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64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

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Impact of the Cav2.3 calcium channel in the genesis of DCI after SAH in vivo

Meeting Abstract

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  • Marcel A. Kamp - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf; Institut für Neurophysiologie, Universität zu Köln
  • Maxine Dibué - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf; Institut für Neurophysiologie, Universität zu Köln; Zentrum für Molekulare Medizin Köln
  • Hans-Jakob Steiger - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf
  • Toni Schneider - Institut für Neurophysiologie, Universität zu Köln; Zentrum für Molekulare Medizin Köln
  • Daniel Hänggi - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocDI.11.06

doi: 10.3205/13dgnc269, urn:nbn:de:0183-13dgnc2692

Published: May 21, 2013

© 2013 Kamp et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Objective: The molecular pathways underlying the pathogenesis of vasospasms and delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) remain poorly understood. Furthermore, L-type calcium (Ca2+) channels and the Cav2.3 containing E-/R-type are suggsted to be involved in the genesis. However, impact of Cav2.3 on the genesis of DCI after SAH has yet not been analyzed in Cav2.3-deficient animals

Method: Totally, 24 C57BL/6J mice were analyzed. After induction of general anesthesia, 50 µl of freshly-drawn blood obtained from the tail vein (or saline for the saline injection group or no injection but perforation of the atlanto-occipital membrane for the sham group) was injected in the cisterna magna. Relative rCBF was evaluated by Laser-Dopplermetry above the S1 and the cerebellar cortex and data were collected 10 minutes before and 10 minutes at the time point of maximal vasospasm 6 hours after SAH. Telemetric electrocorticograms recorded from the S1 by implanted transmitters were continuously collected and were used to calculate absolute power of frequency bands.

Results: Totally, 24 mice (10 Cav2.3 -/- mice and 14 Cav2.3 +/+ animals) were analyzed. Cav2.3 -/- mice displayed a significant rCBF and Conc impairment of S1 (p = .048 and p = .0049, respectively) but not of the cerebellum compared to Cav2.3 +/+ mice after 6 hours. For the saline-injected animals, rCBF and Conc did not significantly differ. Injection of blood into the foramen magnum reduced total ECoG power by an average of 65% in Cav2.3 +/+ animals, whereas total ECoG power was not reduced by that average in Cav2.3-deficient mice.

Conclusions: Cav2.3 containing E-/R-type Ca2+ channels are involved in these genesis of cerebral vasospasms and DCI after SAH in a SAH mouse model. Therefore, this Ca2+ channel should be considered in the development of new therapeutic strategies focusing of DCI.