Abstract
The influence of estrogen on stimulation of inositol phospholipid hydrolysis by norepinephrine and carbamylcholine has been studied by measuring the accumulation of [3H]inositolmonophosphate ([3H]InsP) in cortical, hippocampal and striatal slices from ovariectomized rats. Repeated (but not a single) subcutaneous injections of estradiol benzoate (EB) (2 μg/animal once every 2 days for 10 days) markedly reduced stimulation of inositol phospholipid hydrolysis by norepinephrine in hippocampus and corpus striatum. Conversely, the efficacy of norepinephrine was increased in cortical slices. Estrogen treatment did not affect basal or carbamylcholine-stimulated [3H]InsP formation. In vitro addition of 17β-estradiol (1-100 nM) failed to modify norepinephrine- or carbamylcholine-induced [3H]InsP production in all regions examined. An increased density of α1-adrenergic binding sites in cortical membranes paralleled the enhanced responsiveness of inositol phospholipid hydrolysis to norepinephrine induced by EB treatment in this area, whereas no significant changes in [3H]prazosin binding were found in membranes from hippocampus and corpus striatum. These results indicate that estrogen may affect inositol phospholipid hydrolysis in discrete brain areas, suggesting a complex role for estradiol in modulating noradrenergic receptor activity in the central nervous system.
Original language | English |
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Pages (from-to) | 65-69 |
Number of pages | 5 |
Journal | Brain Research |
Volume | 555 |
Issue number | 1 |
DOIs | |
Publication status | Published - Jul 26 1991 |
Keywords
- Estradiol benzoate
- Inositol phospholipid hydrolysis
- Norepinephrine
ASJC Scopus subject areas
- Developmental Biology
- Molecular Biology
- Clinical Neurology
- Neuroscience(all)