ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Kinetics, Ca2+ dependence, and biophysical properties of integrin-mediated mechanical modulation of transmitter release from frog motor nerve terminals.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 84 citations in OpenAlex.
- Microelectrode-based approaches for studying cholinergic neuromuscular transmission.Biophysical reviews · 2025Review
- Synapses without tension fail to fire in an in vitro network of hippocampal neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Manipulation of Axonal Outgrowth via Exogenous Low Forces.International journal of molecular sciences · 2020Review
- Axonal cytomechanics in neuronal development.Journal of biosciences · 2020Review
- Cytoskeletal Mechanisms of Axonal Contractility.Biophysical journal · 2018Article
- Multiple roles of integrin-α3 at the neuromuscular junction.Journal of cell science · 2017Article
- Mechanical tension modulates local and global vesicle dynamics in neurons.Cellular and molecular bioengineering · 2012Article
- Dry needling - peripheral and central considerations.The Journal of manual & manipulative therapy · 2011Article
- Glial cell line-derived neurotrophic factor protein content in rat skeletal muscle is altered by increased physical activity in vivo and in vitro.Neuroscience · 2011Article
- Influence of integrin-blocking peptide on gadolinium- and hypertonic shrinking-induced neurotransmitter release in rat brain synaptosomes.Neurochemical research · 2008Article
- Activity-dependent regulation of synaptic AMPA receptor composition and abundance by beta3 integrins.Neuron · 2008Article
- C2B polylysine motif of synaptotagmin facilitates a Ca2+-independent stage of synaptic vesicle priming in vivo.Molecular biology of the cell · 2006Article
- Article
- Mechanotransduction by intraganglionic laminar endings of vagal tension receptors in the guinea-pig oesophagus.The Journal of physiology · 2003Article
- Optical measurements of presynaptic release in mutant zebrafish lacking postsynaptic receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Biphasic modulation of synaptic transmission by hypertonicity at the embryonic Drosophila neuromuscular junction.The Journal of physiology · 2002Article
- Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate.The Journal of physiology · 2002Article
- Hypertonicity-induced transmitter release at Drosophila neuromuscular junctions is partly mediated by integrins and cAMP/protein kinase A.The Journal of physiology · 2002Article
- Temperature effect on carbachol-induced depression of spontaneous quantal transmitter release in frog neuromuscular junction.Neurochemical research · 2001Article
- Hypertonic enhancement of transmitter release from frog motor nerve terminals: Ca2+ independence and role of integrins.The Journal of physiology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurotransmitter release from frog motor nerve terminals is strongly modulated by change in muscle length. Over the physiological range, there is an approximately 10% increase in spontaneous and evoked release per 1% muscle stretch. Because many muscle fibers do not receive suprathreshold synaptic inputs at rest length, this stretch-induced enhancement of release constitutes a strong peripheral amplifier of the spinal stretch reflex. The stretch modulation of release is inhibited by peptides that block integrin binding of natural ligands. The modulation varies linearly with length, with a delay of no more than approximately 1-2 msec and is maintained constant at the new length. Moreover, the stretch modulation persists in a zero Ca2+ Ringer and, hence, is not dependent on Ca2+ influx through stretch activated channels. Eliminating transmembrane Ca2+ gradients and buffering intraterminal Ca2+ to approximately normal resting levels does not eliminate the modulation, suggesting that it is not the result of release of Ca2+ from internal stores. Finally, changes in temperature have no detectable effect on the kinetics of stretch-induced changes in endplate potential (EPP) amplitude or miniature EPP (mEPP) frequency. We conclude, therefore, that stretch does not act via second messenger pathways or a chemical modification of molecules involved in the release pathway. Instead, there is direct mechanical modulation of release. We postulate that tension on integrins in the presynaptic membrane is transduced mechanically into changes in the position or conformation of one or more molecules involved in neurotransmitter release, altering sensitivity to Ca2+ or the equilibrium for a critical reaction leading to vesicle fusion.
Indexed as
Identifiers
8994045PMC6573157W2126844149What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.