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60th Annual Meeting of the German Society of Neurosurgery (DGNC)
Joint Meeting with the Benelux countries and Bulgaria

German Society of Neurosurgery (DGNC)

24 - 27 May 2009, Münster

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After ventricular hemorrhage the ATP-sensitive PY2-receptor induces a Ca2+-rise in the cytosol resulting in necrosis but not apoptosis in human astrocytes

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  • W. Scharbrodt - Neurochirugische Klinik, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH
  • Y. Abdallah - Physiologisches Institut, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH
  • S. Kasseckert - Physiologisches Institut, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH
  • H. Piper - Physiologisches Institut, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH
  • D.-K. Böker - Neurochirugische Klinik, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH
  • M. Stein - Neurochirugische Klinik, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH
  • M. Miqdad - Neurochirugische Klinik, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH
  • M. Oertel - Neurochirugische Klinik, Standort Gießen, Universitätsklinikum Gießen und Marburg GmbH

Deutsche Gesellschaft für Neurochirurgie. 60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien. Münster, 24.-27.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. DocMO.12-04

doi: 10.3205/09dgnc083, urn:nbn:de:0183-09dgnc0830

Published: May 20, 2009

© 2009 Scharbrodt 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: Ca2+-is a cofactor of many cellular processes including apoptosis and necrosis. This study’s hypothesis was that bloody CSF from patients after intraventricular hemorrhage may cause a Ca2+-rise which induces apoptosis or necrosis in an in-vitro model of human cerebral astrocytes.

Methods: Human astrocytes were incubated with CSF from patients with intraventicular hemorrhage. In control experiments, native CSF was used. Single cell cytosolic Ca2+-concentrations were measured by fura-2 microfluometry. Three blockers were used: Nimodipine, APB and suramine that blocks the L-type Ca2+-channel, the membrane and endoplasmic reticulum Ca2+-channels; and the ATP-sensitive PY2-rezeptor, respectively. Apoptosis and necrosis were evaluated by staining with Hoechst-3342 and propidium iodide.

Results: Incubation of astrocytes with bloody-CSF provoked a cytosolic Ca2+-rise a typical pattern: after an initial peak, Ca2+ concentration almost returned to baseline but then increased slowly but long lasting over the observation period of 60 min. The Ca2+-rise was significantly blocked by APB and suramin. Nimodipine had no influence on the cytosolic Ca2+-concentration. Incubation of the astrocytes with bloody-CSF induced necrosis but not apoptosis. The blockade of the Ca2+-rise by APB or Suramin reduced necrosis significantly. Nimodipine did not prevent astrocytic necrosis.

Conclusions: Bloody CSF induces an Ca2+-rise leading to necrosis but not to apoptosis in human astrocytes. The cytosolic Ca2+-increase and cellular necrosis depend on the activation of the ATP-sensitive PY2-receptor. Nimodipine had no protective effect on astrocytes in vitro.