Premium
Mutational analysis of dendritic Ca 2+ kinetics in rodent Purkinje cells: role of parvalbumin and calbindin D 28k
Author(s) -
Schmidt Hartmut,
Stiefel Klaus M.,
Racay Peter,
Schwaller Beat,
Eilers Jens
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2003.00013.x
Subject(s) - parvalbumin , chemistry , anatomy , ion channel , electrophysiology , neuroscience , biology , medicine , microbiology and biotechnology , biophysics , receptor , biochemistry
The mechanisms governing the kinetics of climbing fibre‐mediated Ca 2+ transients in spiny dendrites of cerebellar Purkinje cells (PCs) were quantified with high‐resolution confocal Ca 2+ imaging. Ca 2+ dynamics in parvalbumin (PV −/− ) and parvalbumin/calbindin D 28k null‐mutant (PV/CB −/− ) mice were compared with responses in wild‐type (WT) animals. In the WT, Ca 2+ transients in dendritic shafts were characterised by double exponential decay kinetics that were not due to buffered Ca 2+ diffusion or saturation of the indicator dye. Ca 2+ transients in PV −/− PCs reached the same peak amplitude as in the WT but the biphasic nature of the decay was less pronounced, an effect that could be attributed to PV's slow binding kinetics. In contrast, peak amplitudes in PV/CB −/− PCs were about two times higher than in the WT and the decay became nearly monophasic. Numerical simulations indicate that the residual deviation from a single exponential decay in PV/CB −/− is due to saturation of the Ca 2+ indicator dye. Furthermore, the simulations imply that the effect of uncharacterised endogenous Ca 2+ binding proteins is negligible, that buffered diffusion and dye saturation significantly affects spineous Ca 2+ transients but not those in the dendritic shafts, and that neither CB nor PV undergoes saturation in spines or dendrites during climbing fibre‐evoked Ca 2+ transients. Calbindin's medium‐affinity binding sites are fast enough to reduce the peak amplitude of the Ca 2+ signal. However, similar to PV, delayed binding by CB leads to biphasic Ca 2+ decay kinetics. Our results suggest that the distinct kinetics of PV and CB underlie the biphasic kinetics of synaptically evoked Ca 2+ transients in dendritic shafts of PCs.