Estrogen modulates responses of striatal dopamine neurons to MPP+: evaluations using in vitro and in vivo techniques

Arvin, Michael; Fedorkova, Lenka; Disshon, Kimberly A; Dluzen, Dean E.; Leipheimer, Robert E.

doi:10.1016/s0006-8993(00)02511-7

Cited by 40 publications

(15 citation statements)

References 43 publications

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“…Consequently, our results imply that acute high dose of estradiol, which blocked the effects of amphetamine and potentiated the effects of haloperidol on LI, reduced mesolimbic DA function, whereas low dose, which disrupted LI, increased DA release within the nucleus accumbens. Results consistent with both reduction and increase of striatal dopaminergic function by estradiol have been reported for all indices of dopaminergic activity, including receptor levels/binding, membrane dopamine transporter levels, and release, depending on dose and treatment paradigm (Arvin et al, 2000;Bazzett and Becker, 1994;Becker and Beer, 1986;Becker and Rudick, 1999;Di Paolo, 1994, 1982, 1984, 1985Disshon et al, 1998;Disshon and Dluzen, 2000;Dluzen, 1997;Landry et al, 2002;McDermott, 1993;McDermott et al, 1994;Morissette et al, 2008;Morissette and Di Paolo, 1993;Peris et al, 1991;Shieh and Yang, 2008;Thompson and Moss, 1994;Zhou et al, 2002). It has been suggested that antidopaminergic effects are primarily exerted by high doses of estrogen or chronic administration, whereas pro-dopaminergic actions are more associated with lower physiological levels of estrogen (Barber et al, 1976;Becker, 1999;Bedard et al, 1977;Cyr et al, 2002;Di Paolo, 1994;Di Paolo et al, 1981;Hruska and Silbergeld, 1980;McEwen and Alves, 1999;Riddoch et al, 1971).…”

Section: Discussionsupporting

confidence: 76%

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: 76%

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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“…Within the nigrostriatal dopaminergic (NSDA) system, estrogen is well known to modulate tyrosine hydroxylase activity, DA metabolism, DA release and DA receptor characteristics . Of particular relevance to the present report are the neuroprotective properties of estrogen as demonstrated by neurodegenerative responses of the NSDA system to neurotoxins (Arvin et al 2000;. Such findings suggest an involvement of estrogen in the characteristics of PD incidence rates, PD which is more prevalent in males (Diamond et al 1990;Bower et al 1999).…”

supporting

confidence: 52%

Increased dopamine release in vivo by estradiol benzoate from the central amygdaloid nucleus of Parkinson's disease model rats

Liu

Xie

2004

Journal of Neurochemistry

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In addition to the dopaminergic neurons in the nigrostriatal system, the properties of dopaminergic neurons in the mesolimbic system, such as the amygdala, are also of interest and importance because of their specific neuromodulatory effects in the pathophysiology of Parkinson's disease (PD). Using the fast cyclic voltammetry (FCV) technique, we present evidence to indicate that electrically-evoked dopamine (DA) release from the amygdala, especially the central amygdaloid nucleus (CAN), of ovariectomized (OVX) female rats was significantly enhanced with increasing doses of estradiol benzoate (EB; 30, 50 and 100 lg/kg). Impaired DA release from the amygdala of an OVX rat PD model can also be increased by EB treatment (50 lg/kg) to a level similar to that of controls. The well established neuroprotective effects of estrogen may be beneficial for reducing the dysfunction of dopaminergic neurons in mesolimbic structures of rat PD models and PD patients.

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“…This nucleus contains dopaminergic neurons and may be analogous to the nigrostriatal dopaminergic system of tetrapods (Rink & Wullimann 2001). In mammals, these dopaminergic neurons are responsive to oestrogen, and E 2 protects them from degeneration induced by the neurotoxins 6-hydroxydopamine and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; Arvin et al 2000;Murray et al 2003).…”

Section: Discussionmentioning

confidence: 99%

The distributions of the duplicate oestrogen receptors ER-βa and ER-βb in the forebrain of the Atlantic croaker (Micropogonias undulatus): evidence for subfunctionalization after gene duplication

Hawkins¹,

Godwin

Crews

et al. 2005

Proc. R. Soc. B.

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Teleost fishes have three distinct oestrogen receptor (ER) subtypes: ER-a, ER-ba (or ER-g) and ER-bb. ER-ba and ER-bb arose from a duplication of an ancestral ER-b gene early in the teleost lineage. Here, we describe the distribution of the three ER mRNAs in the hypothalamus and cerebellum of the Atlantic croaker to address two issues: the specific functions of multiple ERs in the neuroendocrine system and the evolution and fate of duplicated genes. ER-a was detected in nuclei of the preoptic area (POA) and hypothalamus previously shown to possess ER-as in teleosts. AcER-bb, but not ER-ba, labelling was detected in the magnocellular neurons of the POA, nucleus posterior tuberis, the nucleus recessus posterior and cerebellum. By contrast, acER-ba, but not ER-bb, was detected in the dorsal anterior parvocellular POA and suprachiasmatic nucleus. Both ER-bs were found in posterior parvocellular and ventral anterior POA nuclei, the ventral hypothalamus, and periventricular dorsal hypothalamus. The differences we observed in ER subtype mRNA distribution within well-characterized brain nuclei suggest that ER-ba and ER-bb have distinct functions in the neuroendocrine control of reproduction and behaviour, and provide evidence that the teleost ER-b paralogues have partitioned functions of the ancestral ER-b gene they shared with tetrapods.

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Estrogen modulates responses of striatal dopamine neurons to MPP+: evaluations using in vitro and in vivo techniques

Cited by 40 publications

References 43 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?

Increased dopamine release in vivo by estradiol benzoate from the central amygdaloid nucleus of Parkinson's disease model rats

The distributions of the duplicate oestrogen receptors ER-βa and ER-βb in the forebrain of the Atlantic croaker (Micropogonias undulatus): evidence for subfunctionalization after gene duplication

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