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Subcellular structural plasticity caused by the absence of the fast Ca²⁺ buffer calbindin D-28k in recurrent collaterals of cerebellar Purkinje neurons

  • Orduz, David Laboratory of Neurophysiology, UNI, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
  • Boom, Alain Laboratory of Histology, Neuroanatomy and Neuropathology, UNI, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
  • Gall, David Laboratory of Neurophysiology, UNI, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
  • Brion, Jean-Pierre Laboratory of Histology, Neuroanatomy and Neuropathology, UNI, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
  • Schiffmann, Serge N. Laboratory of Neurophysiology, UNI, Université Libre de Bruxelles (ULB), Bruxelles, Belgium
  • Schwaller, Beat Anatomy, Department of Medicine, University of Fribourg, Switzerland
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    2014
Published in:
  • Frontiers in Cellular Neuroscience. - 2014, vol. 8, p. 364
English Purkinje cells (PC) control spike timing of neighboring PC by their recurrent axon collaterals. These synapses underlie fast cerebellar oscillations and are characterized by a strong facilitation within a time window of <20 ms during paired-pulse protocols. PC express high levels of the fast Ca²⁺ buffer protein calbindin D-28k (CB). As expected from the absence of a fast Ca²⁺ buffer, presynaptic action potential-evoked [Ca²⁺]i transients were previously shown to be bigger in PC boutons of young (second postnatal week) CB-/- mice, yet IPSC mean amplitudes remained unaltered in connected CB–/– PC. Since PC spine morphology is altered in adult CB–/– mice (longer necks, larger spine head volume), we summoned that morphological compensation/adaptation mechanisms might also be induced in CB–/– PC axon collaterals including boutons. In these mice, biocytin-filled PC reconstructions revealed that the number of axonal varicosities per PC axon collateral was augmented, mostly confined to the granule cell layer. Additionally, the volume of individual boutons was increased, evidenced from z-stacks of confocal images. EM analysis of PC–PC synapses revealed an enhancement in active zone (AZ) length by approximately 23%, paralleled by a higher number of docked vesicles per AZ in CB–/– boutons. Moreover, synaptic cleft width was larger in CB–/– (23.8 ± 0.43 nm) compared to wild type (21.17 ± 0.39 nm) synapses. We propose that the morphological changes, i.e., the larger bouton volume, the enhanced AZ length and the higher number of docked vesicles, in combination with the increase in synaptic cleft width likely modifies the GABA release properties at this synapse in CB–/– mice. We view these changes as adaptation/homeostatic mechanisms to likely maintain characteristics of synaptic transmission in the absence of the fast Ca²⁺ buffer CB. Our study provides further evidence on the functioning of the Ca²⁺ homeostasome.
Faculty
Faculté des sciences et de médecine
Department
Département de Médecine
Language
  • English
Classification
Biology
License
License undefined
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Persistent URL
https://folia.unifr.ch/unifr/documents/304223
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