Synaptic plasticity refers to alteration of synaptic activity due to activity or experience. Long-term potentiation(LTP), the most common form of synaptic plasticity, is induced by activation of Ca2+-sensitive intracellular kinases, followed by reinstatement of AMPA receptors to membrane by different molecular processes. If transcription factors are added to the molecular process, gene expression and new protein synthesis occur, and induced synaptic activity is maintained for a while. An important mechanism in the controlling of transcription is acetylation/deacetylation of histone proteins. Histone acetyltransferases(HAT) disrupt the histone-DNA interaction by adding acetyl groups to histone proteins, allowing the chromatin structure to relax and transcription factors to reach the promoter regions of genes and activate transcription. Histone de-acetylase(HDAC), which remove the acetyl group from histone proteins on DNA, ensure that DNA is tightly packaged and makes it difficult for transcription factors to reach DNA. Consequently, it is conceivable that the persistence of induced plasticity is accompanied by a histone acetylation that would allow mRNA transcription of associated genes. Histone acetylation/deacetylation imbalances can cause disorders such as depression and neurodegeneration. It has been reported that chronic stress causes depression by reducing SIRT1 activity in mice and impairs LTP in dentate-gyrus(DG). SIRT1 promotes heterochromatin formation by deacetylating histone polypeptides. Therefore, processes that require gene transcription, such as LTP, are expected to evolve with SIRT1 inhibition. Conversely, SIRT1 has also been reported to be required for LTP. The possible effect of SIRT1 on the induction of LTP may be due to histone acetylation by activating ERK signaling pathway rather than deacetylation. Indeed, it is known that increased ERK activity results in induction of LTP. Although there are studies on a functional relationship between SIRT1 and LTP, it is still not fully clarified. Moreover, to the best of our knowledge, there are no studies on the relationship between LTP defect and SIRT1 in rats with experimental depression models. In this project, it was aimed that HAT and HDAC expression were changed in the hippocampus of rats with a depression model induced by corticosterone, and ERK1/2-CREB pathway disorder in the defect of LTP developed due to these changes, the defect in DNA damage and DNA damage repair mechanism were corrected with Sirtuin1(SIRT1) activator "Resveratrol". Experiments will be performed on 2-month-old male-rats. Rats will be divided into five groups as control-group(CG), depression-group(DG), depression+resveratrol group(DRG), depression+fluxetine group(DFG), and resveratrol-group(RG). Puppies born from normal pregnant rats will be separated from their mothers on the PN21 and will be housed in an environment where suitable conditions are provided until they become young-adults(PN60). During this period, development of the rats will be followed by weekly weight measurements, behavioral experiments will be performed on PN60 days for rats to be taken for behavioral experiment, and the rest will be used for electrophysiological experiments at PN60 days without behavioral experiments. Hippocampal DG will be isolated and used in molecular experiments on the PN62 day of the rats with behavioral experiments and at the end of the electrophysiological experiments of other rats. With these experiments; It was aimed to obtain original data about whether the LTP defect can be corrected with Resveratrol as well as the necessity of histone acetylation in the induction of LTP, whether the DNA damage accompanying the LTP defect and the defects in the DNA damage repair mechanism can be corrected with resveratrol in the hippocampus of rats depressed with corticosterone.