Published in:
Clin Neurophysiol. 2011 Jun;122(6):1117-26. Epub 2010 Oct 13.

Abstract
OBJECTIVE:
Emergence of slow EEG rhythms within the delta frequency band following an ischemic insult of the brain has long been considered a marker of irreversible anatomical damage. Here we investigated whether ischemic adenosine release and subsequent functional inhibition via the adenosine A(1) receptor (A(1)R) contributes to post-ischemic delta activity.
METHODS:
Rats were subjected to episodes of non-injuring transient global cerebral ischemia (GCI) under chloral hydrate anesthesia.
RESULTS:
We found that a GCI lasting only 10s was enough to induce a brief discharge of rhythmic delta activity (RDA) with a peak frequency just below 1 Hz quantified as an increase by twofold of the 0.5-1.5 Hz spectral power. This post-ischemic RDA did not occur following administration of the A(1)R antagonist 8-cyclopentyl-1,3-dipropylxanthine. Nevertheless, a similar RDA could be induced in rats not subjected to GCI, by systemic administration of the A(1)R agonist N(6)-cyclopentyladenosine.
CONCLUSIONS:
Our data suggest that A(1)R activation at levels that occur following cerebral ischemia underlies the transient post-ischemic RDA.
SIGNIFICANCE:
It is likely that the functional, thus potentially reversible, synaptic disconnection by A(1)R activation promotes slow oscillations in the cortical networks. This should be accounted for in the interpretation of early post-ischemic EEG delta activity.


Copyright © 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.