Omega-3 polyunsaturated fatty acids (PUFA) are critical for optimal brain health and are involved in psychiatric and neurological ailments. Here, we report the effects of higher endogenous omega-3 PUFA on memory impairment in the hippocampus by studying mice with transgenic expression of the fat-1 gene that converts omega-6 to omega-3 PUFA. We performed Y-maze and passive avoidance tests to evaluate the memory function of fat-1 mice treated with scopolamine. Fat-1 mice showed induced alternation in the Y-maze test and increased latency in the passive avoidance test. The effects of scopolamine on hippocampal neurogenesis were confirmed by increases in the number of Ki-67- and DCX-positive cells in the fat-1 mice. Western blotting revealed increased brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element-binding protein levels, and lower scopolamine-induced apoptosis based on the cleaved-caspase 3 protein level in fat-1 mice. These findings suggest that higher endogenous omega-3 PUFA prevented granular cell loss, increased BDNF signaling, and decreased apoptosis signaling in scopolamine-treated fat-1 mice. These processes may underlie granular cell survival and suggest potential therapeutic targets for memory impairment.

Omega-3多不饱和脂肪酸（PUFA）对于最佳的大脑健康至关重要，并涉及精神病和神经病。在这里，我们通过研究具有将omega-6 PUFA转化为Omega-6 PUFA的fat-1基因的转基因表达的小鼠，来报告高内源性Omega-3 PUFA对海马体记忆障碍的影响。我们进行了Y迷宫和被动回避测试，以评估用东pol碱治疗的fat-1小鼠的记忆功能。Fat-1小鼠在Y迷宫测试中显示出诱导的交替，在被动回避测试中显示出增加的潜伏期。脂肪1中Ki-67和DCX阳性细胞数量的增加证实了东pol碱对海马神经发生的影响老鼠。Western印迹显示，脂肪-1小鼠中裂解的胱天蛋白酶3蛋白水平提高了脑源性神经营养因子（BDNF）和磷酸化的cAMP反应元件结合蛋白水平，并降低了东-碱诱导的凋亡。这些发现表明，在东pol碱治疗的fat-1小鼠中，较高的内源性omega-3 PUFA可以防止颗粒细胞丢失，增加BDNF信号传导并减少凋亡信号传导。这些过程可能是颗粒细胞存活的基础，并提出了记忆障碍的潜在治疗靶标。