Anxiety-like behaviors and expression of SERT and TPH in the dorsal raphé of estrogen- and fluoxetine-treated ovariectomized rats

Charoenphandhu, Jantarima; Teerapornpuntakit, Jarinthorn; Nuntapornsak, Amporn; Krishnamra, Nateetip; Charoenphandhu, Narattaphol

doi:10.1016/j.pbb.2011.02.023

Cited by 40 publications

(29 citation statements)

References 55 publications

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“…Because all anxiety disorder subtypes are more frequent in females (30) and the anxiolytic effect of fluoxetine is often ineffective in postmenopausal females (52), there is a critical need for a mouse model for use in the study of anxiety in female humans. In light of the altered GABAergic system in the vmPFC and the resulting anxiety phenotype, our findings indicate that LXRβ −/− female mice may provide such a model.…”

Section: Discussionmentioning

confidence: 99%

Anxiety in liver X receptor β knockout female mice with loss of glutamic acid decarboxylase in ventromedial prefrontal cortex

Tan

Dai

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Anxiety disorders are the most prevalent mental disorders in adolescents in the United States. Female adolescents are more likely than males to be affected with anxiety disorders, but less likely to have behavioral and substance abuse disorders. The prefrontal cortex (PFC), amygdala, and dorsal raphe are known to be involved in anxiety disorders. Inhibitory input from the PFC to the amygdala controls fear and anxiety typically originating in the amygdala, and disruption of the inhibitory input from the PFC leads to anxiety, fear, and personality changes. Recent studies have implicated liver X receptor β (LXRβ) in key neurodevelopmental processes and neurodegenerative diseases. In the present study, we used elevated plus-maze, startle and prepulse inhibition, open field, and novel object recognition tests to evaluate behavior in female LXRβ KO (LXRβ −/− ) mice. We found that the female LXRβ −/− mice were anxious with impaired behavioral responses but normal locomotion and memory. Immunohistochemistry analysis revealed decreased expression of the enzyme responsible for GABA synthesis, glutamic acid decarboxylase (65+67), in the ventromedial PFC. Expression of tryptophan hydroxylase 2 in the dorsal raphe was normal. We conclude that the anxiogenic phenotype in female LXRβ −/− mice is caused by reduced GABAergic input from the ventromedial PFC to the amygdala.

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Section: Discussionmentioning

confidence: 99%

Anxiety in liver X receptor β knockout female mice with loss of glutamic acid decarboxylase in ventromedial prefrontal cortex

Tan

Dai

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…We speculated that BPA induced the potential emotional alterations as an 'anxiolytic effect', especially for the female rats at this apparatus. From several adult rat experiments, it is a well-known fact that estrogen is strongly related to the anxiety level (Charoenphandhu et al, 2011;Olivera-Lopez et al, 2008). Further studies are needed to investigate the 'estrogen-like effect' of BPA on female rats.…”

Section: Discussionmentioning

confidence: 99%

Postnatal exposure to low-dose bisphenol A influences various emotional conditions

et al. 2013

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-Bisphenol A (BPA) is one of the 'environmental endocrine disrupters' (EEDs) released by plastics and resin known to interfere with hormonal responses. In this study, female Wistar rats were exposed to low-dose BPA (24 μg/kg/day) during 7 days after giving birth. The male and female offspring, exposed to the BPA through lactation, were evaluated using an open field test (OFT) at the age of six weeks, an elevated plus maze test (EPM) at seven weeks, and a forced swimming test (FST) at nine weeks. The OFT indicated that females were more active than males, and that BPA selectively increased rearing duration in males, thereby eliminating the gender effect. The results of EPM showed that BPA did not enhance the anxiety-like action; rather, it was associated with an anxiolytic-like action in females. In the FST, not only there was an increase in the immobility time, but also there was reduction of latency observed in BPA rats. It indicated that the depression-like responses were clearly enhanced by the postnatal exposure. Altogether, these data suggest that low-dose BPA ingested by neonates through breastfeeding may cause persistent aberrant behaviors that are relevant to emotions.

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“…In studies of acute estradiol exposure in rats, SERT proteins were shown to be upregulated in both the raphe nuclei and the hypothalamus [39,40] . In contrast, chronic estradiol administration in macaques was associated with decreased levels of SERT in the raphe nuclei [41] and increased SERT activity in the basal ganglia and hypothalamic nuclei in several animal studies [30,42] . Yet still, other studies found that treatment with estradiol in OVX macaques either increased or did not change SERT binding in various brain regions, and did not change SERT binding in rats [43] .…”

Section: Estradiol and Serotoninmentioning

confidence: 94%

Effect of Gonadal Hormones on Neurotransmitters Implicated in the Pathophysiology of Obsessive-Compulsive Disorder: A Critical Review

Karpinski

Mattina

Steiner³

2016

Neuroendocrinology

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Obsessive-compulsive disorder (OCD) is a relatively common neuropsychiatric disorder affecting between 1.6 and 3.2% of the population. A number of studies have previously reported increased incidence of OCD, or exacerbation of preexisting symptoms in females during reproductive events. Since these periods are known to involve fluctuating levels of gonadal hormones, these steroids have been suggested to be involved in modulating the course of the disorder. However, to date, only a few studies have measured hormone levels and obsessive-compulsive (OC) symptoms concurrently; thus, direct evidence for this relationship is limited. In turn, investigations into neurotransmission in OC individuals have been more extensive, and have implicated the serotonergic, dopaminergic, and glutamatergic neurotransmitter systems in OCD pathology. There is evidence suggesting that reproductive hormones estrogens and progesterone can modulate neurotransmission in the aforementioned signaling pathways by regulating the expression of receptors and channels, as well as the synthesis and release of the neurotransmitter itself. Overall, estrogen and progesterone appear to enhance serotonin signaling, which has been associated with improved OC symptoms. The effect of the gonadal hormones in dopaminergic and glutamatergic signaling is much more variable, highlighting the need for further research in this field. The existing evidence shows that gonadal hormones can have profound impacts on neurotransmission in the brain, leading to the conclusion that the hormonal fluctuations during reproductive events are a plausible factor contributing to the change in OCD course during these times.

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Anxiety-like behaviors and expression of SERT and TPH in the dorsal raphé of estrogen- and fluoxetine-treated ovariectomized rats

Cited by 40 publications

References 55 publications

Anxiety in liver X receptor β knockout female mice with loss of glutamic acid decarboxylase in ventromedial prefrontal cortex

Anxiety in liver X receptor β knockout female mice with loss of glutamic acid decarboxylase in ventromedial prefrontal cortex

Postnatal exposure to low-dose bisphenol A influences various emotional conditions

Effect of Gonadal Hormones on Neurotransmitters Implicated in the Pathophysiology of Obsessive-Compulsive Disorder: A Critical Review

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