Rapid effects of estrogens on short-term memory: Possible mechanisms

Paletta, Pietro; Sheppard, Paul A. S.; Matta, Richard; Ervin, Kelsy S.J.; Choleris, Elena

doi:10.1016/j.yhbeh.2018.05.019

Cited by 53 publications

(46 citation statements)

References 113 publications

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“…For examples, intracerebroventricular infusion of the GPER agonist G-1 rapidly facilitates the female sexual behavior in estradiol-primed rats (Long et al, 2014(Long et al, , 2017. Activation of GPER in the dorsal hippocampus enhances social and object recognition and memory in the rat within 40 min (Paletta et al, 2018). In spinal cord slice in vitro, G-1 directly depolarizes superficial dorsal horn neurons; in vivo, intrathecal application of G-1 results in pain-related behaviors characterized by caudally directed scratching, biting and licking (Deliu et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…Revankar et al (2005) expressed GPER as a fusion protein with green fluorescent protein (GFP) in COS7 cell (monkey kidney fibroblast) and found that activation of GPER resulted in intracellular Ca 2+ mobilization and synthesis of phosphatidylinositol 3,4,5trisphosphate in the nucleus. Incidentally, GPER is enriched in the hypothalamic-pituitary axis and the hippocampal formation (Paletta et al, 2018), where E2 has been reported to elicit cytosolic Ca 2+ changes. Nevertheless, whether GPER mediates rapid Ca 2+ signaling in neuronal cells is still uncertain.…”

Section: Introductionmentioning

confidence: 99%

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Activation of the G Protein-Coupled Estrogen Receptor Elicits Store Calcium Release and Phosphorylation of the Mu-Opioid Receptors in the Human Neuroblastoma SH-SY5Y Cells

et al. 2019

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Estrogens exert extensive influences on the nervous system besides their well-known roles in regulation of reproduction and metabolism. Estrogens act via the nuclear receptor ERα and ERβ to regulate gene transcription (classical genomic effects). In addition, estrogens are also known to cause rapid non-genomic effects on neuronal functions including inducing fast changes in cytosolic calcium level and rapidly desensitizing the µ type opioid receptor (MOR). The receptors responsible for the rapid actions of estrogens remain uncertain, but recent evidence points to the G proteincoupled estrogen receptor (GPER), which has been shown to be expressed widely in the nervous system. In the current study, we test the hypothesis that activation of GPER may mediate rapid calcium signaling, which may promote phosphorylation of MOR through the calcium-dependent protein kinases in neuronal cells. By qPCR and immunocytochemistry, we found that the human neuroblastoma SH-SY5Y cells endogenously express GPER and MOR. Activation of GPER by 17β-estradiol (E2) and G-1 (GPER selective agonist) evoked a rapid calcium rise in a concentrationdependent manner, which was due to store release rather than calcium entry. The GPER antagonist G15, the PLC inhibitor U73122 and the IP3 receptor inhibitor 2-APB each virtually abolished the calcium responses to E2 or G-1. Activation of GPER stimulated translocation of PKC isoforms (α and ε) to the plasma membrane, which led to MOR phosphorylation. Additionally, E2 and G-1 stimulated c-Fos expression in SH-SY5Y cells in a PLC/IP3-dependent manner. In conclusion, the present study has revealed a novel GPER-mediated estrogenic signaling in neuroblastoma cells in which activation of GPER

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Activation of the G Protein-Coupled Estrogen Receptor Elicits Store Calcium Release and Phosphorylation of the Mu-Opioid Receptors in the Human Neuroblastoma SH-SY5Y Cells

et al. 2019

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“…Oestradiol affects memory formation at all stages: from early formation to consolidation . The cognitive effects of oestradiol are mediated in the brain areas where it is produced, including in the prefrontal cortex and the hippocampus, and are critical for learning and memory .…”

Section: Oestradiol In Learning and Memorymentioning

confidence: 99%

Oestradiol, threat conditioning and extinction, post‐traumatic stress disorder, and prolonged exposure therapy: A common link

Hammoud

Foa

Milad

2019

J Neuroendocrinology

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The accumulating evidence regarding the impact of estradiol on learning and memory synergized studies to examine its influence on enhancing animal's ability to quell fear and anxiety. In this review, we first provide a foundational platform regarding the impact of oestradiol on cellular mechanisms of learning and memory and we review recent advances from rodent and human data showing that oestrogen enhances extinction learning across species. We then propose clinical application to these data.We discuss the potential role of oestradiol variance on the aetiology, maintenance and treatment for post-traumatic stress disorder. Specifically, we argue that the use of oestradiol as an adjunct to prolonged exposure (PE) therapy for PTSD may provide a new treatment approach for enhancing the efficacy of PE in women with PTSD.This could advance our understanding of the mechanisms of PTSD and help tailor sex-specific treatments for this disorder. K E Y W O R D Soestradiol, prolonged exposure therapy, PTSD, threat extinction

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“…All three ER receptors are expressed in the medial amygdala where they enhance social recognition and likely are associated with the functioning of the OTR . Estrogens in the paraventricular nucleus rapidly facilitate social recognition, an effect that was blocked by OTR antagonists in the amygdala (, in preparation), while estrogens in medial preoptic area of female mice have been associated with the rewarding effects of male odors facilitating dopamine release at the level of the ventral tegmental area . It is possible that such interactive mechanism may be associated with the expression of pathogen and toxin disgust associated with ERs.…”

Section: Neurobiology Of Disgust and Pathogen/toxin Avoidancementioning

confidence: 99%

Social neuroscience of disgust

Kavaliers

Ossenkopp

Choleris

2018

Genes Brain and Behavior

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Disgust can be thought of as an affective system that has evolved to detect signs of pathogens, parasite and toxins as well as to stimulate behaviors that reduce the risk of their acquisition. Disgust incorporates social cognitive mechanisms to regulate exposure to and, or anticipate and avoid exposure to pathogens and toxins. Social cognition entails the acquisition of social information about others (ie, social recognition) and from others (ie, social learning). This involves recognizing and assessing other individuals and the pathogen/parasite/contamination/toxin threat they pose and deciding about when and how to interact with and, or avoid them. Social cognition provides a frame-work for examining the expression of disgust and the associated neurobiological mechanisms. Here, we briefly consider the relations between social cognition and pathogen/parasite/toxin avoidance behaviors. We briefly discuss aspects of: (1) the odor mediated social recognition of actual and potentially infected individuals and the impact of parasite/pathogen threat on disgust mate and social partner choice; (2) the roles of "out-groups" (strangers, unfamiliar individuals) and "in-groups" (familiar individuals) in the expression of disgust and pathogen avoidance behaviors; (3) individual and social learning of disgust and empathy for disgust; (4) toxin elicited disgust and anticipatory disgust; (5) the neurobiological mechanisms, and in particular the roles of the nonapeptide, oxytocin and estrogenic mechanism associated with social cognition and the expression of disgust. These findings on the social neuroscience of disgust have a direct bearing on our understanding of the roles of disgust in shaping human and nonhuman social behavior.

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Rapid effects of estrogens on short-term memory: Possible mechanisms

Cited by 53 publications

References 113 publications

Activation of the G Protein-Coupled Estrogen Receptor Elicits Store Calcium Release and Phosphorylation of the Mu-Opioid Receptors in the Human Neuroblastoma SH-SY5Y Cells

Activation of the G Protein-Coupled Estrogen Receptor Elicits Store Calcium Release and Phosphorylation of the Mu-Opioid Receptors in the Human Neuroblastoma SH-SY5Y Cells

Oestradiol, threat conditioning and extinction, post‐traumatic stress disorder, and prolonged exposure therapy: A common link

Social neuroscience of disgust

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