Norepinephrine Regulation of Ventromedial Hypothalamic Nucleus Metabolic-Sensory Neuron 5′-AMP-Activated Protein Kinase Activity: Impact of Estradiol

Mahmood, Akhtar; Uddin, Md. Main; Ibrahim, Mostafa M.H.; Briski, Karen P.

doi:10.3390/ijms21062013

Cited by 3 publications

(1 citation statement)

References 51 publications

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“…Sex hormones affect many, if not all, neurotransmitter systems in myriad ways [140]. Both excitatory and inhibitory effects of estradiol on several neurotransmitters, including glutamatergic [141][142][143][144], GABAergic [145,146], dopaminergic [147][148][149][150][151][152], serotonergic [153][154][155][156][157], and noradrenergic [158][159][160], have been extensively documented. These effects occur via multiple mechanisms (including synthesis [153], release [149], turnover/degradation [161], receptor trafficking [154], and transport [162]) and are dependent on contextual factors, such as receptor subtype [163], brain area [164], developmental stage [165], duration of treatment/time following exposure [166,167], mode of administration [167], and amount of steroid present [168].…”

Section: Signal Transductionmentioning

confidence: 99%

In search of sex-related mediators of affective illness

Sikes-Keilp

Rubinow

2021

Biol Sex Differ

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Sex differences in the rates of affective disorders have been recognized for decades. Studies of physiologic sex-related differences in animals and humans, however, have generally yielded little in terms of explaining these differences. Furthermore, the significance of these findings is difficult to interpret given the dynamic, integrative, and highly context-dependent nature of human physiology. In this article, we provide an overview of the current literature on sex differences as they relate to mood disorders, organizing existing findings into five levels at which sex differences conceivably influence physiology relevant to affective states. These levels include the following: brain structure, network connectivity, signal transduction, transcription/translation, and epigenesis. We then evaluate the importance and limitations of this body of work, as well as offer perspectives on the future of research into sex differences. In creating this overview, we attempt to bring perspective to a body of research that is complex, poorly synthesized, and far from complete, as well as provide a theoretical framework for thinking about the role that sex differences ultimately play in affective regulation. Despite the overall gaps regarding both the underlying pathogenesis of affective illness and the role of sex-related factors in the development of affective disorders, it is evident that sex should be considered as an important contributor to alterations in neural function giving rise to susceptibility to and expression of depression.

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Section: Signal Transductionmentioning

confidence: 99%

In search of sex-related mediators of affective illness

Sikes-Keilp

Rubinow

2021

Biol Sex Differ

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Ventromedial hypothalamic nucleus glycogen regulation of metabolic-sensory neuron AMPK and neurotransmitter expression: role of lactate

Bheemanapally

Ibrahim

Alshamrani

et al. 2021

American Journal of Physiology-Regulatory, Integrative and Comp

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Astrocyte glycogen is dynamically remodeled during metabolic stability and provides oxidizable L-lactate equivalents during neuro-glucopenia. Current research investigated the hypothesis that ventromedial hypothalamic nucleus (VMN) glycogen metabolism controls gluco-stimulatory nitric oxide (NO) and/or gluco-inhibitory gamma-aminobutyric acid (GABA) neuron 5'-AMP-activated protein kinase (AMPK) and transmitter marker, e.g. neuronal nitric oxide synthase (nNOS), glutamate decarboxylase65/67 (GAD) protein expression. Adult ovariectomized estradiol-implanted female rats were injected into the VMN with the glycogen phosphorylase inhibitor 1,4-dideoxy-1,4-imino-D-arabinitol (DAB) before vehicle or L-lactate infusion. Western blot analysis of laser-catapult-microdissected nitrergic and GABAergic neurons showed that DAB caused lactate-reversible up-regulation of nNOS and GAD proteins. DAB suppressed or increased total AMPK content of NO and GABA neurons, respectively, by lactate-independent mechanisms, but lactate prevented drug enhancement of pAMPK expression in nitrergic neurons. Inhibition of VMN glycogen disassembly caused divergent changes in counter-regulatory hormone, e.g. corticosterone (increased) and glucagon (decreased) secretion. Outcomes show that VMN glycogen metabolism controls local gluco-regulatory transmission by means of lactate signal volume. Results implicate glycogen-derived lactate deficiency as a physiological stimulus of corticosterone release. Concurrent normalization of nitrergic neuron nNOS and pAMPK protein and corticosterone secretory response to DAB by lactate infers that the hypothalamic-pituitary-adrenal axis may be activated by VMN NO-mediated signals of cellular energy imbalance.

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The interaction of BDNF with estrogen in the development of hypertension and obesity, particularly during menopause

Zhang,

He,

Pan

et al. 2024

Front. Endocrinol.

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The expression of BDNF in both neuronal and non-neuronal cells is influenced by various stimuli, including prenatal developmental factors and postnatal conditions such as estrogens, dietary habits, and lifestyle factors like obesity, blood pressure, and aging. Central BDNF plays a crucial role in modulating how target tissues respond to these stimuli, influencing the pathogenesis of hypertension, mitigating obesity, and protecting neurons from aging. Thus, BDNF serves as a dynamic mediator of environmental influences, reflecting an individual's unique history of exposure. Estrogens, on the other hand, regulate various processes to maintain overall physiological well-being. Through nuclear estrogen receptors (ERα, ERβ) and the membrane estrogen receptor (GPER1), estrogens modulate transcriptional processes and signaling events that regulate the expression of target genes, such as ERα, components of the renin-angiotensin system (RAS), and hormone-sensitive lipase. Estrogens are instrumental in maintaining the set point for blood pressure and energy balance. BDNF and estrogens work cooperatively to prevent obesity by favoring lipolysis, and counteractively regulate blood pressure to adapt to the environment. Estrogen deficiency leads to menopause in women with low central BDNF level. This review delves into the complex mechanisms involving BDNF and estrogen, especially in the context of hypertension and obesity, particularly among postmenopausal women. The insights gained aim to inform the development of comprehensive therapeutic strategies for these prevalent syndromes affecting approximately 68% of adults.

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Norepinephrine Regulation of Ventromedial Hypothalamic Nucleus Metabolic-Sensory Neuron 5′-AMP-Activated Protein Kinase Activity: Impact of Estradiol

Cited by 3 publications

References 51 publications

In search of sex-related mediators of affective illness

In search of sex-related mediators of affective illness

Ventromedial hypothalamic nucleus glycogen regulation of metabolic-sensory neuron AMPK and neurotransmitter expression: role of lactate

The interaction of BDNF with estrogen in the development of hypertension and obesity, particularly during menopause

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