Ovarian steroids and serotonin neural function

Bethea, Cynthia L.; Pecins‐Thompson, Melanie; Schutzer, William E.; Gundlah, Chrisana; Lü, Zhe

doi:10.1007/bf02914268

Cited by 167 publications

(93 citation statements)

References 239 publications

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“…Estrogen has also been shown to increase the density of 5HT2A receptors in brain regions associated with mood (Fifa and Fillion, 1992). Taken together, these findings suggest that estrogen can facilitate serotonergic transmission by enhancing serotonin synthesis and/or decreasing serotonin reuptake thereby alleviating depressive symptoms (Bethea et al, 1999). Consistent with this, clinical studies have demonstrated estrogen treatment to have antidepressant effects when administered alone (Klaiber et al, 1996) or in combination with serotonergic antidepressants (Halbreich et al, 1995).…”

Section: Interactions Between Serotonin and Ovarian Hormonesmentioning

confidence: 68%

“…Serotonergic neurons in the raphe of the rhesus macaque have also been found to contain estrogen inducible progestin receptors thus providing a direct target for the regulation of serotonergic function by ovarian hormones (Bethea, 1993). Ovarian hormones have also been shown to affect numerous factors regulating serotonin synthesis and serotonin levels in the central nervous system (see Bethea et al, 1999 for review). For example, ovarian hormones promote the induction of tryptophan hydroxylase, the rate-limiting enzyme in the synthesis of serotonin, and reduce serotonin reuptake transporter (SERT) mRNA expression in the raphe nuclei.…”

Section: Interactions Between Serotonin and Ovarian Hormonesmentioning

confidence: 99%

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Estrogen-mediated effects on depression and memory formation in females

Shors

Leuner

2003

Journal of Affective Disorders

158

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Women are twice as likely to suffer from depression as men. It has been proposed that the ovarian hormones estrogen and progesterone contribute to the higher incidence of this potentially debilitating disorder. Depression can also be accompanied by a loss of cognitive performance. Here we review estrogen-mediated effects on depression and memory formation in females. We propose that changes in levels of estrogen are associated with sex differences in learning as well as changes in affect prior to menses, immediately after pregnancy and during perimenopause and the menopausal transition. Finally, we discuss the animal model of depression known as 'learned helplessness' and describe research from our laboratory demonstrating that exposure to an acute stressful experience compromises a female's later ability to acquire certain types of new memories. This response to stressful experience is opposite to that observed in males and is dependent on the presence of estrogen, and more specifically-changing levels of estrogen. This observation indicates that females and males can use different hormonal and neural mechanisms to respond to the same emotional event and underscore the importance of studying the unique and changing biology of females, especially when considering treatment strategies for depression and stress-related illness.

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Section: Interactions Between Serotonin and Ovarian Hormonesmentioning

confidence: 68%

Section: Interactions Between Serotonin and Ovarian Hormonesmentioning

confidence: 99%

Estrogen-mediated effects on depression and memory formation in females

Shors

Leuner

2003

Journal of Affective Disorders

158

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“…Serotonergic function is influenced by sex hormones, 26,27 and serotonin system biological variations by gender have been reported. 28 Mice pups prenatally exposed to agents that can alter serotonergic function, including an SSRI, 29,30 showed permanent sex-specific changes in behavior.…”

Section: Discussionmentioning

confidence: 99%

Prenatal SSRI Use and Offspring With Autism Spectrum Disorder or Developmental Delay

et al. 2014

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WHAT'S KNOWN ON THIS SUBJECT: Serotonin is critical in early brain development, creating concerns regarding prenatal exposure to factors influencing serotonin levels, like selective serotonin reuptake inhibitors (SSRIs). Prenatal SSRI use was recently associated with autism; however, its association with other developmental delays is unclear. WHAT THIS STUDY ADDS:This population-based case-control study in young children provides evidence that prenatal SSRI use may be a risk factor for autism and other developmental delays. However, underlying depression and its genetic underpinnings may be a confounder.abstract OBJECTIVE: To examine associations between prenatal use of selective serotonin reuptake inhibitors (SSRIs) and the odds of autism spectrum disorders (ASDs) and other developmental delays (DDs).METHODS: A total of 966 mother-child pairs were evaluated (492 ASD, 154 DD, 320 typical development [TD]) from the Childhood Autism Risks from Genetics and the Environment (CHARGE) Study, a populationbased case-control study. Standardized measures confirmed developmental status. Interviews with biological mothers ascertained prenatal SSRI use, maternal mental health history, and sociodemographic information. RESULTS:Overall, prevalence of prenatal SSRI exposure was lowest in TD children (3.4%) but did not differ significantly from ASD (5.9%) or DD (5.2%) children. Among boys, prenatal SSRI exposure was nearly 3 times as likely in children with ASD relative to TD (adjusted odds ratio [OR]: 2.91; 95% confidence interval [CI]: 1.07-7.93); the strongest association occurred with first-trimester exposure (OR: 3.22; 95% CI: 1.17-8.84). Exposure was also elevated among boys with DD (OR: 3.39; 95% CI: 0.98-11.75) and was strongest in the third trimester (OR: 4.98; 95% CI: 1.20-20.62). Findings were similar among mothers with an anxiety or mood disorder history. CONCLUSIONS:In boys, prenatal exposure to SSRIs may increase susceptibility to ASD or DD. Findings from published studies on SSRIs and ASD continues to be inconsistent. Potential recall bias and residual confounding by indication are concerns. Larger samples are needed to replicate DD results. Because maternal depression itself carries risks for the fetus, the benefits of prenatal SSRI use should be carefully weighed against potential harms.

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“…Therefore, it can be concluded that the 5-HT 1A receptor subtype is a mediator of the antidepressant-like action of E 2 . Evidences in favor of this hypothesis are the results derived from in vitro and in vivo studies, showing that the 5-HT 1A receptor subtype is a target of estrogens and some estrogen-like compounds (Bethea et al, 1998;Biegon et al, 1983;Mize and Alper, 2000;Mize et al, 2001;Raap et al, 2000;Uphouse, 2000). Indeed, Lu and Bethea (2002) demonstrated that E 2 induces the desensitization of 5-HT 1A receptors in the DRN of monkeys.…”

Section: Discussionmentioning

confidence: 99%

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

Estrada‐Camarena

Fernández‐Guasti

López‐Rubalcava

2005

Neuropsychopharmacol

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The aim of the present study was to explore the possible participation of the 5-HT 1A receptor in the antidepressant-like action of two estrogenic compounds: 17b-estradiol (E 2 ) and ethynil-estradiol (EE 2 ) in the FST. Ovariectomized female Wistar rats were used in all experiments. As a positive control, the effect of the 5-HT 1A receptor agonist, 8-hydroxy-2-(di-n)-propil-aminotetraline (8-OH-DPAT; 0.0625, 0.125, 0.25 and 0.5 mg/kg) alone or in combination with WAY 100635 (0.5 and 1.0 mg/kg) was analyzed in the FST. In order to analyze the participation of the 5-HT 1A receptor in the antidepressant-like actions of estrogens, the effect of the selective antagonist WAY 100635 (0.5 and 1.0 mg/kg) in combination with E 2 (10 mg/rat) and EE 2 (5 mg/rat) was studied in the FST. In this case, WAY 100635 was administered either simultaneously with the estrogens (48 h before the FST test) or 30 min before the FST. On the other hand, a suboptimal dose of 8-OH-DPAT (0.0625 mg/kg), combined with a noneffective dose of E 2 (2.5 mg/rat) or EE 2 (1.25 mg/rat), was tested in the FST. The results showed that 8-OH-DPAT (0.25 and 0.5 mg/kg), E 2 (10 mg/rat), and EE 2 (5 mg/rat), by themselves, exerted an antidepressant-like action. The antagonist to the 5-HT 1A receptor WAY 100635, when applied together with 8-OH-DPAT or E 2 , blocked their antidepressant-like actions, but not the one induced by EE 2 . Interestingly, when the antagonist was applied 30 min before the FST, it was able to cancel the actions of EE 2 on immobility behavior, and had no effect on the actions of E 2. Finally, when a subthreshold dose of 8-OH-DPAT was combined with a noneffective dose of either E 2 or EE 2 , an antidepressant-like action was observed. The results support the notion that the 5-HT 1A receptor is one of the mediators of the antidepressant-like action of E 2 , and could indirectly contribute to the one induced by EE 2 .

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Ovarian steroids and serotonin neural function

Cited by 167 publications

References 239 publications

Estrogen-mediated effects on depression and memory formation in females

Estrogen-mediated effects on depression and memory formation in females

Prenatal SSRI Use and Offspring With Autism Spectrum Disorder or Developmental Delay

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

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