ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Increase in the pool size of releasable synaptic vesicles by the activation of protein kinase C in goldfish retinal bipolar cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 39 citations in OpenAlex.
- Non-canonical type 1 cannabinoid receptor signaling regulates night visual processing in the inner rat retina.iScience · 2024Article
- Trophoblast glycoprotein is required for efficient synaptic vesicle exocytosis from retinal rod bipolar cells.Frontiers in cellular neuroscience · 2023Article
- The Effect of PKCα on the Light Response of Rod Bipolar Cells in the Mouse Retina.Investigative ophthalmology & visual science · 2015Article
- Synaptic mechanisms of adaptation and sensitization in the retina.Nature neuroscience · 2013Article
- SynGAP regulates protein synthesis and homeostatic synaptic plasticity in developing cortical networks.PloS one · 2013Article
- PKC{alpha} is essential for the proper activation and termination of rod bipolar cell response.Investigative ophthalmology & visual science · 2010Article
- The role of ribbons at sensory synapses.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2009Review
- Protein kinase C modulates synaptic vesicle acidification in a ribbon type nerve terminal in the retina.Neurochemistry international · 2008Article
- Phorbol esters target the activity-dependent recycling pool and spare spontaneous vesicle recycling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Distinct roles of different neural cell adhesion molecule (NCAM) isoforms in synaptic maturation revealed by analysis of NCAM 180 kDa isoform-deficient mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Molecular basis of lithium action: integration of lithium-responsive signaling and gene expression networks.Molecular psychiatry · 2003Review
- Specificity emerges in the dissection of diacylglycerol- and protein kinase C-mediated signalling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- A highly Ca2+-sensitive pool of vesicles is regulated by protein kinase C in adrenal chromaffin cells.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secretion from neurons and neuroendocrine cells is enhanced by the activation of protein kinase C (PKC) in various preparations. We have already reported that transmitter (glutamate) release from Mb1 bipolar cells in the goldfish retina is potentiated by the activation of PKC. However, it is not yet settled whether the potentiation is ascribed to the increase in the pool size of releasable synaptic vesicles or in release probability. In the present study, Ca2+ influx and exocytosis were simultaneously monitored by measuring the presynaptic Ca2+ current and membrane capacitance changes, respectively, in a terminal detached from the bipolar cell. The double pulse protocol was used to estimate separately the changes in the pool size and release probability. The activation of PKC by phorbol 12-myristate 13-acetate (PMA) specifically increased the pool size but not the release probability. PKC was activated by PMA even after the Ca2+ influx was blocked by Co2+. In bipolar cells the releasable pool can be divided into two components: one is small and rapidly exhausted, and the other is large and slowly exocytosed. To identify which component is responsible for the increase in the pool size, the effects of PMA and a PKC-specific inhibitor, bisindolylmaleimide I (BIS), on each component were examined. The slow component was selectively increased by PMA and reduced by BIS. Thus, we conclude that the activation of PKC in Mb1 bipolar cells potentiates glutamate release by increasing the pool size of the slow component.
Indexed as
Identifiers
12077174PMC6757743W1524148397What OpenQuestion holds
Registered trials
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