Cholinergic modulation of CRH and non-CRH neurons in Barrington’s nucleus of the mouse

2020 ◽  
Vol 124 (2) ◽  
pp. 443-457
Author(s):  
Masahiro Kawatani ◽  
Keiichi Itoi ◽  
Ashraf Hossain Talukder ◽  
Katsuya Uchida ◽  
Kenji Sakimura ◽  
...  
Keyword(s):  
Muscarinic Receptors ◽  
Nicotinic Receptors ◽  
Corticotropin Releasing Hormone ◽  
Cholinergic Modulation ◽  
Cholinergic Agonists ◽  
Releasing Hormone

This study investigates the effects of bath-applied cholinergic agonists on Barrington’s nucleus (BarN) neurons in vitro. They were either excitatory, through nicotinic receptors, or inhibitory, through muscarinic receptors. Putative corticotropin-releasing hormone (CRH)-expressing neurons in BarN, as well as putative non-CRH-expressing neurons, responded to cholinergic agonists.

Effect of Cholinergic Agonists and Antagonists on Rat Hypothalamic Corticotropin-Releasing Hormone Secretion in vitro

1988 ◽  
Vol 47 (4) ◽  
pp. 303-308 ◽  
Author(s):  
Aldo E. Calogero ◽  
William T. Gallucci ◽  
Renato Bernardini ◽  
Christina Saoutis ◽  
Philip W. Gold ◽  
...  
Keyword(s):  
Hormone Secretion ◽  
Corticotropin Releasing Hormone ◽  
Cholinergic Agonists ◽  
Releasing Hormone ◽  
Cholinergic Agonists And Antagonists

Regulation of CRH-induced secretion of ACTH and corticosterone by SOM230 in rats

2005 ◽  
Vol 153 (3) ◽  
pp. R7-R10 ◽  
Author(s):  
A P Silva ◽  
P Schoeffter ◽  
G Weckbecker ◽  
C Bruns ◽  
H A Schmid
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Hormone ◽  
Acth Secretion ◽  
Releasing Hormone ◽  
Corticosterone Secretion ◽  
Corticosterone Release ◽  
Acth Release

Objective: Adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome is biochemically characterized by increased plasma concentrations of ACTH inducing hypersecretion of cortisol. Somatostatin is known to inhibit ACTH secretion, and in vitro data have shown the inhibition of ACTH secretion by agonists activating sst2 and sst5 receptors. The present study aimed to determine the inhibitory effect of the multireceptor ligand SOM230, compared with the sst2-preferring agonist octreotide, on corticotropin-releasing hormone (CRH)-stimulated secretion of ACTH and corticosterone in rats. Methods: Secretion of ACTH and corticosterone was induced by i.v. application of CRH (0.5 μg/kg) in rats pretreated 1 h before by i.v. application of SOM230 (1, 3, or 10 μg/kg), octreotide (10 μg/kg) or NaCl 0.9%. Results: SOM230 (3 and 10 μg/kg) inhibited CRH-induced ACTH release by 45±3% and 51±2%, respectively, and corticosterone release by 43±5% and 27±16%, respectively. 10 μg/kg of octreotide tended to be less potent at inhibiting ACTH release (34±6% inhibition) and did not alter the secretion of corticosterone. Conclusion: SOM230 has a stronger inhibitory effect on ACTH and corticosterone secretion than octreotide in rats. This difference can be explained by its higher affinity to sst1, sst3 and especially sst5 receptors compared with octreotide.

Immobilization stress rapidly decreases hypothalamic corticotropin-releasing hormone secretion in vitro in the male 344/N Fischer rat

Life Sciences ◽  
1993 ◽  
Vol 53 (3) ◽  
pp. 233-240 ◽  
Author(s):  
Giovanni Cizza ◽  
Richard Kvetnansky ◽  
Maria E. Tartaglia ◽  
Marc R. Blackman ◽  
George P. Chrousos ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Hormone Secretion ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

scholarly journals Corticotropin-releasing hormone (CRH) alters mitochondrial morphology and function by activating the NF-kB-DRP1 axis in hippocampal neurons

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Chiara R. Battaglia ◽  
Silvia Cursano ◽  
Enrico Calzia ◽  
Alberto Catanese ◽  
Tobias M. Boeckers
Keyword(s):  
Hippocampal Neurons ◽  
Morphological Changes ◽  
Mitochondrial Dynamics ◽  
Synaptic Activity ◽  
Mitochondrial Activity ◽  
Mitochondrial Morphology ◽  
Significant Shift ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

AbstractNeuronal stress-adaptation combines multiple molecular responses. We have previously reported that thorax trauma induces a transient loss of hippocampal excitatory synapses mediated by the local release of the stress-related hormone corticotropin-releasing hormone (CRH). Since a physiological synaptic activity relies also on mitochondrial functionality, we investigated the direct involvement of mitochondria in the (mal)-adaptive changes induced by the activation of neuronal CRH receptors 1 (CRHR1). We observed, in vivo and in vitro, a significant shift of mitochondrial dynamics towards fission, which correlated with increased swollen mitochondria and aberrant cristae. These morphological changes, which are associated with increased NF-kB activity and nitric oxide concentrations, correlated with a pronounced reduction of mitochondrial activity. However, ATP availability was unaltered, suggesting that neurons maintain a physiological energy metabolism to preserve them from apoptosis under CRH exposure. Our findings demonstrate that stress-induced CRHR1 activation leads to strong, but reversible, modifications of mitochondrial dynamics and morphology. These alterations are accompanied by bioenergetic defects and the reduction of neuronal activity, which are linked to increased intracellular oxidative stress, and to the activation of the NF-kB/c-Abl/DRP1 axis.

Rat interier splanchnic afferents respond differently to corticotropin-releasing hormone (CRF) and bradykinin intra-arterial injection in vitro

2001 ◽  
Vol 120 (5) ◽  
pp. A717
Author(s):  
Jen Yu Wei ◽  
Yu Hua Wang ◽  
Mulugeta Million ◽  
Yvette Tache ◽  
Angeles C.A.
Keyword(s):  
Corticotropin Releasing Hormone ◽  
Releasing Hormone
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