Synaptotagmin I: A major Ca2+ sensor for transmitter release at a central synapse

Martin Geppert, Yukiko Goda, Robert E Hammer, Cai Li, Thomas W. Rosahl, Charles F. Stevens, Thomas C. Südhof

Research output: Contribution to journalArticle

1082 Citations (Scopus)

Abstract

Mice carrying a mutation in the synaptotagmin I gene were generated by homologous recombination. Mutant mice are phenotypically normal as heterozygotes, but die within 48 hr after birth as homozygotes. Studies of hippocampal neurons cultured from homozygous mutant mice reveal that synaptic transmission is severely impaired. The synchronous, fast component of Ca2+-dependent neurotransmitter release is decreased, whereas asynchronous release processes, including spontaneous synaptic activity (miniature excitatory postsynaptic current frequency) and release triggered by hypertonic solution or α-latrotoxin, are unaffected. Our findings demonstrate that synaptotagmin I function is required for Ca2+-triggering of synchronous neurotransmitter release, but is not essential for asynchronous or Ca2+-independent release. We propose that synaptotagmin I is the major low affinity Ca2+ sensor mediating Ca2+ regulation of synchronous neurotransmitter release in hippocampal neurons.

Original languageEnglish (US)
Pages (from-to)717-727
Number of pages11
JournalCell
Volume79
Issue number4
DOIs
StatePublished - Nov 18 1994

Fingerprint

Synaptotagmin I
Synapses
Neurotransmitter Agents
Transmitters
Neurons
Sensors
Hypertonic Solutions
Excitatory Postsynaptic Potentials
Homologous Recombination
Homozygote
Heterozygote
Synaptic Transmission
Genes
Parturition
Mutation

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

Geppert, M., Goda, Y., Hammer, R. E., Li, C., Rosahl, T. W., Stevens, C. F., & Südhof, T. C. (1994). Synaptotagmin I: A major Ca2+ sensor for transmitter release at a central synapse. Cell, 79(4), 717-727. https://doi.org/10.1016/0092-8674(94)90556-8

Synaptotagmin I : A major Ca2+ sensor for transmitter release at a central synapse. / Geppert, Martin; Goda, Yukiko; Hammer, Robert E; Li, Cai; Rosahl, Thomas W.; Stevens, Charles F.; Südhof, Thomas C.

In: Cell, Vol. 79, No. 4, 18.11.1994, p. 717-727.

Research output: Contribution to journalArticle

Geppert, M, Goda, Y, Hammer, RE, Li, C, Rosahl, TW, Stevens, CF & Südhof, TC 1994, 'Synaptotagmin I: A major Ca2+ sensor for transmitter release at a central synapse', Cell, vol. 79, no. 4, pp. 717-727. https://doi.org/10.1016/0092-8674(94)90556-8
Geppert, Martin ; Goda, Yukiko ; Hammer, Robert E ; Li, Cai ; Rosahl, Thomas W. ; Stevens, Charles F. ; Südhof, Thomas C. / Synaptotagmin I : A major Ca2+ sensor for transmitter release at a central synapse. In: Cell. 1994 ; Vol. 79, No. 4. pp. 717-727.
@article{72bbbbdeb1a44e13844f077aecafea63,
title = "Synaptotagmin I: A major Ca2+ sensor for transmitter release at a central synapse",
abstract = "Mice carrying a mutation in the synaptotagmin I gene were generated by homologous recombination. Mutant mice are phenotypically normal as heterozygotes, but die within 48 hr after birth as homozygotes. Studies of hippocampal neurons cultured from homozygous mutant mice reveal that synaptic transmission is severely impaired. The synchronous, fast component of Ca2+-dependent neurotransmitter release is decreased, whereas asynchronous release processes, including spontaneous synaptic activity (miniature excitatory postsynaptic current frequency) and release triggered by hypertonic solution or α-latrotoxin, are unaffected. Our findings demonstrate that synaptotagmin I function is required for Ca2+-triggering of synchronous neurotransmitter release, but is not essential for asynchronous or Ca2+-independent release. We propose that synaptotagmin I is the major low affinity Ca2+ sensor mediating Ca2+ regulation of synchronous neurotransmitter release in hippocampal neurons.",
author = "Martin Geppert and Yukiko Goda and Hammer, {Robert E} and Cai Li and Rosahl, {Thomas W.} and Stevens, {Charles F.} and S{\"u}dhof, {Thomas C.}",
year = "1994",
month = "11",
day = "18",
doi = "10.1016/0092-8674(94)90556-8",
language = "English (US)",
volume = "79",
pages = "717--727",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "4",

}

TY - JOUR

T1 - Synaptotagmin I

T2 - A major Ca2+ sensor for transmitter release at a central synapse

AU - Geppert, Martin

AU - Goda, Yukiko

AU - Hammer, Robert E

AU - Li, Cai

AU - Rosahl, Thomas W.

AU - Stevens, Charles F.

AU - Südhof, Thomas C.

PY - 1994/11/18

Y1 - 1994/11/18

N2 - Mice carrying a mutation in the synaptotagmin I gene were generated by homologous recombination. Mutant mice are phenotypically normal as heterozygotes, but die within 48 hr after birth as homozygotes. Studies of hippocampal neurons cultured from homozygous mutant mice reveal that synaptic transmission is severely impaired. The synchronous, fast component of Ca2+-dependent neurotransmitter release is decreased, whereas asynchronous release processes, including spontaneous synaptic activity (miniature excitatory postsynaptic current frequency) and release triggered by hypertonic solution or α-latrotoxin, are unaffected. Our findings demonstrate that synaptotagmin I function is required for Ca2+-triggering of synchronous neurotransmitter release, but is not essential for asynchronous or Ca2+-independent release. We propose that synaptotagmin I is the major low affinity Ca2+ sensor mediating Ca2+ regulation of synchronous neurotransmitter release in hippocampal neurons.

AB - Mice carrying a mutation in the synaptotagmin I gene were generated by homologous recombination. Mutant mice are phenotypically normal as heterozygotes, but die within 48 hr after birth as homozygotes. Studies of hippocampal neurons cultured from homozygous mutant mice reveal that synaptic transmission is severely impaired. The synchronous, fast component of Ca2+-dependent neurotransmitter release is decreased, whereas asynchronous release processes, including spontaneous synaptic activity (miniature excitatory postsynaptic current frequency) and release triggered by hypertonic solution or α-latrotoxin, are unaffected. Our findings demonstrate that synaptotagmin I function is required for Ca2+-triggering of synchronous neurotransmitter release, but is not essential for asynchronous or Ca2+-independent release. We propose that synaptotagmin I is the major low affinity Ca2+ sensor mediating Ca2+ regulation of synchronous neurotransmitter release in hippocampal neurons.

UR - http://www.scopus.com/inward/record.url?scp=0028061861&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028061861&partnerID=8YFLogxK

U2 - 10.1016/0092-8674(94)90556-8

DO - 10.1016/0092-8674(94)90556-8

M3 - Article

C2 - 7954835

AN - SCOPUS:0028061861

VL - 79

SP - 717

EP - 727

JO - Cell

JF - Cell

SN - 0092-8674

IS - 4

ER -