NDLI: Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals

Content Provider	PubMed Central
Author	David, Gavriel Barrett, Ellen F.
Copyright Year	2003
Abstract	We investigated how inhibition of mitochondrial Ca2+ uptake affects transmitter release from mouse motor terminals during brief trains of action potentials (500 at 50 Hz) in physiological bath [Ca2+]. When mitochondrial Ca2+ uptake was inhibited by depolarizing mitochondria with antimycin A1 or carbonyl cyanide m-chlorophenyl-hydrazone, the stimulation-induced increase in cytosolic [Ca2+] was greater (> 10 μm, compared to ≤ 1μm in control solution), the quantal content of the endplate potential (EPP) depressed more rapidly (∼84 % depression compared to ∼8 % in controls), and asynchronous release during the stimulus train reached higher frequencies (peak rates of ∼6000 s−1 compared to ∼75 s−1 in controls). These effects of mitochondrial depolarization were not accompanied by a significant change in EPP quantal content or the rate of asynchronous release during 1 Hz stimulation, and were not seen in oligomycin, which blocks mitochondrial ATP synthesis without depolarizing mitochondria. Inhibition of endoplasmic reticular Ca2+ uptake with cyclopiazonic acid also had little effect on stimulation-induced changes in cytosolic [Ca2+] or EPP amplitude. We hypothesize that the high rate of asynchronous release evoked by stimulation during mitochondrial depolarization was produced by the elevation of cytosolic [Ca2+], and contributed to the accelerated depression of phasic release by reducing the availability of releasable vesicles. During mitochondrial depolarization, the post-tetanic potentiation of the EPP observed under control conditions was replaced by a post-tetanic depression with a slow time course of recovery. Thus, mitochondrial Ca2+ uptake is essential for sustaining phasic release, and thus neuromuscular transmission, during and following tetanic stimulation.
Related Links	http://dx.doi.org/10.1113/jphysiol.2002.035196
Starting Page	425
File Format	PDF
ISSN	14697793
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 2
Volume Number	548
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2003-04-15
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Stimulation-induced mitochondrial [Ca2+] elevations in mouse motor terminals: comparison of wild-type with SOD1-G93A

Stimulation-induced changes in [Ca2+] in lizard motor nerve terminals.

Changes in binomial parameters of quantal release at crustacean motor axon terminals during presynaptic inhibition.

Quantal transmitter release mediated by strontium at the mouse motor nerve terminal.

Hypertonic enhancement of transmitter release from frog motor nerve terminals: Ca2+ independence and role of integrins

Quantal secretion at release sites of nerve terminals in toad (Bufo marinus) muscle during formation of topographical maps.

Stimulation-induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminals

Changes in statistical release parameters during prolonged stimulation of preganglionic nerve terminals.

Intermittent ATP release from nerve terminals elicits focal smooth muscle Ca2+ transients in mouse vas deferens

Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals

Similar Documents

Stimulation-induced mitochondrial [Ca2+] elevations in mouse motor terminals: comparison of wild-type with SOD1-G93A

Stimulation-induced changes in [Ca2+] in lizard motor nerve terminals.

Changes in binomial parameters of quantal release at crustacean motor axon terminals during presynaptic inhibition.

Quantal transmitter release mediated by strontium at the mouse motor nerve terminal.

Hypertonic enhancement of transmitter release from frog motor nerve terminals: Ca2+ independence and role of integrins

Quantal secretion at release sites of nerve terminals in toad (Bufo marinus) muscle during formation of topographical maps.

Stimulation-induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminals

Changes in statistical release parameters during prolonged stimulation of preganglionic nerve terminals.

Intermittent ATP release from nerve terminals elicits focal smooth muscle Ca2+ transients in mouse vas deferens

Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals