Abstract
Neuronal endoplasmic reticulum (ER), continuous from soma to dendritic spines, undergoes rapid fragmentation in response to N-methyl-D-aspartate (NMDA) receptor stimulation in hippocampal slices and neuronal primary cultures. Here, we show that ER fragments in the mouse brain following cardiac arrest (CA) induced brain ischemia. The ER structure was assessed in vivo in cortical pyramidal neurons in transgenic mice expressing ER-targeted GFP using two-photon laser scanning microscopy with fluorescence recovery after photobleaching (FRAP). Endoplasmic reticulum fragmentation occurred 1 to 2 minutes after CA and once induced, fragmentation was rapid (<15 seconds). We propose that acute ER fragmentation may be a protective response against severe ischemic stress.Journal of Cerebral Blood Flow & Metabolism advance online publication, 6 April 2011; doi:10.1038/jcbfm.2011.37.
Original language | English |
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Pages (from-to) | 1663-1667 |
Journal | Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism |
Volume | 31 |
DOIs | |
Publication status | Published - 2011 |
Bibliographical note
The information about affiliations in this record was updated in December 2015.The record was previously connected to the following departments: Clinical Memory Research Unit (013242610), Laboratory for Experimental Brain Research (013041000)
Subject classification (UKÄ)
- Cardiology and Cardiovascular Disease