Brain mechanisms of HPA axis regulation: neurocircuitry and feedback in context Richard Kvetnansky lecture

Herman, James P.; Nawreen, Nawshaba; Smail, Marissa A.; Cotella, Evelin M.

doi:10.1080/10253890.2020.1859475

Cited by 89 publications

(103 citation statements)

References 171 publications

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“…Adrenal-derived catecholamines (epinephrine and norepinephrine) and glucocorticoids that are released in the blood in response to stress maintain vital homeostatic functions through binding to their receptors-ARs and GRs, respectively [16][17][18]. The stress signal, perceived or physiological, conveyed through the autonomic sensory nerves or generated within the central nervous system (CNS), leads to hypothalamic sympathetic activation, which initiates the body's response through the activation of the neuroendocrine system [19].…”

Section: Ars and Grs Their Subtypes And Roles In Homeostatic Functionsmentioning

confidence: 99%

“…Cortisol and mineralocorticoids released into circulation then bind to GRs and mediate cellular responses to stress (Figure 1) [23,24]. Impairment of the SAM and HPA axes has been linked to a wide array of neuropsychiatric conditions, and even chronic peripheral diseases [16,17].…”

Section: Ars and Grs Their Subtypes And Roles In Homeostatic Functionsmentioning

confidence: 99%

“…Plasticity in GR-mediated biological processes is complex and influenced by multiple regulatory impacts on its activity [17]. Posttranslational modifications of GR, including phosphorylation, ubiquitination, and acetylation, can also modulate GR activity.…”

Section: Cellular Signaling Through Activation Of Grsmentioning

confidence: 99%

“…Furthermore, communication between the lungs and the brain was needed in order to receive a stress signal in the brain from irritancy stress after ozone exposure. It is noteworthy that ARs and GRs have been implicated in stress adaptation and resiliency, and that the failure of normal functioning of these receptors has been linked not only to neurological ailments but also to peripheral chronic diseases [16,17,19]. Thus, the contribution of these receptors to airpollutant-induced stress responses and subsequent pulmonary, neuronal, and peripheral effects, as well as adaptation, warrant further consideration.…”

Section: Circulating Ligands Of Ars and Grs In Lung-brain Communicationmentioning

confidence: 99%

“…Hypothalamus, the master regulator of environmental cues, receives stress signals from external and internal stressors though autonomic sensory nerves and light signals directly from the suprachiasmatic nucleus (SCN), which is connected to the retina [141]. The hypothalamus integrates the information received to from both sources to generate bodily response through neural and endocrine mechanisms involving the SAM, HPA, and other hormonal axes to direct peripheral immune and metabolic responses via the activation of ARs and GRs [17]. Diurnal oscillations are evolved through complex selfregulatory mechanisms of genes and transcription factors in the brain and other peripheral organs, and work in tandem with adrenergic and glucocorticoid mechanisms to mediate physiological changes to synchronize with changes in activity patterns.…”

Section: Air Pollution's Impact On Circadian Clock Genes and The Potential Mediating Roles Of Ars And Grsmentioning

confidence: 99%

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Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution

Hodge

Henriquez

Kodavanti

2021

Toxics

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Adrenergic receptors (ARs) and glucocorticoid receptors (GRs) are activated by circulating catecholamines and glucocorticoids, respectively. These receptors regulate the homeostasis of physiological processes with specificity via multiple receptor subtypes, wide tissue-specific distribution, and interactions with other receptors and signaling processes. Based on their physiological roles, ARs and GRs are widely manipulated therapeutically for chronic diseases. Although these receptors play key roles in inflammatory and cellular homeostatic processes, little research has addressed their involvement in the health effects of air pollution. We have recently demonstrated that ozone, a prototypic air pollutant, mediates pulmonary and systemic effects through the activation of these receptors. A single exposure to ozone induces the sympathetic–adrenal–medullary and hypothalamic–pituitary–adrenal axes, resulting in the release of epinephrine and corticosterone into the circulation. These hormones act as ligands for ARs and GRs. The roles of beta AR (βARs) and GRs in ozone-induced pulmonary injury and inflammation were confirmed in a number of studies using interventional approaches. Accordingly, the activation status of ARs and GRs is critical in mediating the health effects of inhaled irritants. In this paper, we review the cellular distribution and functions of ARs and GRs, their lung-specific localization, and their involvement in ozone-induced health effects, in order to capture attention for future research.

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Section: Ars and Grs Their Subtypes And Roles In Homeostatic Functionsmentioning

confidence: 99%

Section: Ars and Grs Their Subtypes And Roles In Homeostatic Functionsmentioning

confidence: 99%

Section: Cellular Signaling Through Activation Of Grsmentioning

confidence: 99%

Section: Circulating Ligands Of Ars and Grs In Lung-brain Communicationmentioning

confidence: 99%

Section: Air Pollution's Impact On Circadian Clock Genes and The Potential Mediating Roles Of Ars And Grsmentioning

confidence: 99%

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Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution

Hodge

Henriquez

Kodavanti

2021

Toxics

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Sex differences in the vulnerability of the hippocampus to prenatal stress

Soti

Ranjbar

Kohlmeier

et al. 2022

Developmental Psychobiology

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Distressing events during pregnancy that engage activity of the body's endocrine stress response have been linked with later life cognitive deficits in offspring and associated with developmental changes in cognitive-controlling neural regions. Interestingly, prenatal stress (PS)-induced alterations have shown some sex specificity.Here, we review the literature of animal studies examining sex-specific effect of physical PS on the function and structure of the hippocampus as hippocampal impairments likely underlie PS-associated deficits in learning and memory. Furthermore, the connectivity between the hypothalamic-pituitary-adrenal (HPA) axis and the hippocampus as well as the heavy presence of glucocorticoid receptors (GRs) in the hippocampus suggests this structure plays an important role in modulation of activity within stress circuitry in a sex-specific pattern. We hope that better understanding of sex-specific, PS-related hippocampal impairment will assist in uncovering the molecular mechanisms behind sex-based risk factors in PS populations across development, and perhaps contribute to greater precision in management of cognitive disturbances in this vulnerable population.

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The upregulation of glutamate decarboxylase 67 against hippocampal excitability damage in male fetal rats by prenatal caffeine exposure

Jiao

et al. 2022

Environmental Toxicology

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As a kind of xanthine alkaloid, caffeine is widely present in beverages, food, and analgesic drugs. Our previous studies have shown that prenatal caffeine exposure (PCE) can induce programmed hypersensitivity of the hypothalamic-pituitary-adrenal (HPA) axis in offspring rats, which is involved in developing many chronic adult diseases. The present study further examined the potential molecular mechanism and toxicity targets of hippocampal dysfunction, which might mediate the programmed hypersensitivity of the HPA axis in offspring. Pregnant rats were intragastrically administered with 0, 30, and 120 mg/kg/day caffeine from gestational days (GD) 9-20, and the fetal rats were extracted at GD20. Rat fetal hippocampal H19-7/IGF1R cell line was treated with caffeine, adenosine A2A receptor (A2AR) agonist (CGS-21680) or adenylate cyclase agonist (forskolin) plus caffeine. Compared with the control group, hippocampal neurons of male fetal rats by PCE displayed increased apoptosis and reduced synaptic plasticity, whereas glutamate decarboxylase 67 (GAD67) expression was increased. Moreover, the expression of A2AR was down-regulated, PCE inhibited the cAMP/PKA/CREB/BDNF/TrkB pathway. Furthermore, the results in vitro were consistent with the in vivo study. Both CGS21680 and forskolin could reverse the above alteration caused by caffeine. These results indicated that PCE inhibits the BDNF pathway and mediates the hippocampus's glutamate (Glu) excitotoxicity. The compensatory up-regulation of GAD67 unbalanced the Glu/gammaaminobutyric acid (GABA)ergic output, leading to the impaired negative feedback to the hypothalamus and hypersensitivity of the HPA axis.

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Brain mechanisms of HPA axis regulation: neurocircuitry and feedback in context Richard Kvetnansky lecture

Cited by 89 publications

References 171 publications

Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution

Adrenergic and Glucocorticoid Receptors in the Pulmonary Health Effects of Air Pollution

Sex differences in the vulnerability of the hippocampus to prenatal stress

The upregulation of glutamate decarboxylase 67 against hippocampal excitability damage in male fetal rats by prenatal caffeine exposure

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