Acute and long-term effects of 17β-estradiol on Gi/o coupled neurotransmitter receptor function in the female rat brain as assessed by agonist-stimulated [35S]GTPγS binding

Mize, Amy L.; Alper, Richard H.

doi:10.1016/s0006-8993(00)01998-3

Cited by 90 publications

(72 citation statements)

References 22 publications

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“…The most likely mechanism responsible for the observed PPI effects is that estrogen treatment altered signalling of the 5-HT 1A receptor. Acute estrogen treatment in ovariectomized rats desensitized 5-HT 1A receptor function, as indicated by a reduction in [ 35 S]GTPgS binding (Mize and Alper, 2000;Mize et al, 2001). Further studies are required to investigate if similar mechanisms occur in humans.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Prevents 5-HT1A Receptor-Induced Disruptions of Prepulse Inhibition in Healthy Women

Gogos

Nathan

Guille

et al. 2005

Neuropsychopharmacol

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The sex steroid hormone, estrogen, has been proposed to be protective against schizophrenia. This study examined the effects of estrogen treatment on modulation of prepulse inhibition (PPI) by the serotonin-1A (5-HT 1A ) receptor partial agonist, buspirone. PPI is a model of sensorimotor gating, which is deficient in schizophrenia and other mental illnesses. A total of 11 healthy women were tested following four acute treatment conditions: placebo, buspirone (Buspar; 5 mg), estradiol (Estrofem; 2 mg), and combined buspirone and estradiol. Electromyogram activity was measured across three interstimulus intervals (ISI): 30, 60, and 120 ms. There was no significant effect of either drug treatment on startle amplitude or habituation. At 120 ms ISI, buspirone caused a significant disruption of PPI and pretreatment with estrogen prevented this disruption. Estrogen treatment, administered in the appropriate experimental conditions, prevented PPI deficits induced by 5-HT 1A receptor activation and may therefore also play a protective role in sensorimotor gating deficits in schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Estrogen Prevents 5-HT1A Receptor-Induced Disruptions of Prepulse Inhibition in Healthy Women

Gogos

Nathan

Guille

et al. 2005

Neuropsychopharmacol

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“…Therefore, it can be concluded that the 5-HT 1A receptor subtype is a mediator of the antidepressant-like action of E 2 . Evidences in favor of this hypothesis are the results derived from in vitro and in vivo studies, showing that the 5-HT 1A receptor subtype is a target of estrogens and some estrogen-like compounds (Bethea et al, 1998;Biegon et al, 1983;Mize and Alper, 2000;Mize et al, 2001;Raap et al, 2000;Uphouse, 2000). Indeed, Lu and Bethea (2002) demonstrated that E 2 induces the desensitization of 5-HT 1A receptors in the DRN of monkeys.…”

Section: Discussionmentioning

confidence: 99%

“…Considering this, it could be expected that E 2 stimulates the 5-HT 1A receptor subtype in two different manners: one mechanism, underlying the effects that last from several hours to days, that could involve the activation of intracellular estrogen receptors and the subsequent transcription of the gene that codifies for the 5-HT 1A receptor subtype. The other mechanism, underlying those estrogenic effects that appear in the order of minutes, that implies the activation of the 5-HT 1A receptor subtype and its respective second messenger cascade (Mize and Alper, 2000). The fact that the antidepressant-like actions of E 2 were blocked by WAY 100635 when both compounds were administered simultaneously (48 h before the test) indicates that the 5-HT 1A receptor subtype has a significant participation in the antiimmobility effect induced by this steroid, suggesting a direct interaction with 5-HT 1A receptors.…”

Section: Discussionmentioning

confidence: 99%

Participation of the 5-HT1A Receptor in the Antidepressant-Like Effect of Estrogens in the Forced Swimming Test

Estrada‐Camarena

Fernández‐Guasti

López‐Rubalcava

2005

Neuropsychopharmacol

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The aim of the present study was to explore the possible participation of the 5-HT 1A receptor in the antidepressant-like action of two estrogenic compounds: 17b-estradiol (E 2 ) and ethynil-estradiol (EE 2 ) in the FST. Ovariectomized female Wistar rats were used in all experiments. As a positive control, the effect of the 5-HT 1A receptor agonist, 8-hydroxy-2-(di-n)-propil-aminotetraline (8-OH-DPAT; 0.0625, 0.125, 0.25 and 0.5 mg/kg) alone or in combination with WAY 100635 (0.5 and 1.0 mg/kg) was analyzed in the FST. In order to analyze the participation of the 5-HT 1A receptor in the antidepressant-like actions of estrogens, the effect of the selective antagonist WAY 100635 (0.5 and 1.0 mg/kg) in combination with E 2 (10 mg/rat) and EE 2 (5 mg/rat) was studied in the FST. In this case, WAY 100635 was administered either simultaneously with the estrogens (48 h before the FST test) or 30 min before the FST. On the other hand, a suboptimal dose of 8-OH-DPAT (0.0625 mg/kg), combined with a noneffective dose of E 2 (2.5 mg/rat) or EE 2 (1.25 mg/rat), was tested in the FST. The results showed that 8-OH-DPAT (0.25 and 0.5 mg/kg), E 2 (10 mg/rat), and EE 2 (5 mg/rat), by themselves, exerted an antidepressant-like action. The antagonist to the 5-HT 1A receptor WAY 100635, when applied together with 8-OH-DPAT or E 2 , blocked their antidepressant-like actions, but not the one induced by EE 2 . Interestingly, when the antagonist was applied 30 min before the FST, it was able to cancel the actions of EE 2 on immobility behavior, and had no effect on the actions of E 2. Finally, when a subthreshold dose of 8-OH-DPAT was combined with a noneffective dose of either E 2 or EE 2 , an antidepressant-like action was observed. The results support the notion that the 5-HT 1A receptor is one of the mediators of the antidepressant-like action of E 2 , and could indirectly contribute to the one induced by EE 2 .

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“…There is also evidence that membrane effects of estrogens can activate intracellular signaling pathways involving cyclic AMP (cAMP; [103,170,254]), protein kinase A (PKA; [104,141,266]), the "mitogen activated protein kinases" (or MAP kinases; [39,122,153,205,260,269,276]), and the tyrosine kinases [39]. The activation of these intracellular signaling pathways results primarily in phosphorylations/dephosphorylations producing different kinds of physiological responses such as the decoupling of a receptor from its effector system [141,[171][172][173] or the modulation of the catalytic activity of an enzyme [191]. Finally, as mentioned previously, the activation of these cascades of intracellular events may result in a transcriptional activation caused, for example, by the phosphorylation of CREB (cAMP response element [CRE]-binding protein) which then acts at the level of the cAMP response element notably (CRE; [2,3,46,102,288]).…”

Section: Non-genomic Effects On Cell Functionmentioning

confidence: 99%

Functional significance of the rapid regulation of brain estrogen action: Where do the estrogens come from?

2006

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Estrogens exert a wide variety of actions on reproductive and non-reproductive functions. These effects are mediated by slow and long lasting genomic as well as rapid and transient non-genomic mechanisms. Besides the host of studies demonstrating the role of genomic actions at the physiological and behavioral level, mounting evidence highlights the functional significance of non-genomic effects. However, the source of the rapid changes in estrogen availability that are necessary to sustain their fast actions is rarely questioned. For example, the rise of plasma estrogens at pro-estrus that represents one of the fastest documented changes in plasma estrogen concentration appears too slow to explain these actions. Alternatively, estrogen can be synthesized in the brain by the enzyme aromatase providing a source of locally high concentrations of the steroid. Furthermore, recent studies demonstrate that brain aromatase can be rapidly modulated by afferent inputs, including glutamatergic afferents. A role for rapid changes in estrogen production in the central nervous system is supported by experiments showing that acute aromatase inhibition affects nociception as well as male sexual behavior and that preoptic aromatase activity is rapidly (within min) modulated following mating. Such mechanisms thus fulfill the gap existing between the fast actions of estrogen and their mode of production and open new avenues for the understanding of estrogenic effects on the brain.

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Acute and long-term effects of 17β-estradiol on Gi/o coupled neurotransmitter receptor function in the female rat brain as assessed by agonist-stimulated [35S]GTPγS binding

Cited by 90 publications

References 22 publications

Estrogen Prevents 5-HT1A Receptor-Induced Disruptions of Prepulse Inhibition in Healthy Women

Estrogen Prevents 5-HT1A Receptor-Induced Disruptions of Prepulse Inhibition in Healthy Women

Participation of the 5-HT1A Receptor in the Antidepressant-Like Effect of Estrogens in the Forced Swimming Test

Functional significance of the rapid regulation of brain estrogen action: Where do the estrogens come from?

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