ACTIVITY-INDUCED ELEVATIONS OF INTRACELLULAR CALCIUM-CONCENTRATION INNEURONS OF THE DEEP CEREBELLAR NUCLEI

1. Depolarization-induced changes in the cytosolic free calcium concen tration ([Ca2+](i)) were examined in slice-cultured neurons of the dee p cerebellar nuclei by combined intracellular and multisite fura-2 rec ording techniques. 2. Firing of tetrodotoxin (TTX)-sensitive action po tentials induced by depolarizing current pulses caused large elevation s in somatic as well as proximal dendritic [Ca2+](i). In the dendrites , rise and decay times of [Ca2+](i) were faster than in the soma. [Ca2 +](i) changes associated with depolarizations to less than or equal to -40 mV in the presence of TTX were small compared with changes induced by Na+ spike firing, suggesting that Ca2+ influx through high voltage -activated Ca2+ channels is a major cause for Na+ spike-associated [Ca 2+](i) increases. 3. During sustained Na+ spike firing at a constant f requency (>20 Hz), [Ca2+](i) approached a constant level, after simila r to 1 s in the dendrites and 2 s in the soma, respectively. The ampli tude of the attained level was positively correlated with the firing f requency. We suggest that during tonic activity [Ca2+](i) reaches a st eady state determined by Ca2+ influx and extrusion. 4. TTX-resistant p lateau potentials caused substantially greater [Ca2+](i) increases in the dendrites than in the soma. In the dendrites, plateau-associated C a2+ transients were comparable in amplitude to Ca2+ transients trigger ed by short(50 ms) Na+ spike trains, in the soma, they were considerab ly smaller. 5. Low-threshold spikes (LTSs) in association with a burst of Na+ spikes induced a sharp increase in [Ca2+](i) both in the soma and in dendrites. A major fraction of this increase appeared to be med iated by Na+ spikes, which occurred superimposed on the LTS, and conse quently, only a minor fraction directly by the LTS. 6. We conclude tha t voltage-gated Ca2+ channels are localized both at somatic as well as dendritic sites in neurons of the DCN and mediate Ca2+ influx during Na+ spikes. TTX-resistant plateau potentials appear to be generated in the dendrites and to spread only passively into the soma.