scholarly journals Co-localization of the cannabinoid type 1 receptor with corticotropin-releasing factor-containing afferents in the noradrenergic nucleus locus coeruleus: implications for the cognitive limb of the stress response

2017 ◽  
Vol 222 (7) ◽  
pp. 3007-3023 ◽  
Author(s):  
Ryan R. Wyrofsky ◽  
Beverly A. S. Reyes ◽  
Elisabeth J. Van Bockstaele
Keyword(s):  
Stress Response ◽  
Locus Coeruleus ◽  
Corticotropin Releasing Factor ◽  
Cannabinoid Type 1 Receptor

The Potential Role of a Corticotropin-Releasing Factor Receptor-1 Antagonist in Psychiatric Disorders

CNS Spectrums ◽  
2008 ◽  
Vol 13 (6) ◽  
pp. 467-483 ◽  
Author(s):  
Stephen M. Stahl ◽  
Dana D. Wise
Keyword(s):  
Stress Response ◽  
Psychiatric Disorders ◽  
Stress Responses ◽  
Potential Role ◽  
Corticotropin Releasing Factor ◽  
Recovering Alcoholic ◽  
Mood And Cognition ◽  
Pituitary Adrenal Axis

The hypothalamic-pituitary-adrenal axis is a key mediator of the stress response in humans. The corticotropin-releasing factor (CRF) type 1 receptor (CRFR-1) in the pituitary gland is a gatekeeper for that response, and the CRFR-1 receptor is also present in many other mood- and cognition-related neural structures. Behaviorally, a number of relationships between stress and psychiatric disorders can be observed: chronic or repeated stress is associated with onset of depression; stressors can cause a recovering alcoholic to relapse; overactive stress responses mark many anxiety disorders; and insomnia can arise from an overactive stress response. Thus, a CRFR-1 antagonist could be useful for treating or preventing the consequences of CRF-mediated stress in depression, anxiety, insomnia, and substance abuse.

Dimerization of Corticotropin-Releasing Factor Receptor Type 1 Is Not Coupled to Ligand Binding

2005 ◽  
Vol 25 (4-6) ◽  
pp. 251-276 ◽  
Author(s):  
OLIVER KRAETKE ◽  
BURKHARD WIESNER ◽  
JENNY EICHHORST ◽  
JENS FURKERT ◽  
MICHAEL BIENERT ◽  
...  
Keyword(s):  
Ligand Binding ◽  
Corticotropin Releasing Factor ◽  
Receptor Type

scholarly journals Regulation des Angstverhaltens — zur Rolle neuronaler Netzwerke

BIOspektrum ◽  
2019 ◽  
Vol 25 (7) ◽  
pp. 711-714
Author(s):  
Nina Dedic ◽  
Jan M. Deussing
Keyword(s):  
Stress Response ◽  
Ventral Tegmental Area ◽  
Long Range ◽  
Dopamine Release ◽  
Receptor Type ◽  
Projection Neurons ◽  
Neuronal Circuit ◽  
Brain Reward ◽  
Crh Receptor Type 1

AbstractThe corticotropin-releasing hormone (CRH) system orchestrates the organism’s stress response including the regulation of adaptive be haviours. Here we describe a novel neuronal circuit, which acts anxiety suppressing and positively modulates dopamine release. This anxiolytic circuit comprises inhibitory CRH-expressing, long-range projection neurons within the extended amygdala. These neurons innervate the ventral tegmental area, a prominent brain reward center that expresses high levels of CRH receptor type 1.

scholarly journals Molecular Docking and Molecular Dynamics Simulation Studies of Triterpenes from Vernonia patula with the Cannabinoid Type 1 Receptor

2021 ◽  
Vol 22 (7) ◽  
pp. 3595
Author(s):  
Md Afjalus Afjalus Siraj ◽  
Md. Sajjadur Rahman ◽  
Ghee T. Tan ◽  
Veronique Seidel
Keyword(s):  
Molecular Dynamics ◽  
Molecular Docking ◽  
Molecular Dynamics Simulation ◽  
Binding Affinity ◽  
Docking Studies ◽  
Dynamics Simulation ◽  
Simulation Studies ◽  
Cannabinoid Type 1 Receptor ◽  
Docking Approach

A molecular docking approach was employed to evaluate the binding affinity of six triterpenes, namely epifriedelanol, friedelin, α-amyrin, α-amyrin acetate, β-amyrin acetate, and bauerenyl acetate, towards the cannabinoid type 1 receptor (CB1). Molecular docking studies showed that friedelin, α-amyrin, and epifriedelanol had the strongest binding affinity towards CB1. Molecular dynamics simulation studies revealed that friedelin and α-amyrin engaged in stable non-bonding interactions by binding to a pocket close to the active site on the surface of the CB1 target protein. The studied triterpenes showed a good capacity to penetrate the blood–brain barrier. These results help to provide some evidence to justify, at least in part, the previously reported antinociceptive and sedative properties of Vernonia patula.

scholarly journals Oxidative Stress, Glutathione Metabolism, and Liver Regeneration Pathways Are Activated in Hereditary Tyrosinemia Type 1 Mice upon Short-Term Nitisinone Discontinuation

Genes ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 3
Author(s):  
Haaike Colemonts-Vroninks ◽  
Jessie Neuckermans ◽  
Lionel Marcelis ◽  
Paul Claes ◽  
Steven Branson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Liver Regeneration ◽  
The Body ◽  
Glutathione Metabolism ◽  
Short Term ◽  
Therapeutic Regime ◽  
Tyrosinemia Type 1 ◽  
Hereditary Tyrosinemia

Hereditary tyrosinemia type 1 (HT1) is an inherited condition in which the body is unable to break down the amino acid tyrosine due to mutations in the fumarylacetoacetate hydrolase (FAH) gene, coding for the final enzyme of the tyrosine degradation pathway. As a consequence, HT1 patients accumulate toxic tyrosine derivatives causing severe liver damage. Since its introduction, the drug nitisinone (NTBC) has offered a life-saving treatment that inhibits the upstream enzyme 4-hydroxyphenylpyruvate dioxygenase (HPD), thereby preventing production of downstream toxic metabolites. However, HT1 patients under NTBC therapy remain unable to degrade tyrosine. To control the disease and side-effects of the drug, HT1 patients need to take NTBC as an adjunct to a lifelong tyrosine and phenylalanine restricted diet. As a consequence of this strict therapeutic regime, drug compliance issues can arise with significant influence on patient health. In this study, we investigated the molecular impact of short-term NTBC therapy discontinuation on liver tissue of Fah-deficient mice. We found that after seven days of NTBC withdrawal, molecular pathways related to oxidative stress, glutathione metabolism, and liver regeneration were mostly affected. More specifically, NRF2-mediated oxidative stress response and several toxicological gene classes related to reactive oxygen species metabolism were significantly modulated. We observed that the expression of several key glutathione metabolism related genes including Slc7a11 and Ggt1 was highly increased after short-term NTBC therapy deprivation. This stress response was associated with the transcriptional activation of several markers of liver progenitor cells including Atf3, Cyr61, Ddr1, Epcam, Elovl7, and Glis3, indicating a concreted activation of liver regeneration early after NTBC withdrawal.

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