Effect of estradiol and progesterone on rat dopamine uptake sites
ABSTRACT Striatal dopamine (DA) uptake sites labelled with [3H]GBR-12935 binding were investigated in ovariectomized (OVX) rats acutely treated with 17 beta-estradiol (E2) or progesterone (P). One injection of E2 (100 ng, SC) to OVX rats increased plasma levels of this steroid after 15 min while plasma prolactin (PRL) levels remained unchanged. The E2 injection left striatal [3H]GBR-12935 binding affinity unchanged while the maximum density increased 15 and 30 min after the injection (+24% and +18%, respectively). One injection of P (110 micrograms, SC) to OVX rats increased this steroid plasma level from 15 to 120 min while plasma PRL levels remained unchanged. [3H]GBR-12935 binding density and affinity remained unchanged up to 120 min after the injection. Thus, acutely, E2 but not P, modulated striatal DA uptake sites in OVX rats. The effect of E2 appeared in coincidence with the peak of this steroid plasma concentration. This increase was rapid and is probably nongenomic and suggests a causal effect relationship as well as a presynaptic site of action of E2.
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- "  ) but numerous studies have also identified mechanisms through which E 2 can rapidly alter these systems. For instance, estradiol rapidly increases the activity of tyrosine hydroxylase, the enzyme that constitutes the limiting step in the synthesis of catecholamines , the DA turnover , the number of DA re-uptake sites  and the DA release as measured by in vivo microdialysis  and in vivo voltammettry . Within similarly short latencies, E 2 also uncouples and down-regulates dopamine D2 receptors . "
ABSTRACT: Steroids are generally viewed as transcription factors binding to intracellular receptors and activating gene transcription. Rapid cellular effects mediated via non-genomic mechanisms have however been identified and one report showed that injections of estradiol rapidly stimulate chemoinvestigation and mounting behavior in castrated male rats. It is not known whether such effects take place in other species and what are the cellular underlying mechanisms. We show here that a single injection of estradiol (500 microg/kg) rapidly and transiently activates copulatory behavior in castrated male quail pre-treated with a dose of testosterone behaviorally ineffective by itself. The maximal behavioral effect was observed after 15 min. In a second experiment, the brain of all subjects was immediately collected after behavioral tests performed 15 min after injection. The preoptic area--hypothalamus (HPOA), hindbrain, telencephalon and cerebellum were isolated and monoamines measured by HPLC-ED. Estradiol increased levels of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and 5-HIAA/serotonin ratios in the telencephalon and hindbrain independently of whether animals had mated or not. Estradiol also affected these measures in HPOA and cerebellum but this effect was correlated with the level of sexual activity so that significant effects of the treatment only appeared when sexual activity was used as a covariate. Interactions between estradiol effects and sexual activity were also observed for dopamine in the HPOA and for serotonin in the hindbrain and cerebellum. Together, these data demonstrate that a single estradiol injection rapidly activates male sexual behavior in quail and that this behavioral effect is correlated with changes in monoaminergic activity.Behavioural Brain Research 02/2006; 166(1):110-23. DOI:10.1016/j.bbr.2005.07.017 · 3.39 Impact Factor
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ABSTRACT: Sex steroid hormones influence the dopaminergic systems of the hypothalamus as well as the extrahypothalamic regions of the brain in controlling movement and behavior in both humans and animals. This review focuses on the effects of sex steroids on dopaminergic activity in extrahypothalamic brain areas. Among sex steroids, estrogens have been most extensively investigated, and many studies report that estrogens affect behaviors mediated by the basal ganglia, such as in humans suffering from extrapyramidal disorders. Epidemiological and clinical evidence also suggests an influence of estrogens on the vulnerability threshold for schizophrenia and sex differences in the clinical expression of this disease. Clinical observations point to a role of androgenic hormones in Gilles de la Tourette's syndrome. In normal humans, sex steroids were also shown to influence motor and cognitive performance. Biochemical and behavioral studies in animals have also shown the effect of sex steroids on dopaminergic activity in the basal ganglia; however, both activating and inhibiting effects have been reported. This may partly be explained by effects of the dose, duration of treatment, interval between steroid administration and testing the behavior measured, and the part of the basal ganglia from which the behavior is elicited. In view of the numerous variables that influence net dopaminergic response to steroids, focus will be on the literature using similar experimental conditions to assess the effect of in vivo chronic steroid treatment, acute short-term steroid treatment and the estrous cycle as well as in vitro effects of steroids on dopamine receptors. These experimental paradigms point to two general mechanisms of action of steroids: a rapid short-term non-genomic membrane effect and a slower long-term possibly genomic effect of steroids on dopamine systems. Combining dopaminergic drugs with sex steroids could improve efficacy or reduce side effects associated with these drugs. Examples of such combined treatments in rats and monkeys are presented for delta 9-tetrahydrocannabinol, cocaine, neuroleptics, apomorphine and L-DOPA. A better understanding of steroid-dopamine interactions and the possible isolation of conditions to have only pro or anti dopaminergic activity could then be used to develop combined therapies or to optimize drug treatments that would take into account the patient's sex and endocrine status.Reviews in the neurosciences 01/1994; 5(1):27-41. DOI:10.1515/REVNEURO.19184.108.40.206 · 3.31 Impact Factor
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ABSTRACT: Aging differentially affects receptor function. In the present electrophysiological study we compared neuronal responsiveness to locally applied dopamine D1 and D2 receptor agonist in the striatum of female Fischer 344 rats aged 3 and 26-27 months. In a subgroup of the old rats, the nigrostriatal dopamine bundle was destroyed unilaterally with 6-hydroxydopamine (6-OHDA) to assess receptor plasticity in response to denervation. Spontaneous firing rate of striatal neurons was higher in aged compared to young rats. Higher doses of the D1 agonist SKF 38393 or the D2 agonist quinpirole were required to elicit a 50% change in firing rate in aged compared to young rats. No difference with SKF 38393 or quinpirole was detected between 6-OHDA denervated and control (nonlesioned) striatum in aged rats. Supersensitivity to D2 agonists has been reported following 6-OHDA lesions in young rats. These observations suggest that D2 receptors in aged rat striatum might not be as plastic as in younger rats.Neurobiology of Aging 17(6):877-83. · 4.85 Impact Factor