scholarly journals Adolescent alcohol exposure increases orexin-A/hypocretin-1 in the anterior hypothalamus

Alcohol ◽  
2020 ◽  
Vol 88 ◽  
pp. 65-72
Author(s):  
Leslie R. Amodeo ◽  
Wen Liu ◽  
Derek N. Wills ◽  
Ryan P. Vetreno ◽  
Fulton T. Crews ◽  
...  
2008 ◽  
Vol 145 (1-3) ◽  
pp. 60-64 ◽  
Author(s):  
Kenji Dohi ◽  
Beth Ripley ◽  
Nobuhiro Fujiki ◽  
Hirokazu Ohtaki ◽  
Takefumi Yamamoto ◽  
...  

SLEEP ◽  
2012 ◽  
Vol 35 (2) ◽  
pp. 187-191 ◽  
Author(s):  
Adi Aran ◽  
Irina Shors ◽  
Ling Lin ◽  
Emmanuel Mignot ◽  
Michael S. Schimmel

Epilepsia ◽  
2009 ◽  
Vol 50 (6) ◽  
pp. 1641-1644 ◽  
Author(s):  
Konrad Rejdak ◽  
Ewa Papuć ◽  
Paweł Grieb ◽  
Zbigniew Stelmasiak

2009 ◽  
Vol 10 (2) ◽  
pp. 271
Author(s):  
Paul Christian Baier ◽  
Robert Göder ◽  
Manfred Hallschmid

2019 ◽  
Vol 2019 (4) ◽  
Author(s):  
Paul Coleman ◽  
Luis De Lecea ◽  
Anthony Gotter ◽  
Jim Hagan ◽  
Rebecca Hills ◽  
...  

Orexin receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Orexin receptors [39]) are activated by the endogenous polypeptides orexin-A and orexin-B (also known as hypocretin-1 and -2; 33 and 28 aa) derived from a common precursor, preproorexin or orexin precursor, by proteolytic cleavage and some typical peptide modifications [102]. Currently the only orexin receptor ligand in clinical use is suvorexant, which is used as a hypnotic. Orexin receptor crystal structures have been solved [124, 123].


2016 ◽  
Vol 22 (3) ◽  
pp. 616-628 ◽  
Author(s):  
Samuel W. Centanni ◽  
Elizabeth J. Burnett ◽  
Heather Trantham-Davidson ◽  
L. Judson Chandler

SLEEP ◽  
2002 ◽  
Vol 25 (3) ◽  
pp. 337-339 ◽  
Author(s):  
Takashi Kanbayashi ◽  
Tamami Yano ◽  
Hideaki Ishiguro ◽  
Kentoh Kawanishi ◽  
Shigeru Chiba ◽  
...  

2019 ◽  
Vol 85 (10) ◽  
pp. S210-S211
Author(s):  
Evan Kyzar ◽  
Huaibo Zhang ◽  
John Peyton Bohnsack ◽  
Subhash Pandey

2020 ◽  
Vol 9 (10) ◽  
pp. 3354
Author(s):  
Mojdeh Samzadeh ◽  
Ewa Papuć ◽  
Marzena Furtak-Niczyporuk ◽  
Konrad Rejdak

The effects of status epilepticus on the orexin/hypocretin system have yet to be investigated. The present study aimed to assay orexin-A/hypocretin-1 in the cerebrospinal fluid (CSF) of patients after generalized convulsive status epilepticus (GCSE). The study groups included 20 GCSE patients, 24 patients diagnosed with epilepsy but remaining in remission (ER), and 25 normal controls (CTR). Diagnostic lumbar puncture was performed in GCSE patients within 3–10 days of seizure cessation, as well as in the ER and to CTR subjects. Among all GCSE patients, the outcome was graded according to the modified Rankin Scale (mRS) at 1-month follow-up. Orexin-A levels were measured in unextracted CSF samples, using a commercial radioimmunoassay. There was a significant overall difference in median CSF orexin-A concentrations between GCSE, RE, and CTR patients (p < 0.001). The lowest concentrations were noted in the GCSE group compared to ER (p < 0.001) or CTR (p < 0.001). CSF orexin-A levels in GCSE patients inversely correlated with clinical outcome as assessed on the mRS at 1-month follow-up (r = −0.55; p = 0.1). In conclusion, CSF orexin-A levels may serve as a biomarker of increased turn-over of the peptide or post-SE neuronal damage, and implicates the orexin system in the pathogenesis of SE.


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