Involvement of dopamine and opioids in the motivation to eat: influence of palatability, homeostatic state, and behavioral paradigms.

Rationale: Motivation for food depends on several variables including food palatability, the homeostatic state of the organism, and the nature of the behavior required to obtain the reward. However, few studies to date have tried to evaluate motivation for food considering all these variables at the same time. Since dopamine and opioids have been deeply involved in the regulation of feeding, it is of interest to investigate their role considering all the mentioned variables.

Selective estrogen receptor-alpha but not -beta agonist treatment modulates brain alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors.

Estradiol was previously reported to decrease brain alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA)-receptor-specific binding. The contributions of estrogen receptor subtypes in the estradiol modulation of AMPA receptors and its predominant subunit GluR2 are unknown. These experiments investigated whether an estrogenic receptor subtype is involved in the estradiol effect on AMPA-receptor-specific binding and GluR2 mRNA levels.

ERbeta mediates the estradiol increase of D2 receptors in rat striatum and nucleus accumbens.

Estradiol was previously reported to increase striatal D(2) receptor density. The following experiments investigated the contribution of each estrogen receptor in estradiol modulation of D(2) receptors. Ovariectomized Sprague-Dawley rats were treated for 2 weeks with an agonist for ERalpha, 4,4',4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT), an agonist for ERbeta, 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) and compared to estradiol treatment.

Changes in 5-HT1A receptor binding and G-protein activation in the rat brain after estrogen treatment: comparison with tamoxifen and raloxifene.

Objective: It is thought that an imbalance in serotonergic neurotransmission may underlie many affective disorders. Thus, the serotonin-1A (5-HT1A) receptor is a target for antidepressant and neuroleptic drugs. It has been reported that estrogens modulate serotonergic neurotransmission.

Chronic estrogenic drug treatment increases preproenkephalin mRNA levels in the rat striatum and nucleus accumbens.

Estrogens modulate the expression of preproenkephalin (PPE) in the hypothalamus but little is known for other brain regions. The present study investigated the effect of hormonal withdrawal and replacement therapy on PPE expression in the striatum, nucleus accumbens and cortex. Ovariectomized Sprague-Dawley rats were treated for 2 weeks with estradiol, a specific ligand for estrogen receptor alpha (ERalpha), 4,4',4''-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT) and estrogen receptor beta (ERbeta) 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), or the selective estrogen receptor modulators (SERMs) tamoxifen and raloxifene.

Evaluation of the protective effect of oestradiol against toxicity induced by 6-hydroxydopamine and 1-methyl-4-phenylpyridinium ion (Mpp+) towards dopaminergic mesencephalic neurones in primary culture.

Recent findings suggest that gonadal steroid hormones are neuroprotective and may provide clinical benefits in delaying the development of Parkinson's disease. In this report we investigated the ability of oestradiol to protect mesencephalic dopaminergic neurones cultured in serum-free or serum-supplemented medium from toxicity induced by 6-hydroxydopamine or 1-methyl-4-phenylpyridinium ion (MPP+). The efficiency of both toxins and oestradiol was evaluated by tyrosine hydroxylase (TH) immunocytochemistry, [3H]dopamine ([3H]DA) uptake, length of dopaminergic processes and lactate dehydrogenase (LDH) release measurement.