Estradiol potentiates inhibitory synaptic transmission in the oval bed nucleus of the striaterminalis of male and female rats

Gregory, James Gardner; Hawken, Emily R.; Angelis, Staci; Bouchard, Jean‐François; Dumont, Éric C.

doi:10.1016/j.psyneuen.2019.03.030

Cited by 10 publications

(4 citation statements)

References 53 publications

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“…The labeling of GPER1 in presynaptic sites in the PVN is consistent with evidence showing that GPER1 agonists can influence serotonin release in the PVN (Xu et al, 2009) and suggests an important role for GPER1 in modulating presynaptic neurotransmitter efflux. In addition, the presence of GPER1 in dendrites is also consistent with the ability of GPER1 agonists to modulate postsynaptic inhibitory transmission (Gregory et al, 2019) and the structure of excitatory synapses (Waters et al, 2015) in various brain areas.…”

Section: Discussionsupporting

confidence: 64%

Sex and age influence gonadal steroid hormone receptor distributions relative to estrogen receptor β‐containing neurons in the mouse hypothalamic paraventricular nucleus

Contoreggi

Mazid

Goldstein

et al. 2021

J of Comparative Neurology

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Within the hypothalamic paraventricular nucleus (PVN), estrogen receptor (ER) β and other gonadal hormone receptors play a role in central cardiovascular processes. However, the influence of sex and age on the cellular and subcellular relationships of ERβ with ERα, G‐protein ER (GPER1), as well as progestin and androgen receptors (PR and AR) in the PVN is uncertain. In young (2‐ to 3‐month‐old) females and males, ERβ‐enhanced green fluorescent protein (EGFP) containing neurons were approximately four times greater than ERα‐labeled and PR‐labeled nuclei in the PVN. In subdivisions of the PVN, young females, compared to males, had: (1) more ERβ‐EGFP neurons in neuroendocrine rostral regions; (2) fewer ERα‐labeled nuclei in neuroendocrine and autonomic projecting medial subregions; and (3) more ERα‐labeled nuclei in an autonomic projecting caudal region. In contrast, young males, compared to females, had approximately 20 times more AR‐labeled nuclei, which often colocalized with ERβ‐EGFP in neuroendocrine (approximately 70%) and autonomic (approximately 50%) projecting subregions. Ultrastructurally, in soma and dendrites, PVN ERβ‐EGFP colocalized primarily with extranuclear AR (approximately 85% soma) and GPER1 (approximately 70% soma). Aged (12‐ to 24‐month‐old) males had more ERβ‐EGFP neurons in a rostral neuroendocrine subregion compared to aged females and females with accelerated ovarian failure (AOF) and in a caudal autonomic subregion compared to post‐AOF females. Late‐aged (18‐ to 24‐month‐old) females compared to early‐aged (12‐ to 14‐month‐old) females and AOF females had fewer AR‐labeled nuclei in neuroendrocrine and autonomic projecting subregions. These findings indicate that gonadal steroids may directly and indirectly influence PVN neurons via nuclear and extranuclear gonadal hormone receptors in a sex‐specific manner.

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Section: Discussionsupporting

confidence: 64%

Sex and age influence gonadal steroid hormone receptor distributions relative to estrogen receptor β‐containing neurons in the mouse hypothalamic paraventricular nucleus

Contoreggi

Mazid

Goldstein

et al. 2021

J of Comparative Neurology

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“…128 Studies have revealed that GPER is also expressed in the BNST, amygdala and hippocampus. 129,130 Testosterone's effects on the AVP and OT systems may be mediated directly via its biding at the AR or by ERs after its conversion into 17β-estradiol by the enzyme aromatase (Figure 3). Both AR and ER mechanisms may be at play, as supported by the fact that AVP gene expression in the PVN increases after treatment with 17βestradiol and testosterone in ovariectomized rats.…”

Section: S E X Hormone Modul Ation Of Social Recog Nitionmentioning

confidence: 99%

“…GPER has been found in both the PVN and the SON of male and female rats, where it co‐localizes with both OT and AVP neurons 128 . Studies have revealed that GPER is also expressed in the BNST, amygdala and hippocampus 129,130 …”

Section: Sex Hormone Modulation Of Social Recognitionmentioning

confidence: 99%

Neuroendocrine underpinning of social recognition in males and females

Aspesi

Choleris

2021

J Neuroendocrinology

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Social recognition is an essential skill for the expression of appropriate behaviors towards conspecifics in most social species. Several studies point to oxytocin (OT) and arginine vasopressin (AVP) as key mediators of social recognition in males and females. However, sex differences in social cognitive behaviors highlight an important interplay between OT, AVP and the sex steroids. Estrogens facilitate social recognition by regulating OT action in the hypothalamus and that of OT receptor in the medial amygdala. The role of OT in these brain regions appears to be essential for social recognition in both males and females. Conversely, social recognition in male rats and mice is more dependent on AVP release in the lateral septum than in females. The AVP system comprises a series of highly sexually dimorphic brain nuclei, including the bed nucleus of the stria terminalis, the amygdala and the lateral septum. Various studies suggest that testosterone and its metabolites, including estradiol, influence social recognition in males by modulating the activity of the AVP at V1a receptor. Intriguingly, both estrogens and androgens can affect social recognition very rapidly, through non‐genomic mechanisms. In addition, the androgen metabolites, namely 3α‐diol and 3β‐diol, may also have an impact on social behaviors either by interacting with the estrogen receptors or through other mechanisms. Overall, the regulation of OT and AVP by sex steroids fine tunes social recognition and the behaviors that depend upon it (e.g., social bond, hierarchical organization, aggression) in a sex‐dependent manner. Elucidating the sex‐dependent interaction between sex steroids and neuroendocrine systems is essential for understanding sex differences in the normal and abnormal expression of social behaviors.

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“…Deep brain stimulation of the BNST has yielded sustained symptom relief in obsessions and compulsions in otherwise refractory OCD (Nuttin et al, 1999, 2013; Raymaekers et al, 2017; Winter et al, 2018). A collection of several sexually dimorphic interconnected nuclei, the BNST is part of the extended amygdala with extensive bi-directional connectivity with the CLSTC-loop and beyond (Prewitt and Herman, 1998; McDonald et al, 1999; Dong et al, 2001; Hasue and Shammah-Lagnado, 2002; Dong and Swanson, 2003, 2004b, 2006a,b,c; Rodaros et al, 2007; Li and Kirouac, 2008; Avery et al, 2014; Gregory et al, 2019). Functionally, the BNST filters and/or integrates multiple ascending modalities, mapping with adequate resolution, interoceptive information onto motivational systems for adaptive physiological and behavioral outcomes (Jennings et al, 2013; Kim et al, 2013; Lebow and Chen, 2016).…”

Section: The Bed Nucleus Of the Stria Terminalis (Bnst) In Homeostatimentioning

confidence: 99%

The Bed Nucleus of the Stria Terminalis, Homeostatic Satiety, and Compulsions: What Can We Learn From Polydipsia?

Banasikowski

Hawken

2019

Front. Behav. Neurosci.

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A compulsive phenotype characterizes several neuropsychiatric illnesses – including but not limited to – schizophrenia and obsessive compulsive disorder. Because of its perceived etiological heterogeneity, it is challenging to disentangle the specific neurophysiology that precipitates compulsive behaving. Using polydipsia (or non-regulatory water drinking), we describe candidate neural substrates of compulsivity. We further postulate that aberrant neuroplasticity within cortically projecting structures [i.e., the bed nucleus of the stria terminalis (BNST)] and circuits that encode homeostatic emotions (thirst, hunger, satiety, etc.) underlie compulsive drinking. By transducing an inaccurate signal that fails to represent true homeostatic state, cortical structures cannot select appropriate and adaptive actions. Additionally, augmented dopamine (DA) reactivity in striatal projections to and from the frontal cortex contribute to aberrant homeostatic signal propagation that ultimately biases cortex-dependent behavioral selection. Responding becomes rigid and corresponds with both erroneous, inflexible encoding in both bottom-up structures and in top-down pathways. How aberrant neuroplasticity in circuits that encode homeostatic emotion result in the genesis and maintenance of compulsive behaviors needs further investigation.

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Estradiol potentiates inhibitory synaptic transmission in the oval bed nucleus of the striaterminalis of male and female rats

Cited by 10 publications

References 53 publications

Sex and age influence gonadal steroid hormone receptor distributions relative to estrogen receptor β‐containing neurons in the mouse hypothalamic paraventricular nucleus

Sex and age influence gonadal steroid hormone receptor distributions relative to estrogen receptor β‐containing neurons in the mouse hypothalamic paraventricular nucleus

Neuroendocrine underpinning of social recognition in males and females

The Bed Nucleus of the Stria Terminalis, Homeostatic Satiety, and Compulsions: What Can We Learn From Polydipsia?

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