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Cited by 47Mitochondrial Function and PathologyIon Channels and ReceptorsIon channel regulation and function

Deficiency in parvalbumin, but not in calbindin D-28k upregulates mitochondrial volume and decreases smooth endoplasmic reticulum surface selectively in a peripheral, subplasmalemmal region in the soma of Purkinje cells

Chen, G., Racay, P., Bichet, S., Celio, M.R., Eggli, P., Schwaller, B.·2006·Neuroscience
DOI 10.1016/j.neuroscience.2006.06.008
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Abstract

The Ca(2+)-binding proteins parvalbumin (PV) and calbindin D-28k (CB) are key players in the intracellular Ca(2+)-buffering in specific cells including neurons and have profound effects on spatiotemporal aspects of Ca(2+) transients. The previously observed increase in mitochondrial volume density in fast-twitch muscle of PV-/- mice is viewed as a specific compensation mechanism to maintain Ca(2+) homeostasis. Since cerebellar Purkinje cells (PC) are characterized by high expression levels of the Ca(2+) buffers PV and CB, the question was raised, whether homeostatic mechanisms are induced in PC lacking these buffers. Mitochondrial volume density, i.e. relative mitochondrial mass was increased by 40% in the soma of PV-/- PC. Upregulation of mitochondrial volume density was not homogenous throughout the soma, but was selectively restricted to a peripheral region of 1.5 microm width underneath the plasma membrane. Accompanied was a decreased surface of subplasmalemmal smooth endoplasmic reticulum (sPL-sER) in a shell of 0.5 microm thickness underneath the plasma membrane. These alterations were specific for the absence of the "slow-onset" buffer PV, since in CB-/- mice neither changes in peripheral mitochondria nor in sPL-sER were observed. This implicates that the morphological alterations are aimed to specifically substitute the function of the slow buffer PV. We propose a novel concept that homeostatic mechanisms of components involved in Ca(2+) homeostasis do not always occur at the level of similar or closely related molecules. Rather the cell attempts to restore spatiotemporal aspects of Ca(2+) signals prevailing in the undisturbed (wildtype) situation by subtly fine tuning existing components involved in the regulation of Ca(2+) fluxes.

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Authors
Chen, G., Racay, P., Bichet, S., Celio, M. R., Eggli, P., & Schwaller, B.
Affiliations
  • University of Fribourg (CH)
  • University of Bern (CH)
Corresponding author
Schwaller, B.
ORCID
Venue
Neuroscience
Publisher
Elsevier BV
Published
2006-09
Volume
142
Issue
1
Pages
97-105
ISSN
0306-4522 (ISSN-L)
DOI
10.1016/j.neuroscience.2006.06.008
OpenAlex
W1997317715
Cited by
47
References
64
Citations by year
2026: 2 · 2025: 2 · 2024: 2 · 2022: 1 · 2021: 1 · 2020: 6 · 2019: 5 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 5 · 2013: 2 · 2012: 2
FWCI
0.95
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • reroDoc Digital Library (submittedVersion)
  • BORIS (University Library Bern) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Keywords
parvalbumin, calbindin-D28k, Purkinje cells, mitochondrial volume density, smooth endoplasmic reticulum, calcium homeostasis, calcium buffering, cerebellum, calcium signaling
MeSH terms
Animals, Calcium, Cerebellar Cortex, Endoplasmic Reticulum, Fluorescent Antibody Technique, Mice, Inbred C57BL, Mitochondria, Parvalbumins, Purkinje Cells, Blotting, Western, Electrophoresis, Gel, Two-Dimensional, Mice, Knockout, Statistics, Nonparametric, Microscopy, Electron, Transmission, Mice, Plasma Membrane Calcium-Transporting ATPases, Calbindins, S100 Calcium Binding Protein G

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