|M.Sc Student||Gaitner Michal|
|Subject||Effect of Traumatic Brain Injury and the Glutamergic System|
on Peripheral Benzodiazepine Receptor
|Department||Department of Medicine||Supervisor||Professor Emeritus Moshe Gavish|
Peripheral-type benzodiazepine receptors (PBR) are widely expressed throughout the body, yet different tissues exhibit different paterns of PBR expression. The PBR are genetically conserved from bacteria to man, and are heterodimers composed of three subunits: an isoquinoline carboxamide binding protein (IBP, 18kDa), a voltage-dependent anion channel (VDAC, 32 kDa), and an adenine nucleotide transporter (ANT, 30kDa).
In the present study we have investigated the relative importance of PBR in (TBI) combined with hyperbaric oxygen treatment (HBO) in vivo, and Abeta/glutamate induced apoptosis, in vitro.
The purpose of the in vivo study was to investigate whether PBR may play a role in traumatic brain injury and to evaluate the value of hyperbaric oxygen therapy in treatment of that damage. For this study Sprague -Dawley rats were divided into three groups: (1) sham operated controls, (2) injury alone, (3) injury and HBO. Injured area, hippocampus, hypothalamus, cortex, adrenal and kidney were dissected. Significant increase in PBR expression was observed after TBI in injured area, whereas HBO therapy didn’t show any significant effect. Hippocampus and cortex showed decline in IBP after TBI, while hypothalamus, adrenal, kidney didn't show any significant alterations. In our in vitro study we attempted to investigate the role of IBP in Abeta/glutamate induced apoptosis, using IBP knock out (K.O.) C6 glioma cell lines. Reduced sensitivity to both neurotoxic agents (Abeta, glutamate) was observed in IBP K.O. clones. This decreased sensitivity might indicate the IBPs involvement in Abeta/glutamate induced apoptosis in brain tissue.