Prolonged parent-child separation and pain in adolescence: The role of HPA-axis genetic variations

The article raises the issue of the relationship of parent-child relationships and professional preferences in pedagogical dynasties. Particular attention is paid to the role of the family in the professional development of the individual. It has been suggested that there is a relationship between parent-child relationships and professional preferences.

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GPER-Deficient Rats Exhibit Lower Serum Corticosterone Level and Increased Anxiety-Like Behavior

Neural Plasticity ◽

10.1155/2020/8866187 ◽

2020 ◽

Vol 2020 ◽

pp. 1-22 ◽

Cited By ~ 2

Author(s):

Yi Zheng ◽

Meimei Wu ◽

Ting Gao ◽

Li Meng ◽

Xiaowei Ding ◽

...

Keyword(s):

Hpa Axis ◽

Corticosterone Level ◽

Brain Structures ◽

Ample Evidence ◽

Genetic Ablation ◽

Serum Corticosterone ◽

Underlying Mechanisms ◽

G Protein Coupled ◽

Prolonged Stress

Ample evidence suggests that estrogens have strong influences on the occurrence of stress-related mood disorders, but the underlying mechanisms remain poorly understood. Through multiple approaches, we demonstrate that the G protein-coupled estrogen receptor (GPER) is widely distributed along the HPA axis and in brain structures critically involved in mood control. Genetic ablation of GPER in the rat resulted in significantly lower basal serum corticosterone level but enhanced ACTH release in response to acute restraint stress, especially in the female. GPER-/- rats of either sex displayed increased anxiety-like behaviors and deficits in learning and memory. Additionally, GPER deficiency led to aggravation of anxiety-like behaviors following single-prolonged stress (SPS). SPS caused significant decreases in serum corticosterone in WT but not in GPER-deficient rats. The results highlight an important role of GPER at multiple sites in regulation of the HPA axis and mood.

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The Role of HPA Axis and Allopregnanolone on the Neurobiology of Major Depressive Disorders and PTSD

International Journal of Molecular Sciences ◽

10.3390/ijms22115495 ◽

2021 ◽

Vol 22 (11) ◽

pp. 5495

Author(s):

Felipe Borges Almeida ◽

Graziano Pinna ◽

Helena Maria Tannhauser Barros

Keyword(s):

Hpa Axis ◽

Depressive Disorders ◽

Post Traumatic Stress ◽

Major Depressive ◽

Physiological Adaptations ◽

Suppression Test ◽

Post Traumatic ◽

Major Depressive Disorders ◽

Cortisol Release

Under stressful conditions, the hypothalamic-pituitary-adrenal (HPA) axis acts to promote transitory physiological adaptations that are often resolved after the stressful stimulus is no longer present. In addition to corticosteroids (e.g., cortisol), the neurosteroid allopregnanolone (3α,5α-tetrahydroprogesterone, 3α-hydroxy-5α-pregnan-20-one) participates in negative feedback mechanisms that restore homeostasis. Chronic, repeated exposure to stress impairs the responsivity of the HPA axis and dampens allopregnanolone levels, participating in the etiopathology of psychiatric disorders, such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). MDD and PTSD patients present abnormalities in the HPA axis regulation, such as altered cortisol levels or failure to suppress cortisol release in the dexamethasone suppression test. Herein, we review the neurophysiological role of allopregnanolone both as a potent and positive GABAergic neuromodulator but also in its capacity of inhibiting the HPA axis. The allopregnanolone function in the mechanisms that recapitulate stress-induced pathophysiology, including MDD and PTSD, and its potential as both a treatment target and as a biomarker for these disorders is discussed.

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Genes and hormones of the hypothalamic–pituitary–adrenal axis in post-traumatic stress disorder. What is their role in symptom expression and treatment response?

Journal of Neural Transmission ◽

10.1007/s00702-021-02330-2 ◽

2021 ◽

Author(s):

Susanne Fischer ◽

Tabea Schumacher ◽

Christine Knaevelsrud ◽

Ulrike Ehlert ◽

Sarah Schumacher

Keyword(s):

Hpa Axis ◽

Post Traumatic Stress Disorder ◽

Traumatic Stress ◽

Stress Disorder ◽

Ptsd Symptoms ◽

Post Traumatic Stress ◽

Alternative Treatments ◽

Hypothalamic Pituitary Adrenal ◽

Post Traumatic

Abstract Background Less than half of all individuals with post-traumatic stress disorder (PTSD) remit spontaneously and a large proportion of those seeking treatment do not respond sufficiently. This suggests that there may be subgroups of individuals who are in need of augmentative or alternative treatments. One of the most frequent pathophysiological findings in PTSD is alterations in the hypothalamic–pituitary–adrenal (HPA) axis, including enhanced negative feedback sensitivity and attenuated peripheral cortisol. Given the role of the HPA axis in cognition, this pattern may contribute to PTSD symptoms and interfere with key processes of standard first-line treatments, such as trauma-focused cognitive behavioural therapy (TF-CBT). Methods This review provides a comprehensive summary of the current state of research regarding the role of HPA axis functioning in PTSD symptoms and treatment. Results Overall, there is preliminary evidence that hypocortisolaemia contributes to symptom manifestation in PTSD; that it predicts non-responses to TF-CBT; and that it is subject to change in parallel with positive treatment trajectories. Moreover, there is evidence that genetic and epigenetic alterations within the genes NR3C1 and FKBP5 are associated with this hypocortisolaemic pattern and that some of these alterations change as symptoms improve over the course of treatment. Conclusions Future research priorities include investigations into the role of the HPA axis in day-to-day symptom variation, the time scale in which biological changes in response to treatment occur, and the effects of sex. Furthermore, before conceiving augmentative or alternative treatments that target the described mechanisms, multilevel studies are warranted.

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HPA axis linkage in parent-child dyads: Effects of parent sex, autism spectrum diagnosis, and dyadic relationship behavior

Developmental Psychobiology ◽

10.1002/dev.21537 ◽

2017 ◽

Vol 59 (6) ◽

pp. 776-786 ◽

Cited By ~ 12

Author(s):

Darby E. Saxbe ◽

Ofer Golan ◽

Sharon Ostfeld-Etzion ◽

Yael Hirschler-Guttenberg ◽

Orna Zagoory-Sharon ◽

...

Keyword(s):

Hpa Axis ◽

Autism Spectrum ◽

Dyadic Relationship ◽

Parent Child

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Transient sex-related changes in the mice hypothalamo–pituitary–adrenal (HPA) axis during the acute phase of the inflammatory process

Mediators of Inflammation ◽

10.1155/s0962935193000183 ◽

1993 ◽

Vol 2 (2) ◽

pp. 123-127 ◽

Cited By ~ 12

Author(s):

T. Daneva ◽

E. Spinedi ◽

R. Hadid ◽

M.-C. Jacquier ◽

M. Giacomini ◽

...

Keyword(s):

Sex Difference ◽

Acute Phase ◽

Hpa Axis ◽

Plasma Levels ◽

Potential Role ◽

Post Treatment ◽

Male Mice ◽

Plasma Acth ◽

Endogenous Sex Hormones

The potential role of endogenous sex hormones in regulating hypothalamo–pituitary–adrenal (HPA) axis function was investigated after a single injection of endotoxin in adult (8 week old) BALB/c mice of both sexes. The effect of LPS on plasma ACTH, corticosterone (B), testosterone and oestradiol (E) levels and on anterior pituitary (AP) ACTH and adrenal B contents at different times after treatment was studied. The results indicate that: (a) basal B but not ACTH plasma levels were significantly higher in female than in male mice; (b) LPS significantly increased both ACTH and B plasma levels over the baseline 2 h after injection, both hormone levels being higher in female than in male mice; (c) although plasma ACTH concentrations recovered the basal value at 72 h after LPS in animals of both sexes, plasma B levels returned to the baseline only at 120 h after treatment; (d) E plasma levels significantly increased 2 h after LPS and returned to the baseline at 72 h post-treatment, in both sexes; (e) at 2 h after LPS, testosterone plasma levels significantly decreased in male mice and increased in female mice, recovering the baseline level at 120 and 72 h after LPS, respectively; (f) AP ACTH content was similar in both sexes in basal condition and it was significantly diminished 72 h post-treatment without sex difference; whereas AP ACTH returned to basal content 120 h after LPS in males, it remained significantly decreased in females; (g) basal adrenal B content was higher in female than in male mice, and it significantly increased in both sexes 2 h post-LPS, maintaining this sex difference. Whereas adrenal B returned to basal content 72 h after treatment in male mice, it remained significantly enhanced up to 120 h post-LPS in female animals. The data demonstrate the existence of a clear sexual dimorphism in basal condition and during the acute phase response as well as in the recovery of the HPA axis function shortly after infection.

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