ArticleThe Journal of physiology1997
Voltage-dependent interaction between the muscarinic ACh receptor and proteins of the exocytic machinery.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 88 citations in OpenAlex.
- Voltage Sensors Embedded in G Protein-Coupled Receptors.International journal of molecular sciences · 2024Review
- G Protein-Coupled Receptors Regulated by Membrane Potential.International journal of molecular sciences · 2022Review
- Acetylcholine-Induced Inhibition of Presynaptic Calcium Signals and Transmitter Release in the Frog Neuromuscular Junction.Frontiers in physiology · 2016Article
- Article
- What are the mechanisms for analogue and digital signalling in the brain?Nature reviews. Neuroscience · 2013Review
- A novel fast mechanism for GPCR-mediated signal transduction--control of neurotransmitter release.The Journal of cell biology · 2011Article
- Modulation of M4 muscarinic acetylcholine receptors by interacting proteins.Neuroscience bulletin · 2010Review
- Control of neurotransmitter release: From Ca2+ to voltage dependent G-protein coupled receptors.Pflugers Archiv : European journal of physiology · 2010Review
- Activation of M2 muscarinic receptors leads to sustained suppression of hippocampal transmission in the medial prefrontal cortex.The Journal of physiology · 2009Article
- VAMP2 interacts directly with the N terminus of Kv2.1 to enhance channel inactivation.Pflugers Archiv : European journal of physiology · 2008Article
- Molecular mechanisms that control initiation and termination of physiological depolarization-evoked transmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Intracellular complexes of the beta2 subunit of the nicotinic acetylcholine receptor in brain identified by proteomics.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Synaptic proteins as multi-sensor devices of neurotransmission.BMC neuroscience · 2006Review
- Release of neurotransmitter induced by Ca2+-uncaging: reexamination of the ca-voltage hypothesis for release.Journal of computational neuroscience · 2005Article
- The timing of phasic transmitter release is Ca2+-dependent and lacks a direct influence of presynaptic membrane potential.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Can the Ca2+ hypothesis and the Ca2+-voltage hypothesis for neurotransmitter release be reconciled?Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Ca2+-independent feedback inhibition of acetylcholine release in frog neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Presynaptic M(2) muscarinic receptors are involved in controlling the kinetics of ACh release at the frog neuromuscular junction.The Journal of physiology · 2001Article
- Nociceptin reduces epileptiform events in CA3 hippocampus via presynaptic and postsynaptic mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Long-lasting enhancement of glutamatergic synaptic transmission by acetylcholine contrasts with response adaptation after exposure to low-level nicotine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
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
1. Release of neurotransmitter into the synaptic cleft is the last step in the chain of molecular events following the arrival of an action potential at the nerve terminal. The neurotransmitter exerts negative feedback on its own release. This inhibition would be most effective if exerted on the first step in this chain of events, i.e. a step that is mediated by membrane depolarization. Indeed, in numerous studies feedback inhibition was found to be voltage dependent. 2. The purpose of this study is to investigate whether the mechanism underlying feedback inhibition of transmitter release resides in interaction between the presynaptic autoreceptors and the exocytic apparatus, specifically the soluble NSF-attachment protein receptor (SNARE) complex. 3. Using rat synaptosomes we show that the muscarinic ACh autoreceptor (mAChR) is an integral component of the exocytic machinery. It interacts with syntaxin, synaptosomal-associated protein of 25 kDa (SNAP-25), vesicle-associated membrane protein (VAMP) and synaptotagmin as shown using both cross-linking and immunoprecipitation. 4. The interaction between mAChRs and both syntaxin and SNAP-25 is modulated by depolarization levels; binding is maximal at resting potential and disassembly occurs at higher depolarization. 5. This voltage-dependent interaction of mAChRs with the secretory core complex appears suitable for controlling the rapid, synchronous neurotransmitter release at nerve terminals.
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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.