FORWARD: Preservation of rodent brain cells after cardiac arrest

Tony B. Csoka (
Thu, 16 Apr 1998 14:03:36 -0700

Encouraging news for Alcor members (I'm in the process of joining):

Forwarded from Proceedings of National Academy of Sciences USA

> Vol. 95, Issue 8, 4748-4753, April 14, 1998
> Physiology
> Cardiac arrest in rodents: Maximal duration compatible with a recovery of neuronal activity
> S. Charpak*, and E. Audinat
> * Laboratory of Physiology and Laboratory of Neurobiology, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7637, Ecole Supérieure
> de Physique et de Chimie Industrielles, 10 rue Vauquelin, 75005, Paris, France
> Communicated by Jean Dausset, Centre d'Etude du Polymorphisme Humain, Paris, France, February 12, 1998 (received for review December 8, 1997)
> We report here that during a permanent cardiac arrest, rodent brain tissue is "physiologically" preserved in situ in a particular quiescent state. This state is
> characterized by the absence of electrical activity and by a critical period of 5-6 hr during which brain tissue can be reactivated upon restoration of a simple energy
> (glucose/oxygen) supply. In rat brain slices prepared 1-6 hr after cardiac arrest and maintained in vitro for several hours, cells with normal morphological
> features, intrinsic membrane properties, and spontaneous synaptic activity were recorded from various brain regions. In addition to functional membrane
> channels, these neurons expressed mRNA, as revealed by single-cell reverse transcription-PCR, and could synthesize proteins de novo. Slices prepared after
> longer delays did not recover. In a guinea pig isolated whole-brain preparation that was cannulated and perfused with oxygenated saline 1-2 hr after cardiac arrest,
> cell activity and functional long-range synaptic connections could be restored although the electroencephalogram remained isoelectric. Perfusion of the isolated
> brain with the -aminobutyric acid A receptor antagonist picrotoxin, however, could induce self-sustained temporal lobe epilepsy. Thus, in rodents, the duration
> of cardiac arrest compatible with a short-term recovery of neuronal activity is much longer than previously expected. The analysis of the parameters that regulate
> this duration may bring new insights into the prevention of postischemic damages.