scholarly journals Rats Lacking Dopamine Transporter Display Increased Vulnerability and Aberrant Autonomic Response to Acute Stress

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 842
Author(s):  
Placido Illiano ◽  
Gregory E. Bigford ◽  
Raul R. Gainetdinov ◽  
Marta Pardo
Keyword(s):  
Dopamine Transporter ◽  
Hpa Axis ◽  
Acute Stress ◽  
Female Rats ◽  
Autonomic Response ◽  
Before And After ◽  
Response To Stress ◽  
Vulnerability To Stress ◽  
Body Temperature Increase ◽  
Reduced Temperature

The activity of the hypothalamus–pituitary–adrenal (HPA) axis is pivotal in homeostasis and presides the adaptative response to stress. Dopamine Transporter (DAT) plays a key role in the regulation of the HPA axis. We used young adult female DAT Knockout (KO) rats to assess the effects of DAT ablation (partial, heterozygous DAT+/-, or total, homozygous DAT-/-) on vulnerability to stress. DAT-/- rats show profound dysregulation of pituitary homeostasis, in the presence of elevated peripheral corticosterone, before and after acute restraint stress. During stress, DAT-/- rats show abnormal autonomic response at either respiratory and cardiovascular level, and delayed body temperature increase. DAT+/- rats display minor changes of hypophyseal homeostatic mechanisms. These rats display a similar pituitary activation to that of the control animals, albeit in the presence of higher release of peripheral corticosterone than DAT-/- after stress, and reduced temperature during stress. Our data indicate that DAT regulates the HPA axis at both the central and peripheral level, including autonomic function during stress. In particular, the partial deletion of DAT results in increased vulnerability to stress in female rats, which display central and peripheral alterations that are reminiscent of PTSD, and they might provide new insights in the pathophysiology of this disorder.

scholarly journals Effect of glucocorticoid therapy on adrenal function in children with acute lymphoblastic leukemia

2014 ◽  
Vol 54 (1) ◽  
pp. 15
Author(s):  
Gita Widyapuri ◽  
Djajadiman Gatot ◽  
Aman Bakti Pulungan ◽  
Badriul Hegar
Keyword(s):  
Hpa Axis ◽  
Standard Dose ◽  
Lymphoblastic Leukemia ◽  
Adrenal Function ◽  
High Dose ◽  
Induction Phase ◽  
Acth Test ◽  
Before And After ◽  
Response To Stress ◽  
Cortisol Levels

BackgroundGlucocorticoids play an important role in thetreatment ofacute lymphoblastic leukemia (ALL), but can causeside effects such as suppression of the hypothalamic-pituitaryadrenal (HPA) axis. Suppression of the HPA axis causes adrenal insufficiency, disturbs the cortisol response to stress, and may be a cause of morbidity and mortality in children with ALL.ObjectiveTo evaluate adrenal function in children with ALL afterinduction chemotherapy with high dose glucocorticoids.MethodsThe adrenal function of 20 children with ALL wasevaluated using a standard dose (250 μ g) adrenocorticotropinhormone (ACTH) test performed before and after a 6 week oftreatment with glucocorticoids induction phase chemotherapy,which was followed by a week period tapering off. Adrenalinsuffien cy was defined as blood cortisol level of < 18 μg/dLResultsAdrenal insufficiency was found in 14/20 subjects afterthe induction phase followed by a week period of tapering off.Median cortisol levels pre- and post-stimulation before inductionphase were 14.72 (range 2.0 1- 46. 1) μg/dL and 29.29 (range 21.65 - 55 .15) μg/dL, respectively. Median cortisol levels pre- and poststimulation after induction phase were 5.87 (range 0.2 - 20.53)μg/dL and 10.49 (range 0.33 - 28.69) μg/dL, respectively. Clinicalsigns and symptoms did not differ between those with and withoutadrenal insufficiency.ConclusionOf 20 children with ALL, 14 develop adrenalinsufficiency after a 6-week induction therapy with glucocorticoidsand followed by a week period of tapering off. No specific clinicalsigns and symptoms are identified to be related to the adrenalinsufficiency.

Immunological and psychological responses to psychosocial stress in caregivers of autistic offspring

2011 ◽  
Vol 26 (S2) ◽  
pp. 1580-1580
Author(s):  
S. De Andrés-García ◽  
P. Sariñana-González ◽  
Á. Romero-Martínez ◽  
M.V. Sanchis-Calatayud ◽  
L. Moya-Albiol ◽  
...  
Keyword(s):  
Psychosocial Stress ◽  
Acute Stress ◽  
Immunoglobulin A ◽  
Healthy Population ◽  
Men And Women ◽  
Immunological Responses ◽  
Before And After ◽  
Immunological Effects ◽  
Iga Response ◽  
Response To Stress

IntroductionCaregivers of relatives with chronic diseases has shown lower rest levels of immunoglobulin A than non-caregivers (Gallagher et al., 2008). In response to mental stress, IgA levels used to be increased in healthy population (Okamura et al. 2010). Scarce studies have been focused on immunological effects of caregiving in response to stress, and the results are controversial. To our knowledge, there are no studies stressing this field in chronically stressed populations such as caregivers of autistic offspring.Objectives and aimsEvaluate whether caregivers present different psychosocial and immunological responses to acute stress than non-caregivers, as well as what is the role of gender in these responses.Methods38 caregivers of persons with autism and 35 non-caregivers were exposed to a psychosocial laboratory stress. IgA levels were measured before, during and after a set of several mental tasks, while the state of mood was evaluated before and after the stressors.ResultsCaregivers showed blunted IgA response to stress in men and women compared with non-caregivers, although the response pattern was different for each gender. Moreover, caregivers presented worse mood (depression, anger, fatigue, vigor and total score) than non-caregivers. Moreover, psychological effects of stress are inversely associated with levels of IgA, fundamentally during the task.ConclusionsCaregiving reduces IgA secretion in response to psychosocial stress, although differently in men and women. Further studies are necessary to explore other neuroendocrine factors, together with mood, that could be involved in this buffered response.

Effects of aging on prolactin release after stress in female and male rats

1984 ◽  
Vol 107 (3) ◽  
pp. 337-339 ◽  
Author(s):  
Ljiljana Milenković ◽  
Ljubica Bogić ◽  
Biljana Mušicki ◽  
Jovo V. Martinović
Keyword(s):  
Acute Stress ◽  
Female Rats ◽  
Male Rats ◽  
Elderly Male ◽  
Prolactin Release ◽  
Response To Stress ◽  
Reverse Relationship ◽  
Effects Of Aging ◽  
Sexually Mature ◽  
Intact Rats

Abstract. Young adult and elderly male and female intact rats, as well as chronically ovariectomized (OVX) young and elderly female rats, were subjected to an acute stress by cutting the tip of the tail and prolactin (Prl) concentrations were measured in their blood collected by decapitation at various times thereafter. Maximum concentrations of the hormone were markedly lower in all the three groups of elderly rats than those found in the corresponding young animals, and appeared to occur with a delay in the females, but not in the males. In addition, the Prl-response to stress was attenuated in OVX animals regardless of their age. The result of these experiments, performed at two points on the age scale, suggests that in sexually mature rats of both sexes the stress-induced secretion of Prl is inversely related to the age of the animal and that the reverse relationship is retained in OVX females.

scholarly journals Intrahypothalamic Estradiol Modulates Hypothalamus-Pituitary-Adrenal-Axis Activity in Female Rats

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 3337-3344 ◽  
Author(s):  
J. Liu ◽  
P. H. Bisschop ◽  
L. Eggels ◽  
E. Foppen ◽  
E. Fliers ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Restraint Stress ◽  
Acute Stress ◽  
Plasma Corticosterone ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Stress Exposure ◽  
Ici 182,780 ◽  
Hpa Axis Activity

Estrogen plays an important role in the regulation of the hypothalamus-pituitary-adrenal (HPA)-axis, but the neuroendocrine pathways and the role of estrogen receptor (ER) subtypes involved in specific aspects of this interaction remain unknown. In a first set of experiments, we administered estradiol (E2) intravenously, intracerebroventricularly, and by intrahypothalamic microdialysis to ovariectomized rats to measure plasma corticosterone (CORT) concentrations from carotid artery blood. Systemic infusion of E2 did not increase plasma CORT, but intracerebroventricular E2 induced a 3-fold CORT increase (P = 0.012). Local E2 infusions in the hypothalamic paraventricular nucleus (PVN) significantly increased plasma CORT (P &lt; 0.001). A similar CORT increase was seen after PVN infusion of the ERα agonist propylpyrazoletriol, whereas the ERβ agonist diarylpropiolnitrile had no effect. In a second set of experiments, we investigated whether E2 modulates the HPA-axis response to acute stress by administering E2 agonists or its antagonist ICI 182,780 into the PVN during restraint stress exposure. After 30 min of stress exposure, plasma CORT had increased 5.0-fold (P &lt; 0.001). E2 and propylpyrazoletriol administration in the PVN enhanced the stress-induced plasma CORT increase (8-fold vs. baseline), whereas ICI 182,780 and diarylpropiolnitrile reduced it, as compared with both E2 and vehicle administration in the PVN. In conclusion, central E2 modulates HPA-axis activity both in the basal state and during restraint stress. In the basal condition, the stimulation is mediated by ERα-sensitive neurons, whereas during stress, it is mediated by both ERα and ERβ.

HPA axis responses to acute stress and adrenalectomy during adjuvant-induced arthritis in the rat

1993 ◽  
Vol 264 (1) ◽  
pp. R179-R185 ◽  
Author(s):  
M. S. Harbuz ◽  
R. G. Rees ◽  
S. L. Lightman
Keyword(s):  
Hpa Axis ◽  
Anterior Pituitary ◽  
Acute Stress ◽  
Corticotropin Releasing Factor ◽  
Adjuvant Induced Arthritis ◽  
Response To Stress ◽  
Chronic Activation ◽  
Severity Of The Disease ◽  
Proenkephalin A ◽  
Pathological Situation

Adjuvant-induced arthritis results in chronic activation of the hypothalamo-pituitary-adrenal (HPA) axis. In the Piebald-Viral-Glaxo (PVG) rat, however, corticotropin-releasing factor (CRF) mRNA in the parvocellular paraventricular nucleus (pPVN) of the hypothalamus was reduced, and the normal corticosterone and CRF mRNA responses to acute stress were inhibited. The proenkephalin A mRNA response to stress in the pPVN was maintained, implying a specific inhibition of the CRF mRNA responses in this pathological situation. Adrenalectomy at day 0 (the time of adjuvant injection), day 13 (just before inflammation), or day 19 (submaximal inflammation) resulted in a marked increase in CRF mRNA compared with day 21 adrenal-intact arthritic animals. However, levels were below those of nonarthritic adrenalectomized rats, demonstrating that the inhibition of CRF mRNA associated with arthritis is not simply due to changes in glucocorticoid feedback. Proopiomelanocortin mRNA in the anterior pituitary was markedly increased in all adrenalectomized arthritic animals above the increase seen in sham-adrenalectomized day-21 arthritic rats. Adrenalectomy was always associated with an increase in the severity of the disease.

Effects of Physical Training on Endocrine and Autonomic Response to Acute Stress

2001 ◽  
Vol 15 (2) ◽  
pp. 114-121 ◽  
Author(s):  
A. Salvador ◽  
J. Ricarte ◽  
E. González-Bono ◽  
L. Moya-Albiol
Keyword(s):  
Physical Training ◽  
Acute Stress ◽  
Skin Conductance Level ◽  
Free Testosterone ◽  
Autonomic Response ◽  
Before And After ◽  
Training Impact ◽  
Acute Stressor ◽  
Study Heart Rate ◽  
Transitory State

Abstract The effects of physical training on autonomic response to acute stress are controversial. In this study, heart rate (HR) and skin conductance level (SCL) were continuously recorded in response to a mental stressor in a sample of elite athletes before and after a period of training and competition. The free testosterone to cortisol ratio (FTCR) and the Profile of Mood States (POMS) were used as markers of training impact. After the training, the men and women showed a significant FTCR decrement, although mood and the autonomic response to the acute stressor were not strongly altered. Although men showed significantly lower HR values after training, the results suggest that subjects suffered a transitory state of hormonal overstrain rather than a serious problem of adaptation to training.

Aerodynamic and Acoustic Voice Measures Before and After an Acute Public Speaking Stressor

2020 ◽  
Vol 63 (10) ◽  
pp. 3311-3325
Author(s):  
Brittany L. Perrine ◽  
Ronald C. Scherer
Keyword(s):  
Fundamental Frequency ◽  
Salivary Cortisol ◽  
Public Speaking ◽  
Stress System ◽  
Before And After ◽  
Subglottal Pressure ◽  
Response To Stress ◽  
System Activation ◽  
Speaking Fundamental Frequency ◽  
Pituitary Adrenal Axis

Purpose The goal of this study was to determine if differences in stress system activation lead to changes in speaking fundamental frequency, average oral airflow, and estimated subglottal pressure before and after an acute, psychosocial stressor. Method Eighteen vocally healthy adult females experienced the Trier Social Stress Test (TSST) to activate the hypothalamic–pituitary–adrenal axis. The TSST includes public speaking and performing mental arithmetic in front of an audience. At seven time points, three before the stressor and four after the stressor, the participants produced /pa/ repetitions, read the Rainbow Passage, and provided a saliva sample. Measures included (a) salivary cortisol level, (b) oral airflow, (c) estimated subglottal pressure, and (d) speaking fundamental frequency from the second sentence of the Rainbow Passage. Results Ten of the 18 participants experienced a hypothalamic–pituitary–adrenal axis response to stress as indicated by a 2.5-nmol/L increase in salivary cortisol from before the TSST to after the TSST. Those who experienced a response to stress had a significantly higher speaking fundamental frequency before and immediately after the stressor than later after the stressor. No other variable varied significantly due to the stressor. Conclusions This study suggests that the idiosyncratic and inconsistent voice changes reported in the literature may be explained by differences in stress system activation. In addition, laryngeal aerodynamic measures appear resilient to changes due to acute stress. Further work is needed to examine the influence of other stress systems and if these findings hold for dysphonic individuals.

scholarly journals Kidney Injury Caused by Preeclamptic Pregnancy Recovers Postpartum in a Transgenic Rat Model

2021 ◽  
Vol 22 (7) ◽  
pp. 3762
Author(s):  
Sarah M. Kedziora ◽  
Kristin Kräker ◽  
Lajos Markó ◽  
Julia Binder ◽  
Meryam Sugulle ◽  
...  
Keyword(s):  
Rat Model ◽  
Renal Damage ◽  
Kidney Injury ◽  
Tissue Growth ◽  
Female Rats ◽  
Male Rats ◽  
Renal Diseases ◽  
Transgenic Rat ◽  
Increased Risk ◽  
Before And After

Preeclampsia (PE) is characterized by the onset of hypertension (≥140/90 mmHg) and presence of proteinuria (>300 mg/L/24 h urine) or other maternal organ dysfunctions. During human PE, renal injuries have been observed. Some studies suggest that women with PE diagnosis have an increased risk to develop renal diseases later in life. However, in human studies PE as a single cause of this development cannot be investigated. Here, we aimed to investigate the effect of PE on postpartum renal damage in an established transgenic PE rat model. Female rats harboring the human-angiotensinogen gene develop a preeclamptic phenotype after mating with male rats harboring the human-renin gene, but are normotensive before and after pregnancy. During pregnancy PE rats developed mild tubular and glomerular changes assessed by histologic analysis, increased gene expression of renal damage markers such as kidney injury marker 1 and connective-tissue growth factor, and albuminuria compared to female wild-type rats (WT). However, four weeks postpartum, most PE-related renal pathologies were absent, including albuminuria and elevated biomarker expression. Only mild enlargement of the glomerular tuft could be detected. Overall, the glomerular and tubular function were affected during pregnancy in the transgenic PE rat. However, almost all these pathologies observed during PE recovered postpartum.

scholarly journals The co-chaperone Fkbp5 shapes the acute stress response in the paraventricular nucleus of the hypothalamus of male mice

2021 ◽  
Author(s):  
Alexander S. Häusl ◽  
Lea M. Brix ◽  
Jakob Hartmann ◽  
Max L. Pöhlmann ◽  
Juan-Pablo Lopez ◽  
...  
Keyword(s):  
Stress Response ◽  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Acute Stress ◽  
Negative Regulator ◽  
Neuron Activity ◽  
Cell Type ◽  
Specific Expression ◽  
Acute Stress Response ◽  
Cell Type Specific

AbstractDisturbed activation or regulation of the stress response through the hypothalamic-pituitary-adrenal (HPA) axis is a fundamental component of multiple stress-related diseases, including psychiatric, metabolic, and immune disorders. The FK506 binding protein 51 (FKBP5) is a negative regulator of the glucocorticoid receptor (GR), the main driver of HPA axis regulation, and FKBP5 polymorphisms have been repeatedly linked to stress-related disorders in humans. However, the specific role of Fkbp5 in the paraventricular nucleus of the hypothalamus (PVN) in shaping HPA axis (re)activity remains to be elucidated. We here demonstrate that the deletion of Fkbp5 in Sim1+ neurons dampens the acute stress response and increases GR sensitivity. In contrast, Fkbp5 overexpression in the PVN results in a chronic HPA axis over-activation, and a PVN-specific rescue of Fkbp5 expression in full Fkbp5 KO mice normalizes the HPA axis phenotype. Single-cell RNA sequencing revealed the cell-type-specific expression pattern of Fkbp5 in the PVN and showed that Fkbp5 expression is specifically upregulated in Crh+ neurons after stress. Finally, Crh-specific Fkbp5 overexpression alters Crh neuron activity, but only partially recapitulates the PVN-specific Fkbp5 overexpression phenotype. Together, the data establish the central and cell-type-specific importance of Fkbp5 in the PVN in shaping HPA axis regulation and the acute stress response.

Sign in / Sign up

Export Citation Format

Share Document