Johnnie M. Moore-Dotson

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Neurotransmitter release varies between neurons due to differences in presynaptic mechanisms such as Ca(2+) sensitivity and timing. Retinal rod bipolar cells respond to brief dim illumination with prolonged glutamate release that is tuned by the differential release of GABA and glycine from amacrine cells in the inner retina. To test if differences among(More)
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.(More)
Synaptotagmin (syt) I is a Ca(2+) sensor that has been thought to trigger all vesicle secretion with similar mechanisms. However, given the calcium and stimulation requirements of small clear, and large dense core vesicles, we hypothesized that syt I expression differentially regulates vesicle release. Therefore, in this study, we generated multiple stable(More)
PURPOSE Recent studies suggest that the neural retinal response to light is compromised in diabetes. Electroretinogram studies suggest that the dim light retinal rod pathway is especially susceptible to diabetic damage. The purpose of this study was to determine whether diabetes alters rod pathway signaling. METHODS Diabetes was induced in C57BL/6J mice(More)
21 Neurotransmitter release varies between neurons due to differences in presynaptic 22 mechanisms such as Ca 2+-sensitivity and timing. Retinal rod bipolar cells respond to brief dim 23 illumination with prolonged glutamate release that is tuned by the differential release of GABA 24 and glycine from amacrine cells in the inner retina. To test if(More)
28 The timing of neurotransmitter release from neurons can be modulated by many presynaptic 29 mechanisms. The retina uses synaptic ribbons to mediate slow graded glutamate release from 30 bipolar cells that carry photoreceptor inputs. However, many inhibitory amacrine cells, which 31 modulate bipolar cell output, spike and do not have ribbons for graded(More)
BACKGROUND The function of synaptotagmins (syt) in Ca2+-dependent transmitter release has been attributed primarily to Ca2+-dependent isoforms such as syt I. Recently, syt IV, an inducible Ca2+-independent isoform has been implicated in transmitter release. We postulated that the effects of syt IV on transmitter release are dependent on the expression of(More)
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