ISSN:
1471-4159
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
: Repeated administration of electroconvulsive shock (ECS) increases [3H]prazosin binding to α1-adrenoceptors in rat cerebral cortex. In contrast, [3H]WB4101 binding in cortex has been reported to be unchanged after ECS. [3H]Prazosin labels two α1-adrenoceptor subtypes, termed α1a and α1b, whereas [3HJWB4101 labels the α1a subtype preferentially. The purpose of this study was to determine whether ECS increases one or both α1-adrenoceptor subtypes in rat cerebral cortex. We found that treatment of rats with ECS once daily for 10–12 days increased [3H]prazosin binding in cortex by about 25% but did not significantly alter [3H]WB4101 binding to α1a-adrenoceptors. Measurement of α1a and α1b receptors by competition analysis of the selective α1a antagonist 5-methylurapidil against [3H]prazosin and measurement of [3H]prazosin binding in homogenates preincubated with chlorethylclonidine, which alkylates α1b binding sites, also indicated that the ECS-indiced increase in α1-adrenoceptors is confined to the α1b subtype. In contrast to its effect on [3H]prazosin binding, ECS did not increase phosphoinositide hydrolysis as measured by [3H]inositol 1-phosphate accumulation in slices of rat cerebral cortex stimulated by either norepinephrine or phenylephrine. The failure of ECS to increase [3H]inositol 1-phosphate accumulation stimulated by phenylephrine, which is a partial agonist for this response, suggests that spare receptors do not account for the apparent absence of effect of ECS on α1-adrenoceptor-mediated phosphoinositide hydrolysis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1471-4159.1991.tb06350.x
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