ArticleThe Journal of physiology1995
Calcium in the nerve terminals of chick ciliary ganglia during facilitation, augmentation and potentiation.
Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- Post-tetanic potentiation in the rat calyx of Held synapse.The Journal of physiology · 2005Article
- Augmentation increases vesicular release probability in the presence of masking depression at the frog neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Cumulative inactivation of N-type CaV2.2 calcium channels modified by alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Synaptically driven calcium transients via nicotinic receptors on somatic spines.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Depletion of calcium in the synaptic cleft of a calyx-type synapse in the rat brainstem.The Journal of physiology · 1999Article
- Stimulation-induced changes in [Ca2+] in lizard motor nerve terminals.The Journal of physiology · 1997Article
- Probabilistic secretion of quanta and the synaptosecretosome hypothesis: evoked release at active zones of varicosities, boutons, and endplates.Biophysical journal · 1997Article
- Calcium in sympathetic varicosities of mouse vas deferens during facilitation, augmentation and autoinhibition.The Journal of physiology · 1997Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The calyciform nerve terminals of chick ciliary ganglia were loaded with the calcium indicators calcium green 1 or fura-2. These were used to determine the change in calcium concentration in the terminal, [Ca2+]t, following short (10 impulses) and long (600 impulses) trains of high-frequency (30 Hz) stimulation. 2. Following a single impulse or a short train, the elevated [Ca2+]t declined along two exponentials with time constants similar to slow (F2) facilitation (0.52 s) and augmentation (4.0 s). After a long train elevated [Ca2+]t declined eventually along a single exponential with the time constant of post-tetanic potentiation (162 s). [Ca2+]t was not elevated through long-term potentiation. 3. Addition of Ba2+ (0.75 mM) to the extracellular solution slowed only the decline of [Ca2+]t associated with augmentation. The addition of the nitric oxide donor sodium nitroprusside did not affect [Ca2+]t following short or long trains. 4. Removal of extracellular calcium (buffered with EGTA) and the blockade of calcium channels with Cd2+ completely prevented the changes in [Ca2+]t. 5. The soma of ciliary ganglion cells were loaded with calcium green and the postganglionic nerves stimulated with a single impulse or a short train of impulses. Following stimuli, the elevated [Ca2+]t declined along a single exponential with a time constant similar to F2 facilitation with no augmentation component evident. 6. The results are discussed in terms of the hypothesis that each impulse in a train gives an equal increment of residual Ca2+ to a compartment for secretion and that Ca2+ is removed from the compartment by three first-order kinetics processes associated with F2 facilitation, augmentation and post-tetanic potentiation.
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