2-B-O04-4 〇鹿内 浩樹^1,2、進藤 つぐみ¹、尾崎 和音¹、大橋 敦子¹、大塚 郁夫³、菱本 明豊³、泉 剛^1,2 Hiroki Shikanai^1,2, Tsugumi Shindo¹, Kazune Ozaki¹, Atsuko Ohashi¹, Ikuo Otsuka³, Akitoyo Hishimoto³, Takeshi Izumi^{1,2 1}北海道医療大・薬、²北海道医療大・先端研究推進センター、³神戸大・院医・精神医学分野 ¹Dept. Pharmacol., Fac. Pharmaceut. Sci., Health Sci. Univ. Hokkaido, ²Adv. Res. Promotion Ctr., Health Sci. Univ. Hokkaido, ³Dept. Psychiatry, Kobe Univ. Grad., Sch., Medicine Telomere length is one of the key components of cell lifespan and is maintained by the telomerase reverse transcriptase (TERT), an elongation enzyme for telomere. Increased TERT activity has been reported in cancer cells, while abnormal shortening of telomere length has been reported in several diseases such as diabetes and hypertension. We also reported an abnormal shortening of telomere length in the blood and brain of suicide victims. In this study, we investigated the relationship between depression and brain telomeres using an animal model of depression. We evaluated adult rats exposed to juvenile stress as an animal model of depression. Model rats showed prolonged immobility time in the forced swimming test. Abnormal shortening of telomere length was observed in the medial prefrontal cortex and dorsal hippocampus of model rats. TERT was significantly decreased in the hippocampus of model rats. Shortening of telomere length and decrease of TERT in the hippocampus of model rats were restored by repeated administration of escitalopram. Furthermore, we found abnormal signaling of GSK3β and β-catenin, which are depression-related genes and transcriptional regulators of TERT, in the hippocampus of model rats. These results provide novel pathophysiological insights into depression.