Competition by monophenolic estrogens and catecholestrogens for high-affinity uptake of [3H](−)-norepinephrine into synaptosomes from rat cerebral cortex and hypothalamus

Participation of the 5-HT1A Receptor in the Antidepressant-Like Effect of Estrogens in the Forced Swimming Test

“…In this point, it is important to mention that the behavioral profile induced by EE 2 alone was similar to that produced by mixed reuptake inhibitors that act at both the noradrenergic and serotonergic systems, such as venlafaxine and duloxetine in the FST, that is, these compounds produce a decrease in immobility with a concomitant increase in both swimming and climbing behaviors (Rénéric and Lucki, 1998). Furthermore, in vitro studies have shown that EE 2 inhibits both serotonin and noradrenaline transporters with a similar potency (Michel et al, 1987;Ghraf et al, 1983). At present, data on the mechanism of action of EE 2 on neurotransmitter systems are derived only from in vitro studies and there are no data from behavioral studies.…”

“…An important difference between these two estrogens is that the natural estrogen E 2 is more potent at the serotonergic than at the noradrenergic system in decreasing re-uptake sites (Ghraf et al, 1983;Michel et al, 1987), while the synthetic steroidal compound EE 2 inhibits with a comparable efficacy the serotonergic and catecholaminergic sites (Ghraf et al, 1983;Michel et al, 1987). Both estrogens have been used in clinical practice as contraceptive and/or hormonal restitution therapies (Soares et al, 2001).…”

Antidepressant-Like Effect of Different Estrogenic Compounds in the Forced Swimming Test

“…On the other hand, in vitro studies demonstrate that estrogens can interact, at several levels, with the dopaminergic, the noradrenergic, and the serotonergic systems (Attali et al, 1997;Bethea et al, 1998;Biegon et al, 1983;Cyr et al, 2000;McEwen, 1999;Rubinow et al, 1998). For example, estrogens can inhibit the function of the monoaminergic transporter (Ghraf et al, 1983;Michel et al, 1987;Wilson et al, 1988) and interact with either 5-HT 1A , 5-HT 2A , or b-adrenergic receptors in several brain areas (Biegon et al, 1983;Fink et al, 1996;Kendall et al, 1982;Mize and Alper, 2000;Ö sterlund et al, 1999;Raap et al, 2000;Sumner and Fink, 1995). Interestingly, estrogenic compounds modify those neurotransmitter systems that are targets of antidepressant treatments.…”

“…It is important to mention that the estrogenic activity on each of these systems varies depending on the estrogen nature (Chang and Chang, 1999;Ghraf et al, 1983;Michel et al, 1987). Thus, the natural estrogen E 2 decreases both serotonin and noradrenaline reuptake sites, being more potent at the serotonergic than at the noradrenergic system (Ghraf et al, 1983;Michel et al, 1987).…”

Participation of the Monoaminergic System in the Antidepressant-Like Actions of Estrogens: A Review in Preclinical Studies

“…Several studies reported that estrogenic compounds can influence noradrenergic neurotransmission through an interaction with the noradrenergic transporter and the MAO or tyrosine hydroxylase enzymes. For example, in vitro studies have shown that E2, EE2, DES and some catechol-estrogens such as 2-hydroxy-EE2 (2-OH-EE2) and 2-hydroxy-E1 (2-OHE) inhibit NA reuptake sites in synaptosomes from the cerebral cortex and hypothalamus of rats that resulted in increased levels of NA in the synaptic cleft (Ghraf et al, 1983). In line with these findings, acute E2 administration to ovariectomized rats decreased NA reuptake rate in the hypothalamus (Hiemke et al, 1985) and increases mRNA levels of tyrosine hydroxylase in the locus coeruleus (Serova et al, 2002).…”