The effects of experimental brain damage induced by epilepsy model on the behaviour of basal cells in the subventricular zone, olfactory bulb and olfactory mucosa

It is known that neurogenesis continues in two spesific regions of adultmammalian brain, namely the Subventricular zone and that there is a considerableamount of multipotent neural precursors in other parts of adult mammalian brain. Theaim of our study was to establish the behaviours of progenitor cells in theSubventricular zone and basal cells in the olfactory epithelium in a Lithium-Pilocarpinemodel of experimental brain damage. It is determined that damage caused by statusepilepticus increased neurogenesis and that apoptosis played a part in this process. It isknown that intranasal administration of zinc sulphate causes cell death in the receptorneurons of the olfactory epithelium and that basal cells subsequently reproduce anddifferentiate to form new olfactory receptor neurons. We aimed to explore whetherconcurrent stimulation of the cells in the subventricular zone and the progenitor cells ofthe olfactory epithelium caused any changes in comparison to separate stimulation ofeither of them. We found that brain damage induced by epilepsy model increased theneurogenesis in SVZ and that the changes in the olfactory epithelium followingintranasal administration of zinc sulphate were reversible. Understanding themechanisms underlying the increase in neurogenesis following the damage duringadulthood will contribute to the development of new methods that can be used in thetreatment of neurodegenerative diseases.Key words; Status epilepticus, Subventricular zone, Olfactory bulb, adultneurogenesis, zinc sulphate, olfactory epithelium.