Attenuation of estradiol on the reduction of striatal dopamine by amphetamine in ovariectomized rats

Abstract

Amphetamine (AMPH) is a highly addictive drug of abuse which exhibits toxicity to dopaminergic neurons in long-term abusers. Estrogen seems to show neuroprotection in dopamine (DA) deficit caused by AMPH. The present study was to investigate the effects of estradiol on the levels of striatal DA in ovariectomized (Ovx) rats treated with or without AMPH. Female rats were Ovx for 2 weeks before administration of AMPH (5 mg/kg/day, i.p.) with or without 17beta-estradiol benzoate (EB) (25 microg/kg/day, s.c.) for 7 days. The striatal tissues were collected, homogenized with DA mobile phase, and centrifuged. The concentrations of DA in the supernatants were detected by HPLC. The protein expressions of dopamine transporter (DAT), vesicular monoamine transporter 2 (VMAT-2), and tyrosine hydroxylase (TH) were analyzed by Western blotting. The results indicated that AMPH could attenuate DA level significantly in striatum (P < 0.01). Comparing to control groups, administration of either EB or EB plus AMPH increased DA level (P < 0.01). The protein expression of striatal DAT was significant greater (P < 0.01) in rats treated with AMPH plus EB than AMPH treated animals. These results suggest that the DA levels in striatum can be enhanced by EB via an increase of DAT expression following administration of AMPH.

DiOlistic Labeling of Neurons in Tissue Slices: A Qualitative and Quantitative Analysis of Methodological Variations

“…DiI labeling of tissues fixed with 4% paraformaldehyde resulted in diffuse, indiscriminate labeling and extremely high background, regardless of whether the tissue section was 150 or 300 μm thick. Based on our experience, we are surprised that fixation with 4% paraformaldehyde prior to labeling with DiI has been reported successfully by other groups (Gan et al, 2000; Moolman et al, 2004; Oberheim et al, 2008; Yu et al, 2009; Cui et al, 2010; Li et al, 2010). We can imagine that different combinations of aldehyde concentration and fixation durations could produce acceptable results.…”

Sex-Dependent Antipsychotic Capacity of 17β-Estradiol in the Latent Inhibition Model: A Typical Antipsychotic Drug in Both Sexes, Atypical Antipsychotic Drug in Males

“…Both reduction and increase of striatal dopaminergic function by 17b-estradiol have been reported for all indices of dopaminergic activity, including receptor levels/binding, membrane Sex-dependent antipsychotic capacity of 17b-estradiol M Arad and I Weiner dopamine transporter levels, and release, depending on dose and treatment paradigm (Arvin et al, 2000;Becker, 1999;Chavez et al, 2010;Di Paolo, 1994;Disshon et al, 1998;Dluzen and Horstink, 2003;McDermott, 1993;Morissette et al, 2008;Morissette and Di Paolo, 1993;Peris et al, 1991;Shieh and Yang, 2008;Thompson and Moss, 1994;Yu et al, 2009;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 levels of estrogen (Barber et al, 1976;Becker, 1999;Bedard et al, 1977;Chavez et al, 2010;Cyr et al, 2002;Di Paolo, 1994;Di Paolo et al, 1981;Hruska and Silbergeld, 1980;McEwen and Alves, 1999;Riddoch et al, 1971;Yu et al, 2009). Although the specific mechanisms by which 17b-estradiol exerts its dose-dependent effects on LI observed here remain to be elucidated, if both effects are indeed DA-mediated, this would imply that low 17b-estradiol doses exert a propsychotic action.…”

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

“…The rats were divided into 7 different groups (n = 10). Group 1: Control sham-operated male rats (underwent all surgical procedures without I/R in normal rats); group 2: male rats with bilateral renal I/R; ischemia was produced for 50 min, followed by 48 h reperfusion; group 3: control sham-operated female rats (underwent all surgical procedures without I/R or ovariectomy); group 4: female rats with bilateral ovariectomy (Ovx); group 5: female rats with bilateral renal I/R (I/R); ischemia was produced for 50 min, followed by 48 h reperfusion; group 6: female rats with bilateral renal I/R done 4 weeks after bilateral ovariectomy (Ovx+I/R); group 7: female rats with bilateral renal I/R done 4 weeks after bilateral ovariectomy treated with estrogen supplementation (25 μg/kg/day; SC) for 3 weeks starting 1 week after the ovariectomy (Ovx+E+I/R) (Yu et al 2009) …”