Anti-HCRTR2 (aa 263-282) polyclonal antibody

Orexigenic hormones are a group of hormones that can up-regulate appetite. Current studies have shown that orexigenic hormones also play important roles in stress responses and may be implicated in regulation of fear memory. However, these conclusions lack evidence from human studies. In this study, we examined associations between orexigenic hormone genes and fear-related mental disorders by investigating main, G x E, and G x G effects of ghrelin and orexin gene single nucleotide polymorphisms (SNPs) on human posttraumatic stress disorder (PTSD) symptoms in 1134 Chinese earthquake survivors. SNPs Leu72Met of the GHRL gene (rs696217), Ile408Val of the HCRTRI gene (rs2271933) and Val308Ile of the HCRTR2 gene (rs2653349) were genotyped. None of the SNPs showed significant main or G x E effects. However, a significant interaction effect between GHRL rs696217 and HCRTRI rs2271933 was found to predict the PTSD Checklist (PCL-5) total score (P = 0.007). Further analysis revealed different interaction patterns in males and females. For females, the rs2271933 G allele was associated with an increased PCL-5 total score (B = 2.59, P = 0.024) when the rs696217 genotype TT/TG was present. For males, the rs696217 T allele is associated with an increased PCL-5 total score (B =. 3.62, P = 0.040) when the rs2271933 genotype GG/GA was present. These current findings expand our knowledge of physiological function of the orexigenic hormone system, and suggest its involvement in development of fear related mental disorders such as PTSD.

Studies point to an increased hereditary risk of cluster headache. HCRTR2 gene rs2653349 and ADH4 gene rs1800759 polymorphisms have been associated with cluster headache susceptibility. Also, GNB3 rs5443 polymorphism, associated with increased signal transduction via GPCRs, seems to influence triptan treatment response. DNA from 114 cluster headache patients and 570 non-related controls, representing a general Southeastern European Caucasian (SEC) population, was extracted from buccal swabs and genotyped using real-time PCR. Gene distribution for the rs2653349 was GG = 79.8%, GA = 18.4%, and AA = 1.8% for patients and GG = 79.1%, GA = 19.1%, and AA = 1.8% for controls. The frequency of the mutated A allele was 11.0% for patients and 11.3% for controls. The frequencies for rs5443 were CC = 44.7%, CT = 44.7%, and TT = 10.5% for patients and CC = 43.9%, CT = 42.6%, and TT = 13.5% for controls. The frequency of the mutated T allele was 32.9% for patients and 34.8% for controls. A 2.7-fold more frequent appearance of the mutated T allele was observed in patients with better triptan treatment response, although not statistically significant. For rs1800759, the frequencies were CC = 36.0%, CA = 43.0%, and AA = 21.0% for patients and CC = 34.0%, CA = 50.2%, and AA = 15.8% for controls. The frequency of the mutated A allele was 42.5% and 40.9% for patients and controls, respectively. The mutated T allele of GNB3 rs5443 polymorphism was more prevalent in patients with better triptan treatment response, indicating a possible trend of association between this polymorphism and triptan treatment response in SEC population. According to our observation, no association of HCRTR2 rs2653349 and ADH4 rs1800759 polymorphisms and cluster headache in SEC population could be documented.