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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.

Original publication

DOI

10.1016/j.clinph.2010.09.015

Type

Journal article

Journal

Clin Neurophysiol

Publication Date

06/2011

Volume

122

Pages

1117 - 1126

Keywords

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