ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Differential regulation of transmitter release by presynaptic and glial Ca2+ internal stores at the neuromuscular synapse.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 99 citations in OpenAlex.
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- Purinergic Tuning of the Tripartite Neuromuscular Synapse.Molecular neurobiology · 2023Review
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- Primary Cilia in Glial Cells: An Oasis in the Journey to Overcoming Neurodegenerative Diseases.Frontiers in neuroscience · 2021Review
- Calcium Signaling in Schwann cells.Neuroscience letters · 2020Review
- dBcAMP Rescues the Neurons From Degeneration in Kainic Acid-Injured Hippocampus, Enhances Neurogenesis, Learning, and Memory.Frontiers in behavioral neuroscience · 2020Article
- Review of animal models of bipolar disorder that alter ion regulation.Neuroscience and biobehavioral reviews · 2019Review
- Sympathomimetics regulate neuromuscular junction transmission through TRPV1, P/Q- and N-type CaMolecular and cellular neurosciences · 2019Article
- Clinical relevance of terminal Schwann cells: An overlooked component of the neuromuscular junction.Journal of neuroscience research · 2018Review
- Emerging roles of mitochondria in synaptic transmission and neurodegeneration.Current opinion in physiology · 2018Article
- Activity-induced CaeLife · 2018Article
- Ultrafast and Slow Cholinergic Transmission. Different Involvement of Acetylcholinesterase Molecular Forms.Molecules (Basel, Switzerland) · 2017Review
- New perspectives on amyotrophic lateral sclerosis: the role of glial cells at the neuromuscular junction.The Journal of physiology · 2017Review
- LKB1 Regulates Mitochondria-Dependent Presynaptic Calcium Clearance and Neurotransmitter Release Properties at Excitatory Synapses along Cortical Axons.PLoS biology · 2016Article
- Organelle-Specific Sensors for Monitoring CaFrontiers in synaptic neuroscience · 2016Review
- Perisynaptic Schwann Cells at the Neuromuscular Synapse: Adaptable, Multitasking Glial Cells.Cold Spring Harbor perspectives in biology · 2015Review
- Ca2+ Diffusion through Endoplasmic Reticulum Supports Elevated Intraterminal Ca2+ Levels Needed to Sustain Synaptic Release from Rods in Darkness.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Schwann cells sense and control acetylcholine spillover at the neuromuscular junction by α7 nicotinic receptors and butyrylcholinesterase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
Corrections and comments
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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
The differential regulation of synaptic transmission by internal Ca(2+) stores of presynaptic terminals and perisynaptic Schwann cells (PSCs) was studied at the frog neuromuscular junction. Thapsigargin (tg), an inhibitor of Ca(2+)-ATPase pumps of internal stores, caused a transient Ca(2+) elevation in PSCs, whereas it had no effect on Ca(2+) stores of presynaptic terminals at rest. Tg prolonged presynaptic Ca(2+) responses evoked by single action potentials with no detectable increase in the resting Ca(2+) level in nerve terminals. However, Ca(2+) accumulation was observed during high frequency stimulation. Tg induced a rapid rise in endplate potential (EPP) amplitude, accompanied by a delayed and transient increase. The effects appeared presynaptic, as suggested by the lack of effects of tg on the amplitude and time course of miniature EPPs (MEPPs). However, MEPP frequency was increased when preparations were stimulated tonically (0.2 Hz). The delayed and transient increase in EPP amplitude was occluded by injections of the Ca(2+) chelator BAPTA into PSCs before tg application, whereas a rise in intracellular Ca(2+) in PSCs induced by inositol 1,4,5-triphosphate (IP(3)) injections potentiated transmitter release. Furthermore, increased Ca(2+) buffering capacity after BAPTA injection in PSCs resulted in a more pronounced synaptic depression induced by high frequency stimulation of the motor nerve (10 Hz/80 sec). It is concluded that presynaptic Ca(2+) stores act as a Ca(2+) clearance mechanism to limit the duration of transmitter release, whereas Ca(2+) release from glial stores initiates Ca(2+)-dependent potentiation of synaptic transmission.
Indexed as
Identifiers
11245676PMC6762618W1718658880What 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.