Calcium buffering in rodent olfactory bulb granule cells and mitral cells.

In the mammalian olfactory bulb, axonless granule cells (GCs) mediate self- and lateral inhibitory interactions between mitral cells (MCs) via reciprocal dendrodendritic synapses. Calcium signals in the GC dendrites and reciprocal spines appear to decay unusually slowly, hence GC calcium handling might contribute to the known asynchronous release at this synapse. By recording fluorescence transients of different Ca(2+)-sensitive dyes at variable concentrations evoked by backpropagating action potentials (APs) and saturating AP trains we extrapolated Ca(2+) dynamics to conditions of zero added buffer for juvenile rat GC apical dendrites and spines and MC lateral dendrites. Resting [Ca(2+)] was at approximately 50 nM in both GC dendrites and spines. The average endogenous GC buffer capacities (kappa(E)) were within a range of 80-90 in the dendrites and 110-140 in the spines. The extrusion rate (gamma) was estimated as 570 s(-1) for dendrites and 870 s(-1) for spines and the decay time constant as approximately 200 ms for both. Single-current-evoked APs resulted in a [Ca(2+)] elevation of approximately 250 nM. Calcium handling in juvenile and adult mouse GCs appeared mostly similar. In MC lateral dendrites, we found AP-mediated [Ca(2+)] elevations of approximately 130 nM with a similar decay to that in GC dendrites, while kappa(E) and gamma were roughly 4-fold higher. In conclusion, the slow GC Ca(2+) dynamics are due mostly to sluggish Ca(2+) extrusion. Under physiological conditions this slow removal may well contribute to delayed release and also feed into other Ca(2+)-dependent mechanisms that foster asynchronous output from the reciprocal spine.