Glucocorticoid action in the anterior pituitary gland: Insights from corticotroph physiology

Shipston, Michael J.

doi:10.1016/j.coemr.2022.100358

Cited by 9 publications

(2 citation statements)

References 80 publications

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“…As lower-affinity MRs become saturated with stress-induced increases in GC, GRs become activated and work to turn GC production back down ( Figure 1B ). GR expressed in cells of the PVN, anterior pituitary, and adrenal glands bind GC at these higher concentrations, resulting in inhibition of output at every level of the HPA axis (Kim and Iremonger, 2019 ; Shipston, 2022 ). This is a critical component of HPA axis functionality, reducing production of ACTH and CRH and preventing excessive corticosteroid release over extended periods of time in order to maintain homeostasis after exposure to stress.…”

Section: Stress and Tbi Activate Glucocorticoid Receptor Signalingmentioning

confidence: 99%

Context is key: glucocorticoid receptor and corticosteroid therapeutics in outcomes after traumatic brain injury

Taylor,

Kokiko-Cochran

2024

Front. Cell. Neurosci.

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Traumatic brain injury (TBI) is a global health burden, and survivors suffer functional and psychiatric consequences that can persist long after injury. TBI induces a physiological stress response by activating the hypothalamic-pituitary-adrenal (HPA) axis, but the effects of injury on the stress response become more complex in the long term. Clinical and experimental evidence suggests long lasting dysfunction of the stress response after TBI. Additionally, pre- and post-injury stress both have negative impacts on outcome following TBI. This bidirectional relationship between stress and injury impedes recovery and exacerbates TBI-induced psychiatric and cognitive dysfunction. Previous clinical and experimental studies have explored the use of synthetic glucocorticoids as a therapeutic for stress-related TBI outcomes, but these have yielded mixed results. Furthermore, long-term steroid treatment is associated with multiple negative side effects. There is a pressing need for alternative approaches that improve stress functionality after TBI. Glucocorticoid receptor (GR) has been identified as a fundamental link between stress and immune responses, and preclinical evidence suggests GR plays an important role in microglia-mediated outcomes after TBI and other neuroinflammatory conditions. In this review, we will summarize GR-mediated stress dysfunction after TBI, highlighting the role of microglia. We will discuss recent studies which target microglial GR in the context of stress and injury, and we suggest that cell-specific GR interventions may be a promising strategy for long-term TBI pathophysiology.

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Section: Stress and Tbi Activate Glucocorticoid Receptor Signalingmentioning

confidence: 99%

Context is key: glucocorticoid receptor and corticosteroid therapeutics in outcomes after traumatic brain injury

Taylor,

Kokiko-Cochran

2024

Front. Cell. Neurosci.

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“…6,147 Research is ongoing to identify promising therapeutic targets within the HPA axis. [149][150][151] Studies of CRH receptor antagonists have not reported significant improvements in depression, and the effects of glucocorticoid receptors in the treatment of depression are inconsistent. 6,75,152 On the other hand, targeted antagonism of the V 1b receptor is a promising treatment approach in patients with depression.…”

Section: Dovepressmentioning

confidence: 99%

Targeting the Arginine Vasopressin V1b Receptor System and Stress Response in Depression and Other Neuropsychiatric Disorders

Kanes¹,

Dennie²,

Perera³

2023

NDT

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A healthy stress response is critical for good mental and overall health and promotes neuronal growth and adaptation, but the intricately balanced biological mechanisms that facilitate a stress response can also result in predisposition to disease when that equilibrium is disrupted. The hypothalamic-pituitary-adrenal (HPA) axis neuroendocrine system plays a critical role in the body’s response and adaptation to stress, and vasopressinergic regulation of the HPA axis is critical to maintaining system responsiveness during chronic stress. However, exposure to repeated or excessive physical or emotional stress or trauma can shift the body’s stress response equilibrium to a “new normal” underpinned by enduring changes in HPA axis function. Exposure to early life stress due to adverse childhood experiences can also lead to lasting neurobiological changes, including in HPA axis function. HPA axis impairment in patients with depression is considered among the most reliable findings in biological psychiatry, and chronic stress has been shown to play a major role in the pathogenesis and onset of depression and other neuropsychiatric disorders. Modulating HPA axis activity, for example via targeted antagonism of the vasopressin V 1b receptor, is a promising approach for patients with depression and other neuropsychiatric disorders associated with HPA axis impairment. Despite favorable preclinical indications in animal models, demonstration of clinical efficacy for the treatment of depressive disorders by targeting HPA axis dysfunction has been challenging, possibly due to the heterogeneity and syndromal nature of depressive disorders. Measures of HPA axis function, such as elevated cortisol levels, may be useful biomarkers for identifying patients who may benefit from treatments that modulate HPA axis activity. Utilizing clinical biomarkers to identify subsets of patients with impaired HPA axis function who may benefit is a promising next step in fine-tuning HPA axis activity via targeted antagonism of the V 1b receptor.

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Long COVID and pituitary dysfunctions: a bidirectional relationship?

di Filippo,

Franzese,

Santoro

et al. 2024

Pituitary

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Glucocorticoid action in the anterior pituitary gland: Insights from corticotroph physiology

Cited by 9 publications

References 80 publications

Context is key: glucocorticoid receptor and corticosteroid therapeutics in outcomes after traumatic brain injury

Context is key: glucocorticoid receptor and corticosteroid therapeutics in outcomes after traumatic brain injury

Targeting the Arginine Vasopressin V1b Receptor System and Stress Response in Depression and Other Neuropsychiatric Disorders

Long COVID and pituitary dysfunctions: a bidirectional relationship?

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