or drug selection experiments. A similar approach has been utilized to investigate the pathophysiological mechanisms of disease in cells with mutations that cause Duchenne muscular dystrophy, 33 cystic fibrosis, 34 or beta thalassemia. 35,36 Although mutations in CLN3 cause neuronal cell death throughout the CNS, the light-sensing photoreceptor cells of the neural retina are the first to succumb, suggesting they are especially sensitive to CLN3 dysfunction and that using them as a disease model may provide critical insight into how CLN3 mutations specifically alter neuronal function, leading to cell death.…”
Section: Crispr-cas9 Correction Of Batten Disease Ipscsmentioning
confidence: 99%