Cited by 155Neuroscience and Neuropharmacology ResearchIon channel regulation and functionIon Channels and Receptors

Parvalbumin Is a Mobile Presynaptic Ca2+Buffer in the Calyx of Held that Accelerates the Decay of Ca2+and Short-Term Facilitation

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Müller, Martin, Felmy, Felix, Schwaller, Beat, Schneggenburger, Ralf·2007·The Journal of Neuroscience

Abstract

Presynaptic Ca 2+signaling plays a crucial role in short-term plasticity of synaptic transmission. Here, we studied the role of mobile endogenous presynaptic Ca 2+buffer(s) in modulating paired-pulse facilitation at a large excitatory nerve terminal in the auditory brainstem, the calyx of Held. To do so, we assessed the effect of presynaptic whole-cell recording, which should lead to the diffusional loss of endogenous mobile Ca 2+buffers, on paired-pulse facilitation and on intracellular Ca 2+concentration ([Ca 2+]i) transients evoked by action potentials. In unperturbed calyces briefly preloaded with the Ca 2+indicator fura-6F, the [Ca 2+]i transient decayed surprisingly fast (τ fast, ∼30 ms). Presynaptic whole-cell recordings made without additional Ca 2+buffers slowed the decay kinetics of [Ca 2+]i and paired-pulse facilitation (twofold to threefold), but the amplitude of the [Ca 2+]i transient was changed only marginally. The fast [Ca 2+]i decay was restored by adding the slow Ca 2+buffer EGTA (50–100 μ m) or parvalbumin (100 μ m), a Ca 2+-binding protein with slow Ca 2+-binding kinetics, to the presynaptic pipette solution. In contrast, the fast Ca 2+buffer fura-2 strongly reduced the amplitude of the [Ca 2+]i transient and slowed its decay, suggesting that the mobile endogenous buffer in calyces of Held has slow, rather than fast, binding kinetics. In parvalbumin knock-out mice, the decay of [Ca 2+]i and facilitation was slowed approximately twofold compared with wild-type mice, similar to what is observed during whole-cell recordings in rat calyces of Held. Thus, in young calyces of Held, a mobile Ca 2+buffer with slow binding kinetics, primarily represented by parvalbumin, accelerates the decay of spatially averaged [Ca 2+]i and paired-pulse facilitation.

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Authors
Müller, M., Felmy, F., Schwaller, B., & Schneggenburger, R.
Affiliations
  • École Polytechnique Fédérale de Lausanne (CH)
  • Ludwig-Maximilians-Universität München (DE)
  • University of Fribourg (CH)
Venue
The Journal of Neuroscience
Published
2007-02-28
Volume
27
Issue
9
Pages
2261-2271
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W1975952480
Cited by
155
References
46
Citations by year
2026: 4 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 4 · 2021: 7 · 2020: 4 · 2019: 5 · 2018: 7 · 2017: 1 · 2016: 8 · 2015: 9 · 2014: 11 · 2013: 10 · 2012: 8
FWCI
5.97
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
  • Zurich Open Repository and Archive (University of Zurich)
Funders
  • National Science Foundation
  • Deutsche Forschungsgemeinschaft (TP B1)
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (100400, 3100A0)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords
parvalbumin, calyx of Held, paired-pulse facilitation, short-term plasticity, calcium transients, fura-2, EGTA, auditory brainstem, excitatory synapses
MeSH terms
Animals, Brain Stem, Calcium, Calcium-Binding Proteins, Mice, Inbred C57BL, Synaptic Transmission, Neuronal Plasticity, Parvalbumins, Rats, Wistar, Receptors, Presynaptic, Mice, Knockout, Patch-Clamp Techniques, Mice, Rats, In Vitro Techniques

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