ArticleThe Journal of physiology1999
Protein kinase C potentiates transmitter release from the chick ciliary presynaptic terminal by increasing the exocytotic fusion probability.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 85 citations in OpenAlex.
- Alzheimer's Pathology Enhances Excitatory Synaptic Input and Integration in VTA Dopamine Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- PKC-dependent enhancement of glutamate input to VTA dopamine neurons in 3xTg-AD mice.bioRxiv : the preprint server for biology · 2025Article
- Interferon-γ augments GABA release in the developing neocortexFrontiers in cellular neuroscience · 2022Article
- Article
- Application of High-Throughput Assays to Examine Phospho-Modulation of the Late Steps of Regulated Exocytosis.High-throughput · 2017Article
- Calcium-dependent phosphorylation regulates neuronal stability and plasticity in a highly precise pacemaker nucleus.Journal of neurophysiology · 2011Article
- Rapid activation of dormant presynaptic terminals by phorbol esters.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Dynamic modulation of phasic and asynchronous glutamate release in hippocampal synapses.Journal of neurophysiology · 2010Article
- beta-Phorbol ester-induced enhancement of exocytosis in large mossy fiber boutons of mouse hippocampus.The journal of physiological sciences : JPS · 2009Article
- Phorbol esters modulate spontaneous and Ca2+-evoked transmitter release via acting on both Munc13 and protein kinase C.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Phosphorylation of SNAP-25 at Ser187 mediates enhancement of exocytosis by a phorbol ester in INS-1 cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Munc13-1 C1 domain activation lowers the energy barrier for synaptic vesicle fusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Myristoylated alanine rich C kinase substrate (MARCKS) heterozygous mutant mice exhibit deficits in hippocampal mossy fiber-CA3 long-term potentiation.Hippocampus · 2006Article
- Phosphorylation-dependent low-frequency depression at phasic synapses of a crayfish motoneuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- PKC-induced sensitization of Ca2+-dependent exocytosis is mediated by reducing the Ca2+ cooperativity in pituitary gonadotropes.The Journal of general physiology · 2005Article
- Ca2+ influx-independent synaptic potentiation mediated by mitochondrial Na(+)-Ca2+ exchanger and protein kinase C.The Journal of cell biology · 2003Article
- Priming of excitatory synapses by alpha1 adrenoceptor-mediated inhibition of group III metabotropic glutamate receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Phorbol esters and neurotransmitter release: more than just protein kinase C?British journal of pharmacology · 2003Review
- Sensitization of regulated exocytosis by protein kinase C.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The giant presynaptic terminal of chick ciliary ganglion was used to examine how protein kinase C (PKC) modulates neurotransmitter release. Cholinergic excitatory postsynaptic currents (EPSCs) were recorded under whole-cell voltage clamp. 2. Although the EPSC was potentiated by phorbol ester (phorbol 12-myristate 13-acetate, PMA; 0.1 microM) in a sustained manner, the nicotine-induced current was unaffected. PMA increased the quantal content to 2.4 +/- 0.4 (n = 9) of control without changing the quantal size. 3. The inactive isoform of PMA, 4alpha-PMA, showed no significant effect on EPSCs. The PMA-induced potentiation was antagonized by two PKC inhibitors with different modes of action, sphingosine (20 microM) and bisindolylmaleimide I (10 microM). 4. When stimulated by twin pulses of short interval, the second EPSC was on average larger than the first EPSC (paired-pulse facilitation; PPF). PMA significantly decreased the PPF ratio with a time course similar to that of the potentiation of the first EPSC. 5. PMA did not affect resting [Ca2+]i or the action potential-induced [Ca2+]i increment in the giant presynaptic terminals. 6. The effect of PMA was less at 10 mM [Ca2+]o than at 1 mM [Ca2+]o. 7. When a train of action potentials was generated with a short interval, the EPSC was eventually depressed and reached a steady-state level. The recovery process followed a simple exponential relation with a rate constant of 0.132 +/- 0.029 s-1. PMA did not affect the recovery rate constant of EPSCs from tetanic depression. In addition, PMA did not affect the steady-state EPSC which should be proportional to the refilling rate of the readily releasable pool of vesicles. 8. These results conflict with the hypothesis that PKC upregulates the size of the readily releasable pool or the number of release sites. PKC appears to upregulate the Ca2+ sensitivity of the process that controls the exocytotic fusion probability.
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