Influence of Oestrogenic Compounds on Monoamine Transporters in Rat Striatum

Saux, Maryvonne Le; Paolo, Thérèse Di

doi:10.1111/j.1365-2826.2005.01380.x

Cited by 72 publications

(61 citation statements)

References 42 publications

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“…OVX had been proposed to model gonadal hormone withdrawal occurring at menopause (Bosse and Di Paolo, 1995;Le Saux and Di Paolo, 2006;Vaillancourt et al, 2002). In support of this notion, we showed previously that OVX disrupts LI and impairs the efficacy of APDs to restore LI in OVX rats, in line with reduced APD efficacy reported in menopausal women with schizophrenia .…”

Section: Discussionsupporting

confidence: 69%

Contrasting Effects of Increased and Decreased Dopamine Transmission on Latent Inhibition in Ovariectomized Rats and Their Modulation by 17β-Estradiol: An Animal Model of Menopausal Psychosis?

Arad

Weiner

2010

Neuropsychopharmacol

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Women with schizophrenia have later onset and better response to antipsychotic drugs (APDs) than men during reproductive years, but the menopausal period is associated with increased symptom severity and reduced treatment response. Estrogen replacement therapy has been suggested as beneficial but clinical data are inconsistent. Latent inhibition (LI), the capacity to ignore irrelevant stimuli, is a measure of selective attention that is disrupted in acute schizophrenia patients and in rats and humans treated with the psychosisinducing drug amphetamine and can be reversed by typical and atypical APDs. Here we used amphetamine (1 mg/kg)-induced disrupted LI in ovariectomized rats to model low levels of estrogen along with hyperfunction of the dopaminergic system that may be occurring in menopausal psychosis, and tested the efficacy of APDs and estrogen in reversing disrupted LI. 17b-Estradiol (50, 150 mg/kg), clozapine (atypical APD; 5, 10 mg/kg), and haloperidol (typical APD; 0.1, 0.3 mg/kg) effectively reversed amphetamine-induced LI disruption in sham rats, but were much less effective in ovariectomized rats; 17b-estradiol and clozapine were effective only at high doses (150 mg/kg and 10 mg/kg, respectively), whereas haloperidol failed at both doses. Haloperidol and clozapine regained efficacy if coadministered with 17b-estradiol (50 mg/kg, an ineffective dose). Reduced sensitivity to dopamine (DA) blockade coupled with spared/potentiated sensitivity to DA stimulation after ovariectomy may provide a novel model recapitulating the combination of increased vulnerability to psychosis with reduced response to APD treatment in female patients during menopause. In addition, our data show that 17b-estradiol exerts antipsychotic activity.

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Section: Discussionsupporting

confidence: 69%

Contrasting Effects of Increased and Decreased Dopamine Transmission on Latent Inhibition in Ovariectomized Rats and Their Modulation by 17β-Estradiol: An Animal Model of Menopausal Psychosis?

Arad

Weiner

2010

Neuropsychopharmacol

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“…For example, subcutaneous administration of DPN produced antianxiety behavior, which is believed to be mediated in the brain (34). In addition, subcutaneous administration of DPN produced an increase in striatal dopamine transporter binding that was similar to that observed following subcutaneous administration of EB (21). Finally, subcutaneous administration of PPT increased progesterone receptor mRNA expression in the arcuate nucleus and ventromedial hypothalamus (18).…”

mentioning

confidence: 68%

Acute activation of ERα decreases food intake, meal size, and body weight in ovariectomized rats

Santollo¹,

Wiley²,

Eckel³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

117

119

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Santollo J, Wiley MD, Eckel LA. Acute activation of ER␣ decreases food intake, meal size, and body weight in ovariectomized rats. Am J Physiol Regul Integr Comp Physiol 293: R2194-R2201, 2007. First published October 17, 2007; doi:10.1152/ajpregu.00385.2007.-Estradiol exerts many of its actions by coupling with two nuclear estrogen receptor (ER) proteins, ER␣, and ER␤.While the acute, anorexigenic effect of estradiol appears to involve such a mechanism, the relative contributions of ER␣ and ER␤ are equivocal. To address this problem, food intake was monitored in ovariectomized (OVX) rats following acute administration of a selective ER␣ agonist (4,4Ј,4ЈЈ-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol, PPT; dose range ϭ 0 -200 g), a selective ER␤ agonist (2,3-bis(4-hydroxyphenyl)-propionitrile, DPN; dose range ϭ 0 -600 g), and a physiological (4 g) dose of estradiol benzoate (EB). While PPT-treated rats displayed dosedependent decreases in daily food intake and body weight, neither of these measures was influenced by any dose of DPN. In addition, DPN failed to modulate the anorexigenic effect of PPT when the two ER agonists were coadministered. Meal pattern analysis revealed that the anorexigenic effect of 75 g PPT (a dose of PPT that produced a similar decrease in daily food intake as 4 g EB) was mediated by a decrease in meal size, not meal number. Thus, PPT, like EB and endogenous estradiol, decreases food intake by selectively affecting the controls of meal size. The finding that acute administration of 75 g PPT failed to induce a conditioned taste aversion suggests that the anorexigenic effect of this dose of PPT is not secondary to malaise. Taken together, our findings demonstrate that selective activation of ER␣ decreases food intake, body weight, and meal size in the ovariectomized rat. 4,4Ј,4ЈЈ-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol; 2,3-bis(4-hydroxyphenyl)-propionitrile; food intake; estradiol THE OVARIAN HORMONE ESTRADIOL exerts an inhibitory effect on food intake that is particularly well characterized in the rat. For example, the periovulatory increase in estradiol secretion in female rats is associated with a phasic decrease in food intake during estrus (4,8,12), and bilateral ovariectomy promotes sustained hyperphagia (33). Available data involving estradiol benzoate (EB) or progesterone replacement alone and in combination provide evidence that the hyperphagia displayed by ovariectomized (OVX) rats is mediated solely by the postsurgical decline in estradiol secretion (2, 17).Food intake is defined by the product of meal size and meal number over a given period of time. Accordingly, any change in food intake must involve a change in one or both of these parameters. Because meal size and meal number are independently controlled in the rat (32), an important first step in identifying the mechanism underlying estradiol's anorexigenic effect involved a detailed analysis of the spontaneous feeding patterns of cycling and EB-treated OVX rats. Such studies revealed that estradiol decreases food ...

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“…The dopamine transporter, DAT, is a protein that mediates the active reuptake of dopamine from the synapse and is a principal regulator of dopaminergic neurotransmission, dopamine receptor 1 and 2 (D 1 and D 2 , respectively) are modulated by 17β-estradiol and testosterone. Experiments using ovariectomized adult rats have shown a significant reduction of DAT levels in the NAcc and Striatum, which is restored to normal levels after E 2 replacement or the use of diarylpropionitrile (a selective ERβ agonist) and tamoxifen (selective estrogen receptor modulator) [45][46][47][48]. In the same model, levels of D 1 in mPOA are decreased after E 2 replacement [49].…”

Section: Sex Hormones Dopaminergic Neurotransmission and Addictionmentioning

confidence: 73%

Sex Hormones: Role in Neurodegenerative Diseases and Addiction

Pinto¹,

Castillo²,

RamónSotomayor-Zárate³

2018

Sex Hormones in Neurodegenerative Processes and Diseases

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The brain is a complex organ in charge of regulating the homeostasis of our body and behaviors such as motivation, reward, memory, and movement control, between others. These behaviors are regulated by dopaminergic neurons, which can be modulated by several stimuli throughout the life of an individual. For example, early exposure to sex hormones or endocrine disruptors during critical period of neuronal development affects dopaminergic pathways permanently, producing some disorders such as drug addiction. On the other hand, current knowledge regarding neurodegeneration in Parkinson and Alzheimer diseases pointed out the neuroprotection that estradiol can exert, but contradictory information can also be found in the literature. To know the underlying mechanisms that are related to the above mentioned diseases will help to improve health policies and treatments development.

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Influence of Oestrogenic Compounds on Monoamine Transporters in Rat Striatum

Cited by 72 publications

References 42 publications

Contrasting Effects of Increased and Decreased Dopamine Transmission on Latent Inhibition in Ovariectomized Rats and Their Modulation by 17β-Estradiol: An Animal Model of Menopausal Psychosis?

Contrasting Effects of Increased and Decreased Dopamine Transmission on Latent Inhibition in Ovariectomized Rats and Their Modulation by 17β-Estradiol: An Animal Model of Menopausal Psychosis?

Acute activation of ERα decreases food intake, meal size, and body weight in ovariectomized rats

Sex Hormones: Role in Neurodegenerative Diseases and Addiction

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