Estrogen Regulation of Genes Important for K+ Channel Signaling in the Arcuate Nucleus

Roepke, Troy A.; Malyala, Anna; Bosch, Martha A.; Kelly, Martin J.; Rønnekleiv, Oline K.

doi:10.1210/en.2007-0605

Cited by 81 publications

(97 citation statements)

References 78 publications

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“…The effects of ovariectomy and estradiol treatment, however, did not differ between wild-type mice and a different strain of GPR30 Ϫ/Ϫ mice (795). A second novel ER, Gq-mER, is expressed on the cell membranes of proopiomelanocortin (POMC), dopamine, and GABA neurons in the arcuate nucleus of the hypothalamus (576,601,602). Gq-mER reduces the activation of potassium channels on GABA B and -opioid receptors and affects the expression of NPY and other neuropeptides involved in the control of energy homeostasis.…”

Section: Er Mechanisms Controlling Eatingmentioning

confidence: 99%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

408

349

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(HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-␣ (ER␣) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.neuroendocrinology; estrogens; testosterone; eating disorders; obesity SEX DIFFERENCES ARE PERVASIVE in physiology and medicine (51,64,73,109,110,466,797,826). The controls of eating and energy homeostasis are no exceptions. It was observed approximately 100 years ago that removal of the ovaries leads to marked accretion of adipose tissue in rats (697), that daily food intake expressed as kilocalories per gram body weight differs between male and female rats (778), and that food intake varies regularly through the ovarian cycle in intact female rats (674, 779). Sex differences in eating have been the subject of physiological research ever since. The clinical relevance of this work is increasingly evident. In the United States, women are approximately threefold more vulnerable than men to psychiatric eating disorders (346,351) and approximately twofold more vulnerable to severe and morbid obesity (BMI Ն 35 and 40 kg/m 2 , respectively, mass/height 2 ) (226). Women also appear to suffer more from these disorders in terms of physical and psychological functioning and quality of life (24,84,273,292,465,531,762). The increased obesity burden suffered by women is reflected in the fact that Ͼ80% of bariatric surgery patients in the U...

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Section: Er Mechanisms Controlling Eatingmentioning

confidence: 99%

Sex differences in the physiology of eating

Asarian

Geary²

2013

American Journal of Physiology-Regulatory, Integrative and Comp

408

349

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“…Studies are forthcoming on the cross-talk between rapid membrane-initiated and long-term nuclear-initiated steroid actions (Lagrange et al, 1994, Lagrange et al, 1997, Wagner et al, 2001b, Vasudevan et al, 2001, Kow and Pfaff, 2004, Malyala et al, 2005, Qiu et al, 2006b, Qiu et al, 2006a, Roepke et al, 2007. For example, it has been found that both acute effects of E2 and the transcriptional changes alter excitability of hypothalamic neurons , Malyala et al, 2005, Qiu et al, 2006a.…”

Section: β-Estradiol and Gnrh Neurosecretionmentioning

confidence: 99%

Membrane-initiated estrogen signaling in hypothalamic neurons

Kelly

Rønnekleiv

2008

Molecular and Cellular Endocrinology

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SummaryIt is well known that many of the actions of 17β-estradiol (E2) in the central nervous system are mediated via intracellular receptor/transcription factors that interact with steroid response elements on target genes. However, there is compelling evidence for membrane steroid receptors for estrogen in hypothalamic and other brain neurons. But it is not well understood how estrogen signals via membrane receptors, and how these signals impact not only membrane excitability but also gene transcription in neurons. Indeed, it has been known for sometime that E2 can rapidly alter neuronal activity within seconds, indicating that some cellular effects can occur via membrane delimited events. In addition, E2 can affect second messenger systems including calcium mobilization and a plethora of kinases to alter cell signaling. Therefore, this review will consider our current knowledge of rapid membrane-initiated and intracellular signaling by E2 in the hypothalamus, the nature of receptors involved and how they contribute to homeostatic functions. KeywordsERα; ERβ; GPCR (G protein-coupled receptor); mER (membrane estrogen receptor that is a GPCR) Electrophysiological studies in the 1960's and 1970's suggested that gonadal steroids could directly modulate the electrical activity of hypothalamic neurons

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“…Potential targets for E 2 's rapid, nonclassical actions include membrane ERs and/or other membrane targets, which likely involve activation of several signal transduction pathways and/or second messengers, such as MAPK, extracellular signal-regulated kinase, phosphatidylinositol-3-kinase, or adenylyl cyclase cascades [27][28][29][30][31][32][33][34][35][36][37]. Indeed, we have found that co-administration of E 2 to the hippocampus with a MAPK inhibitor blocked the facilitating actions of E 2 for inhibitory avoidance performance (Figure 3).…”

Section: Rapid And/or Membrane Actions In the Hippocampus For E 2 'S mentioning

confidence: 99%

Rapid and estrogen receptor beta mediated actions in the hippocampus mediate some functional effects of estrogen

Walf

Frye

2008

Steroids

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The steroid hormone, estradiol (E 2 ), has numerous targets in the central nervous system, including the hippocampus, which plays a key role in cognition and affective behavior. This review focuses on our evidence from studies in rodents that E 2 has diverse mechanisms in the hippocampus for its functional effects E 2 has rapid, membrane-mediated effects in the hippocampus to enhance cognitive performance. Administration of E 2 to the hippocampus of rats for 10 minutes following training enhances performance in a hippocampus-mediated task. Increased cell firing in the hippocampus occurs within this short time frame. Furthermore, administration of free E 2 or an E 2 conjugate, E 2 :bovine serum albumin (BSA), to the hippocampus produces similar performance-enhancing effects in this task, suggesting that E 2 has membrane actions in the hippocampus for these effects. Further evidence that E 2 has rapid, membrane-mediated effects is that co-administration of E 2 and inhibitors of mitogen activated protein kinase (MAPK), rather than intracellular E 2 receptors (ERs) or protein synthesis, attenuate the enhancing effects of E 2 in this task. Despite these data that demonstrate E 2 can have rapid and/or membrane-mediated effects in the hippocampus, there is clear evidence to suggest that intracellular ERs, particularly the β (rather than α) isoform of ERs, may be important targets for E 2 's functional effects for hippocampal processes. Administration of ligands that are specific for ERβ, but not ERα, have enhancing effects on hippocampal processes similar to that of E 2 (which has similar affinity for ERα and ERβ). These effects are attenuated when ERβ expression is knocked down in transgenic models or with central administration of antisense oligonucleotides. Thus, there may be a convergence of E 2 's actions through rapid, membranemediated effects and intracellular ERs and in the hippocampus for these functional effects.

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Estrogen Regulation of Genes Important for K+ Channel Signaling in the Arcuate Nucleus

Cited by 81 publications

References 78 publications

Sex differences in the physiology of eating

Sex differences in the physiology of eating

Membrane-initiated estrogen signaling in hypothalamic neurons

Rapid and estrogen receptor beta mediated actions in the hippocampus mediate some functional effects of estrogen

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