Faculté des sciences

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, Peter ; Bichet, S. ; Celio, Marco R. ; Eggli, P. ; Schwaller, Beat

In: Neuroscience, 2006, vol. 142, no. 1, p. 97-105

The Ca²⁺-binding proteins parvalbumin (PV) and calbindin D-28k (CB) are key players in the intracellular Ca²⁺-buffering in specific cells including neurons and have profound effects on spatiotemporal aspects of Ca²⁺ transients. The previously observed increase in mitochondrial volume density in fast-twitch muscle of PV−/− mice is viewed as a specific compensation mechanism to... Plus

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    Summary
    The Ca²⁺-binding proteins parvalbumin (PV) and calbindin D-28k (CB) are key players in the intracellular Ca²⁺-buffering in specific cells including neurons and have profound effects on spatiotemporal aspects of Ca²⁺ 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 Ca²⁺ homeostasis. Since cerebellar Purkinje cells (PC) are characterized by high expression levels of the Ca²⁺ 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 μm width underneath the plasma membrane. Accompanied was a decreased surface of subplasmalemmal smooth endoplasmic reticulum (sPL-sER) in a shell of 0.5 μm 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 Ca²⁺ homeostasis do not always occur at the level of similar or closely related molecules. Rather the cell attempts to restore spatiotemporal aspects of Ca²⁺ signals prevailing in the undisturbed (wildtype) situation by subtly fine tuning existing components involved in the regulation of Ca²⁺ fluxes.