Exposure to a traumatic event is required for the diagnosis of posttraumatic stress disorder (PTSD). It was first suggested that PTSD represents a normative response to exposure to extreme stressors, but it soon became evident that only a minority of individuals who experience a traumatic event will develop the disorder. However, the relation between psychopathological events, the phenomenology of the trauma, and neurobiological changes related to PTSD is not totally understood. The symptoms of PTSD are believed to reflect stress-induced changes in neurobiological systems representing an inadequate adaptation of neurobiological systems to exposure to severe stressors. Attempts are made to relate different neurobiological changes to the specific features represented in PTSD. It is not clear whether certain neurobiological changes in PTSD reflect preexisting vulnerability or consequences of trauma exposure. It is known that early life environmental events have persisting effects on central nervous tissue structure and function, a phenomenon called "developmental programming." Further it is knownthat glucocorticoid hormone mediators may be involved in this process. Itwas suggested that changes in the glucocorticoid system are mediated by tissue-specific changes in gene expression. Recent studies suggest that epigenetic mechanisms may play an important role in the interplay between stress exposure and genetic vulnerability. In preclinical studies it was firstsuggested that epigenetic mechanisms may be involved in the modulation ofgene expression in response to stressful stimuli. Recently, epigenetic differences in a neuron-specific glucocorticoid receptor (NR3C1) promoter between postmortem hippocampus obtained from suicide victims with a history ofchildhood abuse and those from either suicide victims with no childhood abuse or controls were found, indicating the involvement of these mechanisms in human adaptation to stress. (Abstract truncated at 2000 characters)
B.04 Guest lecture
COBISS.SI-ID: 27538649Organisation of the Meeting of Slovenian Biochemical Society and Genetic Society of Slovenia with international participation
B.01 Organiser of a scientific meeting
COBISS.SI-ID: 247452672Use of psychoactive substances goes way back in human history. Reasons for individuals or groups that lead to use are complex and versatile, and are combined of many different factors, from social environment to genetic background. Scientific studies of addiction from legal and illegal drugs showed that in the development of addiction are included various factors, which because of their combined effects lead to addiction. For the development of addiction only one factor is not enough, so we assume there has to be a combination of more. Among legal drugs alcohol and nicotine are the most abundant in the world, and among illegal cannabis (Cannabis indica), also known as marijuana. Use of cannabis is because of its effects, relaxation, and euphoria very popular among young, especially men. From the view of social factors is use of cannabis tightly associated with poor education outcome. Beside that it is also linked to increased risk for development of psychiatric disorders, especially schizophrenia. The latter is therefore one of the key reasons for in-depth studies of the cannabis and its active substance on central nervous system.
F.35 Other
COBISS.SI-ID: 29486297Extensive number of different studies, from animal models to clinical and family studies, supports an important role of genetic background and epigenetic factors besides the effects of environmental milieu on the variability of pain response. So far precise mechanisms of pain perception and transmission in the central nervous system have not been fully understood. However, comprehensive data imply that the disinhibition and imbalance of the neurotransmitters serotonin and norepinephrine might play the key roles. Both neurotransmitters have complex pathways, comprised of numerous receptors, autoreceptors, transporters and enzymes. Recently it has been shown that clinically relevant inter-individual differences in pain perception and regulation are importantly influenced by a tri-allelic polymorphism in serotonin transporter gene. In the central nervous system there is another important group of proteins, neurotrophins, that regulate cell growth and survival, differentiation, apoptosis, and cytoskeleton restructuring. Dysregulation of brain-derived neurotrophic factor has been found in individuals with traumatic brain injury and post-traumatic stress disorder, with chronic pain as one of common clinical features. Genomics has a promising potential to contribute to advances in the elucidation of pain mechanisms and control. With modern laboratory techniques that enable identification of candidate genes by linkage mapping, whole-genome association and single gene association studies, genes responsible for different pain disorders could be pointed to in the near future. Knowledge of the genetic factors could further support another important issue – personalized medicine – which could improve efficacy of pain management and lower adverse event profiles.
B.04 Guest lecture
COBISS.SI-ID: 29475801