Subcellular structural plasticity caused by the absence of the fast Ca(2+) buffer calbindin D-28k in recurrent collaterals of cerebellar Purkinje neurons.

ABSTRACT: 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 Ca(2+) buffer protein calbindin D-28k (CB). As expected from the absence of a fast Ca(2+) buffer, presynaptic action potential-evoked [Ca(2+)]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 C

SUBMITTER: Orduz D 

PROVIDER: S-EPMC4220698 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature