Corticotropin-releasing hormone receptor subtypes in the rat anterior pituitary after two types of restraint stress

The stress response in anterior pituitary (AP) is mediated by corticotropin-releasing hormone (CRH) acting through CRH-R1 and -R2, however, the function of CRH-R2 in AP is still not fully elucidated. We used 1-h long restraint (IMO) as well as restraint combined with water immersion (IMO+C). Using real-time PCR we quantified mRNA expression of CRH-R1, CRH-R2α-soluble and -insoluble, and cAMP response element binding (CREB), with reference gene GAPDH. In control AP, CRH-R1 mRNA was up to 20-fold higher than levels of CRH-R2α-soluble or CRH-R2α-insoluble mRNA. IMO reduced CRH-R1 mRNA to 47% and 63% of control levels 1 and 2 h after the onset of stressor, respectively, while IMO+C did not produce significant changes. Our data demonstrated that these stressors did not change CRH-R2α mRNA, unlike the very significant response of CRH-R1 to IMO

Could ethanol-induced alterations in the expression of glutamate transporters in testes contribute to the effect of paternal drinking on the risk of abnormalities in the offspring?

It has been known that a preconception paternal alcoholism impacts adversely on the offspring but the mechanism of the effect is uncertain. Several findings suggest that there are signalling systems in testis that are analogous to those known to be altered by alcoholism in brain. We propose that chronic alcohol affects these systems in a manner similar to that in brain. Specifically, we hypothesise that excessive alcohol may disturb glutamatergic-like signalling in testis by increasing expression of the glutamate transporter GLAST (EAAT1). We discuss ways how to test the hypothesis as well as potential significance of some of the tests as tools in the diagnostics of chronic alcoholism

Original paper<br>Two candidate gene polymorphisms in ADHD children: a case-control study of catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAOB) genes

Introduction: Attention-deficit hyperactivity disorder (ADHD) is a common polygenic heritable disorder. We have investigated the relationship between ADHD and polymorphisms of catechol-O-methyltransferase (COMT) and monoaminooxidase B (MAOB) genes. It is well known that COMT and MAOB are metabolising enzymes that degrade biogenic amines and control the levels of these neurotransmitters in the central nervous system. An association has been previously observed between the Val158Met polymorphism of catechol-O-methyltransferase (COMT) gene and ADHD. The gene of monoamine oxidase B (MAOB) has also been suggested to play a role in psychiatric disorders and behavioural traits. Moreover, MAO inhibitors have been shown to be effective in the treatment of ADHD. Material and methods: 118 boys with ADHD and 153 controls aged from 7 to 13 years were included in this study. PCR methods for the detection of the studied polymorphisms were used. Fisher’s exact test was performed to assess the association between the studied groups. Results: There was no statistically significant difference in the genotype frequency of COMT (p=0.321) or MAOB (p=0.087) gene polymorphisms between the hyperactive group of boys and the control group of boys. Conclusions: Our study supports the results of the previous studies: these two polymorphisms do not play the main role in the pathogenesis of ADHD