scholarly journals Role of 11β-HSD type 1 in abnormal HPA axis activity during immune-mediated arthritis

2018 ◽  
Vol 7 (2) ◽  
pp. 385-394 ◽  
Author(s):  
Janko Sattler ◽  
Jinwen Tu ◽  
Shihani Stoner ◽  
Jingbao Li ◽  
Frank Buttgereit ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Hpa Axis ◽  
Brain Regions ◽  
Chronic Arthritis ◽  
Arthritis Model ◽  
Acute Arthritis ◽  
Immune Mediated ◽  
The Central Nervous System ◽  
Hpa Axis Activity

Patients with chronic immune-mediated arthritis exhibit abnormal hypothalamo-pituitary-adrenal (HPA) axis activity. The basis for this abnormality is not known. Immune-mediated arthritis is associated with increased extra-adrenal synthesis of active glucocorticoids by the 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme. 11β-HSD1 is expressed in the central nervous system, including regions involved in HPA axis regulation. We examined whether altered 11β-HSD1 expression within these regions contributes to HPA axis dysregulation during arthritis. The expression of 11β-HSD1, and other components of glucocorticoid signaling, were examined in various brain regions and the pituitary gland of mice with experimentally induced arthritis. Two arthritis protocols were employed: The K/BxN spontaneous arthritis model for chronic arthritis and the K/BxN serum transfer arthritis model for acute arthritis. 11β-HSD1 mRNA (Hsd11b1) was expressed in the hippocampus, hypothalamus, cortex, cerebellum and pituitary gland. Hypothalamic Hsd11b1 expression did not change in response to arthritis in either model. Pituitary Hsd11b1 expression was however significantly increased in both chronic and acute arthritis models. Hippocampal Hsd11b1 was decreased in acute but not chronic arthritis. Chronic, but not acute, arthritis was associated with a reduction in hypothalamic corticotropin-releasing hormone and arginine vasopressin expression. In both models, serum adrenocorticotropic hormone and corticosterone levels were no different from non-inflammatory controls. These findings demonstrate inflammation-dependent regulation of Hsd11b1 expression in the pituitary gland and hippocampus. The upregulation of 11β-HSD1 expression in the pituitary during both chronic and acute arthritis, and thus, an increase in glucocorticoid negative feedback, could contribute to the abnormalities in HPA axis activity seen in immune-mediated arthritis.

scholarly journals Leptin’s hunger-suppressing effects are mediated by the hypothalamic–pituitary–adrenocortical axis in rodents

2019 ◽  
Vol 116 (27) ◽  
pp. 13670-13679 ◽  
Author(s):  
Rachel J. Perry ◽  
Jon M. Resch ◽  
Amelia M. Douglass ◽  
Joseph C. Madara ◽  
Aviva Rabin-Court ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Hpa Axis ◽  
Homeostatic Regulation ◽  
Adaptive Responses ◽  
Cns Neurons ◽  
The Central Nervous System ◽  
Hpa Axis Activity ◽  
The Brain ◽  
Stimulation Of

Leptin informs the brain about sufficiency of fuel stores. When insufficient, leptin levels fall, triggering compensatory increases in appetite. Falling leptin is first sensed by hypothalamic neurons, which then initiate adaptive responses. With regard to hunger, it is thought that leptin-sensing neurons work entirely via circuits within the central nervous system (CNS). Very unexpectedly, however, we now show this is not the case. Instead, stimulation of hunger requires an intervening endocrine step, namely activation of the hypothalamic–pituitary–adrenocortical (HPA) axis. Increased corticosterone then activates AgRP neurons to fully increase hunger. Importantly, this is true for 2 forms of low leptin-induced hunger, fasting and poorly controlled type 1 diabetes. Hypoglycemia, which also stimulates hunger by activating CNS neurons, albeit independently of leptin, similarly recruits and requires this pathway by which HPA axis activity stimulates AgRP neurons. Thus, HPA axis regulation of AgRP neurons is a previously underappreciated step in homeostatic regulation of hunger.

Mechanism of the induction of brain c-Fos-positive neurons by lipid absorption

2007 ◽  
Vol 292 (1) ◽  
pp. R268-R273 ◽  
Author(s):  
Chun-Min Lo ◽  
Liyun Ma ◽  
Dian Ming Zhang ◽  
Rachel Lee ◽  
Abby Qin ◽  
...  
Keyword(s):  
Arcuate Nucleus ◽  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Lipid Absorption ◽  
Neuronal Activation ◽  
Positive Neuron ◽  
The Central Nervous System ◽  
Chylomicron Formation ◽  
The Brain

Many gastrointestinal meal-related signals are transmitted to the central nervous system via the vagus nerve and thereby control changes in meal size. The c-Fos-positive neuron has been used as a marker of neuronal activation after lipid meals to examine the contribution of a selective macronutrient on brain neurocircuit activity. In rats fed Intralipid, the c-Fos-positive neurons were highly stimulated in the nucleus of the solitary tract (NTS) and in the hypothalamus, including the paraventricular nucleus (PVN), arcuate nucleus of the hypothalamus (ARC), and ventromedial hypothalamus at 4 h lipid feeding. However, c-Fos-like immunoreactivity was markedly attenuated in these brain regions when chylomicron formation/secretion was blocked by Pluronic L-81. After lymph was diverted from the lymph cannulated animals, the rats had a lower number of c-Fos-positive cells in the NTS and ARC. In contrast, the rats had higher c-Fos-positive neurons in PVN. The present study also revealed that c-Fos-positive neurons induced by feeding of Intalipid were abolished by CCK type 1 receptor antagonist, Lorglumide. We conclude that the formation and/or secretion of chylomicron are critical steps for initiating neuronal activation in the brain.

Stress and the Serotonergic System, Observations from Pet Imaging

2017 ◽  
Vol 41 (S1) ◽  
pp. S19-S19
Author(s):  
M. Spies ◽  
R. Lanzenberger
Keyword(s):  
Hpa Axis ◽  
Acute Stress ◽  
Antidepressant Treatment ◽  
Brain Regions ◽  
The Other ◽  
Serotonergic System ◽  
Other Hand ◽  
Positron Emission ◽  
Hpa Axis Activity

IntroductionStress response and the neuroendocrinologic factors through which it is mediated are disturbed in anxiety and in affective disorders. While acute stress is thought to result in hypothalamus-pituitary-adrenal- (HPA) axis hyperactivity (Varghese 2001), chronic stress may result in decreased HPA-response (Booji 2013). Antidepressant treatment, on the other hand, is thought to realign HPA–axis activity (Schüle 2007).On the other hand, dysregulation within the serotonergic neurotransmitter system is understood as a central moderator in the pathophysiology of affective and anxiety disorders. Serotonergic transmission both regulates- and is regulated by- glucocortocoids. Cortisol results in an increase in serotonin synthesis and release while serotonergic transmission is thought to downregulate HPA-axis activity (Lanfumey, 2008). Positron emission tomography (PET) studies have demonstrated the link between the serotonergic system and the HPA-axis in humans in vivo. For example, a negative correlation between cortisol and 5HT1A receptor levels in various brain regions has been shown (Lanzenberger, 2010). SERT expression, on the other hand, was shown using PET to be positively related to HPA-axis reactivity (Frokjaer 2013).Methodsn.a.AimsAvailable literature on interactions between the HPA-axis and the serotonergic system will be discussed with a focus on data acquired via PET studies.Resultsn.a.ConclusionsThe interaction between the serotonergic system and the HPA-axis is likely bilateral and may be understood as a neurobiological link by which stress may foster the development of depression and anxiety.Disclosure of interestM. Spies has received travel grants from AOP Orphan Pharmaceuticals AG, Janssen-Cilag Pharma Gmbh, and Eli Lilly, workshop participation from Eli Lilly, and speaker honoraria from Janssen-Cilag Pharma Gmbh. R. Lanzenberger received travel grants and conference speaker honoraria from AstraZeneca, Lundbeck A/S, Roche Austria GmbH, Dr. Willmar Schwabe GmbH & Co. KG, AOP Orphan Pharmaceuticals, and Janssen-Cilag Pharma Gmbh.

The Influence of HPA-Axis Activity on Aggression

2008 ◽  
Author(s):  
Robina Khan ◽  
Katja Bertsch ◽  
Ewald Naumann ◽  
Menno R. Kruk ◽  
Patrick Britz ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Hpa Axis Activity

Effects of alprazolam on cholecystokinin-tetrapeptide (CCK-4) induced panic and hypothalamic-pituitary-adrenal (HPA) axis activity

2004 ◽  
Vol 36 (05) ◽  
Author(s):  
D Eser ◽  
P Zwanzger ◽  
S Aicher ◽  
C Schüle ◽  
TC Baghai ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Hypothalamic Pituitary Adrenal ◽  
Hpa Axis Activity

METABOLIC STUDIES WITH 131I-LABELED THYROXINE. II.

1963 ◽  
Vol 44 (3) ◽  
pp. 475-480 ◽  
Author(s):  
R. Grinberg
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Optic Nerve ◽  
Pituitary Gland ◽  
Time Interval ◽  
Time Intervals ◽  
Pituitary Glands ◽  
The Central Nervous System ◽  
Tentative Explanation

ABSTRACT Radiologically thyroidectomized female Swiss mice were injected intraperitoneally with 131I-labeled thyroxine (T4*), and were studied at time intervals of 30 minutes and 4, 28, 48 and 72 hours after injection, 10 mice for each time interval. The organs of the central nervous system and the pituitary glands were chromatographed, and likewise serum from the same animal. The chromatographic studies revealed a compound with the same mobility as 131I-labeled triiodothyronine in the organs of the CNS and in the pituitary gland, but this compound was not present in the serum. In most of the chromatographic studies, the peaks for I, T4 and T3 coincided with those for the standards. In several instances, however, such an exact coincidence was lacking. A tentative explanation for the presence of T3* in the pituitary gland following the injection of T4* is a deiodinating system in the pituitary gland or else the capacity of the pituitary gland to concentrate T3* formed in other organs. The presence of T3* is apparently a characteristic of most of the CNS (brain, midbrain, medulla and spinal cord); but in the case of the optic nerve, the compound is not present under the conditions of this study.

Sign in / Sign up

Export Citation Format

Share Document