CART petidinin sıçan beyninde tirozin hidroksilaz ile ko-lokalizasyonu

ÖZET Akut kokain ve amfetamin uygulamasından sonra belirli beyin bölgelerinde artan bir transkript (mRNA) olarak tanımlanan CART ("Cocaine and Amphetamine Regulated Transcript"), beyin kaynaklı ve yapısı bilinen hiç bir peptid ya da proteine benzemeyen yeni bir peptiddir. CART aday bir nörotransmiter veya kotransmiterdir. Beyindeki lokalizastonu CART' m bir çok işlevle ilgili olabileceğini düşündürmektedir. CART'ın beyinde kendine özgü bir dağılımı vardır, nöronlarda, sinir terminallerinde ve sinaptik veziküllerde bulunur. CART'ın beslenme davranışını değiştirebildiği gösterilmiştir. Bir çok nöropeptid nörotransmiterler beyinde daha klasik kabul edilen nörotransmiterlerle birlikte bulunur. CART'ın GABA ve asetil kolin transferaz ile ko- lokalize olduğuna dair histokimyasal kanıtlar vardır. Bu çalışmada CART, katekolamin sentezleyen nöronlarda bulunmuştur. Bu bulgu CART'ın bir nörotransmiter ya da kotransmiter olarak rolünü desteklemekle birlikte, noradrenerjik sistemle etkileşimlerinin anlaşılmasına da yardımcı olabilecektir54 SUMMARY CART (cocaine and amphetamine regulated transcript), initially described as a transcript (mRNA) increasing after acute cocaine and amphetamine administration, is a novel, brain-enriched peptide without homology to any known protein or peptide. CART is a putative peptide neurotransmitter/cotransmitter. Its localization in the brain suggests an involvement of CART in many processes. It has a unique distribution in the brain where it is found in neurons, nerve terminals and synaptic vesicles. It has been demonstrated that CART may alter feeding behavior. Many neuropeptide neurotransmitters are colocalized in the brain with more classic neurotransmitters. There is histochemical evidence that CART co-localizes with GABA and cholin acetyl transferase. In this study CART was found in neurons that synthesize catecholamines. This finding provides further support to the role of CART as a neurotransmitter/cotransmitter and can help elucidate its interaction with noradrenergic system

The role of BDNF and HPA axis in the neurobiology of burnout syndrome

Chronic stress is known to affect the HPA axis. The few clinical studies which have been conducted on HPA-axis function in burnout have produced inconsistent results. The etiological relationship between sBDNF and burnout has not yet been studied. The aim of the current study was to investigate the role of BDNF and HPA axis in the neurobiology of burnout. In the current study 37 clinically diagnosed burnout participants were compared with 35 healthy controls in terms of BDNF, HPA axis, burnout symptoms, depression, anxiety and psychosomatic complaints. Basal serum cortisol, sBDNF and cortisol level after 1 mg DST was sampled. We found no significant differences in terms of HPA-axis function (for basal serum cortisol, p =0.592: for cortisol level after I mg DST, p=0.921), but we did find lowered sBDNF levels in burnout group (88.66 +/- 18.15 pg/ml) as compared to healthy controls (102.18 +/- 20.92 pg/ml) and the difference was statistically significant (p=0.005). Logistic Regression Analysis revealed that emotional exhaustion (p=0.05), depersonalization (p=0.005) and depression (p=0.025) were significantly associated with burnout. sBDNF levels correlated negatively with emotional exhaustion (r=-,268, p=0.026), depersonalization (r=-,333, p=0.005) and correlated positively with competence (r=0.293, p=0.015) sub-scales of burnout inventory. However, there were no significant relationships between cortisol levels and sBDNF levels (r=0.80, p=0.51), depression, anxiety, psychosomatic complaints and burnout inventory. Our results suggest that low BDNF might contribute to the neurobiology of burnout syndrome and it seems to be associated with burnout symptoms including altered mood and cognitive functions. (C) 2008 Elsevier Inc. All rights reserved