Investigation of acute inflammatory pain sensitivity among WAG/RİJ epileptic rats with behavioral tests and molecular mechanisms

The common comorbidities epilepsy with pain syndromes including migraine, neuropathic pain and fibromyalgia lead to investigations and discovery of altered pain sensitivity in epilepsy but there is no an information that whether the increased pain sensitivity in epilepsia involves inflammatory pain. The aim of this thesis study was to investigate the acute inflammatory pain sensitivity and its mechanisms in absence epilepsy. Genetic animal model of WAG/Rij rats with epileptic symptoms were used and peripheral inflammation was induced with intraplantar injection of zymosan to hind paw. Acute pain sensitivity was determined at basal conditions and after induction of inflammation by using behavioral pain tests including the thermal pain sensitivity (thermal plantar test) and the mechanical pain sensitivity (electronic von Frey tests). Following behavioral pain tests, the pain related mediators and receptors (transient receptor potential vaniloid 1 (TRPV1), N-methyl-D-aspartate (NMDA R), neurokinin 1 receptor (NK1 receptor) and interleukin 1 beta (IL-1beta)) expression levels in peripheral (dorsal root (DRG) and trigeminal ganglia (TG)) and central pain pathways (reticular thalamic nucleus (RTN), rostral ventromedial medulla (RVMN), periaqueductal grey (PAG) matter and anterior cingulate cortex (ACC)) in the sacrificed animals was investigated by real time polymerase chain reaction. Induction of inflammation caused asignificant decrease in pain threshold in both heat and mechanical stimulated pain. Interleukin 1beta mRNA levels was higher in all tissues except in DRG. TRPV1 mRNA levels was higher in all tissue samples except in RVMN. NK1 receptor was higher in all tissues except TG. The results obtained from this thesis study indicates that increased pain sensitivity was developped in WAG/Rij epileptic rats as a result of peripheral inflammation but does not clarify whether the mechanism of increased pain sensitivity result from mainly from central or peripheral mechanisms. Key Words: Epilepsy, inflammatory pain, pain sensitivity, TRP V1, zymosan