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.
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Adenosine, Adenosine A1 Receptor Antagonists, Animals, Delta Rhythm, Disease Models, Animal, Electrocardiography, Electroencephalography, Heart Rate, Ischemic Attack, Transient, Male, Rats, Rats, Wistar, Receptor, Adenosine A1, Statistics, Nonparametric, Theophylline, Xanthines