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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 189, Supplement 653
The 86th Annual Meeting of The German Physiological Society
3/25/2007-3/28/2007
Hannover, Germany


IONIC MECHANISMS CONTROLLING DAMPENED NEURONAL OSCILLATIONS IN THE NUCLEUS RETICULARIS THALAMI
Abstract number: S04-2

Cueni1 L, Canepari1 M, Lujan1 R, Watanabe1 M, Bond1 CT, Adelman1 JP, Luthi1 A

1Divsion of Pharmacology & Neurobiology, Biozentrum, Universitt Basel

Thalamic neurons and networks are classically known for their bursting and pacemaking capacities that are central to the generation of synchronized oscillations in the thalamocortical system. Although it is increasingly recognized that an elaborate Ca2+ signaling system, containing both high-voltage-activated (HVA) and low-threshold (T-type) Ca2+ currents and multiple intracellular Ca2+ messenger pathways, underlies thalamic oscillations, little is known about the dynamics of intracellular Ca2+ transients and how these shape ionic events generating the oscillations. To gain quantitative insight into thalamic Ca2+ signaling and associated ionic events, we study the oscillatory properties of the neurons within the nucleus reticularis thalami (nRt) using electrophysiological, imaging, and molecular techniques. Cells in the nRt show an oscillatory pattern characterized by vigorous oscillatory burst discharges that are, however, limited to a few cycles, and then fade away, reflecting an intrinsic dampening of oscillatory bursting. Our data reveal a complex scenario of T-type-mediated Ca2+ signaling. T-currents provide a strong Ca2+ signal in nRt dendrites that is rapidly and selectively detected by SK channels, but also by endoplasmic Ca2+ sequestration mechanisms, enabling a dampened oscillatory activity in these neurons.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 189, Supplement 653 :S04-2

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