Abstract
Norepinephrine (NE)-stimulated inositol phospholipid hydrolysis ("PI breakdown") in rat cerebral cortical miniprisms was used as a measure of alpha 1-adrenoceptor function following serotonin and/or NE depletion. The use of ascorbic acid to prevent autooxidation of the NE during the PI breakdown assay was found to be warranted. Treatment of rats with 5,7-dihydroxytryptamine and DSP4 produced selective depletions of serotonin (79-95%) and NE (69-85%), respectively, in cortical and hippocampal brain regions. The degree of cortical NE-stimulated PI breakdown in the lesioned animals was not significantly different from that in the control animals, suggesting that under the conditions used, serotonin and NE depletion do not lead to a changed sensitivity of alpha 1-adrenoceptors coupled to PI breakdown in the rat cortex.
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