• Christiane Meyer, Annika Kettner, Ulla Hochenegg, Lena Rubi, Karlheinz Hilber, Xaver Koenig, Stefan Boehm, Matej Hotka, and Helmut Kubista.
• Center of Physiology and Pharmacology, Department of Neurophysiology and -pharmacology, Medical University of Vienna, Waehringerstrasse 13a, 1090 Vienna, Austria. Electronic address: chrissi-mey@web.de.
• Neuroscience. 2021 Aug 1; 468: 265281265-281.

AbstractSince their discovery in the 1960s, the term paroxysmal depolarization shift (PDS) has been applied to a wide variety of reinforced neuronal discharge patterns. Occurrence of PDS as cellular correlates of electrographic spikes during latent phases of insult-induced rodent epilepsy models and their resemblance to giant depolarizing potentials (GDPs) nourished the idea that PDS may be involved in epileptogenesis. Both GDPs and - in analogy - PDS may lead to progressive changes of neuronal properties by generation of pulsatile intracellular Ca2+ elevations. Herein, a key element is the gating of L-type voltage gated Ca2+ channels (LTCCs, Cav1.x family), which may convey Ca2+ signals to the nucleus. Accordingly, the present study investigates various insult-associated neuronal challenges for their propensities to trigger PDS in a LTCC-dependent manner. Our data demonstrate that diverse disturbances of neuronal function are variably suited to induce PDS-like events, and the contribution of LTCCs is essential to evoke PDS in rat hippocampal neurons that closely resemble GDPs. These PDS appear to be initiated in the dendritic sub-compartment. Their morphology critically depends on the position of recording electrodes and on their rate of occurrence. These results provide novel insight into induction mechanisms, origin, variability, and co-existence of PDS with other discharge patterns and thereby pave the way for future investigations regarding the role of PDS in epileptogenesis.Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.

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