P86 | THE EFFECTS OF NICOTINIC ACETYLCHOLINE RECEPTOR INHIBITION ON THE EXPRESSION OF BRAIN DERIVED NEUROTROPHIC FACTOR IN THE OLFACTORY BULB ORGANOTYPIC SLICE CULTURES

I. Atasoy¹, S. Yilmazer², D. Gezen Ak³, E. Dursun³ | ¹Medical Biology Department, İstabul University-Cerrahpasa Faculty of Medicine Istanbul, Türkiye; ²Department of Medical Biology Halic University, Faculty of Medicine, Istanbul, Türkiye; ³Brain and Neurodegenerative Disorders Research Laboratories, Department of Neuroscience, Institute of Neurological Sciences, Istanbul University-Cerrahpasa, Istanbul, Türkiye

Olfactory bulb (OB) exhibits high levels of nicotinic acetylcholine receptor (nAChR) expression and receive strong cholinergic input from the basal forebrain. Acetylcholine is important modulator in olfactory related memory. It has been suggested that Ach and nicotinic acetylcholine receptor may have an important role in odor discrimination and modulation of smell memory. Demonstration of the role of BDNF signaling in olfactory bulb neurogenesis provided the first link between disruptions in neurotrophin signaling and olfactory behavioural performance. Impaired olfactory function appears to be one of the earliest detectable functional alterations in Alzheimer disease^1,2. Methods In the study; organotypic olfactory bulb slice cultures, which allows to obtain results closest to in vivo models by protecting tissue architecture and microenvironment were generated. Specific nAChR a7 antagonist methylcaconitine (MLA) was applied to the organotypic slices. Effects of these treatments on Brain derived neurotrophic factor (BDNF) and nAChR a7 receptor expressions, were determined at protein level by Western blot method. Regional localizations of these proteins in the olfactory bulb were also examined by immunofluorescence method. Results it was shown that the application of MLA, caused a decrease in nAChR α7 expression in the olfactory bulb. Low-dose MLA application in olfactory bulb, caused a decrease in BDNF protein levels at the early period. Our findings indicate that Acetylcholine through its receptor could have direct or indirect outcome on synaptic plasticity by regulating protein expression levels of nAChR a7 and BDNF by a dose and time dependent manner. Our immunohistochemical results showed that nAChR α7 is concentrated in the glomerular layer, outer plexiform and inner plexiform layers in the olfactory bulb. BDNF is located in the olfactory neuron layer and glomerular layer. Conclusion: Our results indicated that cholinergic activity through nAChR α7 receptor may contribute to the maintenance of synaptic plasticity in the olfactory bulb.