Slow changes in Ca2+ cause prolonged release from GABAergic retinal amacrine cells
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چکیده
منابع مشابه
Slow changes in Ca2(+) cause prolonged release from GABAergic retinal amacrine cells.
The timing of neurotransmitter release from neurons can be modulated by many presynaptic mechanisms. The retina uses synaptic ribbons to mediate slow graded glutamate release from bipolar cells that carry photoreceptor inputs. However, many inhibitory amacrine cells, which modulate bipolar cell output, spike and do not have ribbons for graded release. Despite this, slow glutamate release from b...
متن کاملSlow changes in Ca cause prolonged release from GABAergic retinal amacrine cells
Eggers ED, Klein JS, Moore-Dotson JM. Slow changes in Ca cause prolonged release from GABAergic retinal amacrine cells. J Neurophysiol 110: 709–719, 2013. First published May 8, 2013; doi:10.1152/jn.00913.2012.—The timing of neurotransmitter release from neurons can be modulated by many presynaptic mechanisms. The retina uses synaptic ribbons to mediate slow graded glutamate release from bipola...
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Calcium influx into cultured retinal amacrine cells is followed by a small, slow, inward current that we show here results from the operation of electrogenic Na-Ca exchange. The activity of the exchanger is shown to correlate with the magnitude of the Ca2+ load and to depend on both the Ca2+ and Na+ gradients. Li+ is unable to substitute for Na+ and in the absence of Na+, slow tail currents are...
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Understanding the regulation of L-type voltage-gated Ca(2+) current is an important component of elucidating the signaling capabilities of retinal amacrine cells. Here we ask how the cytosolic Ca(2+) environment and the balance of Ca(2+)-dependent effectors shape native L-type Ca(2+) channel function in these cells. To achieve this, whole cell voltage clamp recordings were made from cultured am...
متن کاملCalcium from internal stores triggers GABA release from retinal amacrine cells.
The Ca(2+) that promotes transmitter release is generally thought to enter presynaptic terminals through voltage-gated Ca(2+)channels. Using electrophysiology and Ca(2+) imaging, we show that, in amacrine cell dendrites, at least some of the Ca(2+) that triggers transmitter release comes from endoplasmic reticulum Ca(2+) stores. We show that both inositol 1,4,5-trisphosphate receptors (IP(3)Rs)...
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ژورنال
عنوان ژورنال: Journal of Neurophysiology
سال: 2013
ISSN: 0022-3077,1522-1598
DOI: 10.1152/jn.00913.2012