Abstract

We have previously reported that rats exhibited audiogenic myoclonus at 3 days after cardiac arrest. This phenomenon peaked at 14 days, gradually tapered off at older ages, and disappeared in most rats by 60 days following cardiac arrest. Because treatment with the 5-HT 2-selective agonist, (±)-1-2,5-dimethoxy-4-iodophenyl-2-aminopropane (DOI) significantly attenuated audiogenic myoclonus in these postcardiac-arrest rats, the involvement of 5-HT 2 receptors in posthypoxic stimulus-sensitive myoclonus was suggested. In the current study, we, therefore, examined the binding properties of 5-HT 2 receptors in the rat brain at various time points following cardiac arrest. The affinity constant of [ 3H]ketanserin binding to 5-HT 2 receptors in cortical membranes of rats did not change. In contrast, B max values were found to be reduced at 3 and 14 days after cardiac arrest with some recovery after 60 days. Taken together with previous results, these results indicate that hypoactivity of central 5-HT 2 neurotransmission may underlie the development of posthypoxic stimulus-sensitive myoclonus in rats.

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