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      Estrogen Regulation of Dopamine Release in the Nucleus Accumbens: Genomic-and Nongenomic-Mediated Effects

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      Journal of Neurochemistry

      Wiley

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          Abstract

          The ability of estrogen to modulate mesolimbic dopamine (DA) was examined using in vivo voltammetry. Estrogen priming (5 micrograms, 48 h) of ovariectomized (ovx) female rats resulted in a slight decrease in K(+)-stimulated DA release measured in the nucleus accumbens: this decrease was accompanied by a significant increase in both DA reuptake and DA clearance times. Following estrogen priming nomifensine, a potent inhibitor of the DA uptake carrier, was still able to potentiate K(+)-stimulated DA release and alter the time course of DA availability, but the response was attenuated compared with ovx controls. Direct infusion of 17 beta-estradiol hemisuccinate (17 beta-E, 20-50 pg) into the nucleus accumbens resulted in a biphasic potentiation of K(+)-stimulated release. An initial increase in release was observed 2 min after 17 beta-E infusion; this increase, although reduced by 15 min, was still significantly higher than control values. A subsequent potentiation was observed 60 min after the initial 17 beta-E infusion; this response remained for at least an additional 60 min. Nomifensine did not significantly alter K(+)-stimulated DA release following 17 beta-E infusion, but was still able to potentiate the total time DA was available extracellularly. These data suggest that the mesolimbic A10 DA neurons that terminate in the nucleus accumbens can be modulated in vivo by estrogen and that this modulation may be mediated by both genomic (long term) and nongenomic (short term) mechanisms.

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          Most cited references 47

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          Atlas of estradiol-concentrating cells in the central nervous system of the female rat.

           D Pfaff,  M Keiner (1973)
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            Direct effect of 17 beta-estradiol on striatum: sex differences in dopamine release.

            The nigrostriatal dopamine (DA) system is sexually dimorphic. In female but not male rats, striatal DA activity is modulated by gonadal steroid hormones. Ovariectomy (OVX) decreases striatal DA release and turnover. Estrogen replacement restores the response to that of the intact female in estrus. In contrast, castration (CAST) of male rats has no effect on the stimulated release of DA from striatal tissue. This report addresses the question: Does estrogen act directly on the striatum to induce changes in DA release? Physiological concentrations of 17 beta-estradiol and other steroids or a nonsteroidal estrogen analog were applied directly to striatal tissue maintained in an in vitro superfusion system. The effect of hormonal treatments on the responsiveness of striatal DA terminals to stimulation was examined in tissue from OVX females and intact and CAST male rats. The results are summarized as follows: (1) Infusion of 17 beta-estradiol (p less than 0.01) and diethylstilbestrol (p less than 0.05) increased amphetamine (AMPH)-stimulated striatal DA release from striatal tissue of OVX female rats compared with the effect of cholesterol. 17 alpha-Estradiol also tended to potentiate the striatal DA response to AMPH, but this result was not statistically significant (p less than 0.062). 17 beta-Estradiol had no effect on AMPH-stimulated DA release from striatal tissue of intact male rats. (2) The KCl-stimulated release of DA from striatal tissue of OVX rats exposed in vitro to 100 pg/ml 17 beta-estradiol (a physiological dose) was significantly greater (p less than 0.05) than the response after exposure to vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)
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              Non-genomic and genomic effects of steroids on neural activity.

               Bruce McEwen (1991)
              Steroid hormones are recognized as producing their major long-term effects on cell structure and function via intracellular receptors acting on the expression of genes. There is now increasing evidence that steroids also affect the surface of cells and alter ion permeability, as well as release of neurohormones and neurotransmitters. Progesterone appears to be one of the most active of the steroids, and its naturally produced metabolites and some synthetic analogs show activities that are different from the parent steroid. Other steroids, such as estrogens and adrenal steroids and their naturally produced and synthetic analogs, also show membrane effects. Bruce McEwen reviews evidence that synergistic interactions occur between non-genomic and genomic actions of steroids.
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                Author and article information

                Journal
                Journal of Neurochemistry
                Wiley
                00223042
                14714159
                May 1994
                June 28 2008
                : 62
                : 5
                : 1750-1756
                Article
                10.1046/j.1471-4159.1994.62051750.x
                8158125
                © 2008

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