ArticleThe Journal of physiology1999
Two components of transmitter release from the chick ciliary presynaptic terminal and their regulation by protein kinase C.
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 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Evolving insights regarding mechanisms for the inhibition of insulin release by norepinephrine and heterotrimeric G proteins.American journal of physiology. Cell physiology · 2012Review
- Effects of strontium on the permeation and gating phenotype of calcium channels in hair cells.Journal of neurophysiology · 2008Article
- 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
- Increase in the pool size of releasable synaptic vesicles by the activation of protein kinase C in goldfish retinal bipolar cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Probing fundamental aspects of synaptic transmission with strontium.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- mu-Opioid receptor inhibits N-type Ca2+ channels in the calyx presynaptic terminal of the embryonic chick ciliary ganglion.The Journal of physiology · 2000Article
- Stimulation of exocytosis without a calcium signal.The Journal of physiology · 1999Review
Corrections and comments
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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. A study was made of the effects of phorbol ester (phorbol 12-myristate 13-acetate, PMA, 0.1 microM) on the two components of evoked transmitter release, namely the fast synchronous and the slow asynchronous components, from the giant presynaptic terminal of the chick ciliary ganglion. The excitatory postsynaptic currents (EPSCs) were recorded under whole-cell voltage clamp of the postsynaptic neuron. 2. The decay time constant of the slow component was prolonged by replacing Ca2+ with Sr2+. In 5 mM [Sr2+]o the fast component decayed with a time constant of 2.6 +/- 1.4 ms whereas the slow component decayed with a time constant of 19 +/- 7 ms. 3. When stimulated with twin pulses with a short interpulse interval, the fast component of the second EPSC was often depressed whereas the slow component was usually facilitated. Both components were positively dependent on [Sr2+]o in a saturable manner, but the fast component approached its maximum at a lower [Sr2+]o than the slow component. 4. PMA potentiated both the fast and slow components to a similar extent and with a similar time course. For each component, the effect of PMA was less potent at high [Sr2+]o than at low [Sr2+]o. For either the fast or the slow component the PMA-induced potentiation was accompanied by a reduction in the paired-pulse ratio (PPR). 5. Despite the different dissociation constant for dextran-conjugated fura-2, the fluorescent ratio for intraterminal [Sr2+] ([Sr2+]i) decayed to the baseline after the nerve-evoked increment with a time course similar to that for [Ca2+]i, suggesting that intraterminal Sr2+ is buffered less efficiently than Ca2+. PMA did not increase the [Sr2+]i transients produced by stimulation of the presynaptic oculomotor nerve. 6. It is suggested that protein kinase C (PKC) modulates both the fast and slow components through common molecular mechanisms that upregulate the Sr2+ sensitivity of the vesicle fusion probability.
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