Supralinear dendritic Ca(2+) signalling in young developing CA1 pyramidal cells

Pohle, J. and Bischofberger, J.. (2014) Supralinear dendritic Ca(2+) signalling in young developing CA1 pyramidal cells. Journal of Physiology, 592 (22). pp. 4931-4949.

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Official URL: https://edoc.unibas.ch/61420/

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Although Ca(2+) is critically important in activity-dependent neuronal development, not much is known about the regulation of dendritic Ca(2+) signals in developing neurons. Here, we used ratiometric Ca(2+) imaging to investigate dendritic Ca(2+) signalling in rat hippocampal pyramidal cells during the first 1-4 weeks of postnatal development. We show that active dendritic backpropagation of Nav channel-dependent action potentials (APs) evoked already large dendritic Ca(2+) transients in animals aged 1 week with amplitudes of approximately 150 nm, similar to the amplitudes of approximately 160 nM seen in animals aged 4 weeks. Although the AP-evoked dendritic Ca(2+) load increased about four times during the first 4 weeks, the peak amplitude of free Ca(2+) concentration was balanced by a four-fold increase in Ca(2+) buffer capacity kappas ( approximately 70 vs. approximately 280). Furthermore, Ca(2+) extrusion rates increased with postnatal development, leading to a slower decay time course ( approximately 0.2 s vs. approximately 0.1 s) and more effective temporal summation of Ca(2+) signals in young cells. Most importantly, during prolonged theta-burst stimulation dendritic Ca(2+) signals were up to three times larger in cells at 1 week than at 4 weeks of age and much larger than predicted by linear summation, which is attributable to an activity-dependent slow-down of Ca(2+) extrusion. As Ca(2+) influx is four-fold smaller in young cells, the larger Ca(2+) signals are generated using four times less ATP consumption. Taken together, the data suggest that active backpropagations regulate dendritic Ca(2+) signals during early postnatal development. Remarkably, during prolonged AP firing, Ca(2+) signals are several times larger in young than in mature cells as a result of activity-dependent regulation of Ca(2+) extrusion rates.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Division of Physiology > Cellular Neurophysiology (Bischofberger)
UniBasel Contributors:Bischofberger, Josef
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Cambridge University Press
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:28 Jul 2020 13:49
Deposited On:17 Jul 2020 08:25

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