Kooshki Razieh, Anaeigoudari Akbar, Abbasnejad Mehdi, Askari-Zahabi Khadijeh, Esmaeili-Mahani Saeed
Department of Biology, Faculty of Sciences, Lorestan University, Khorramabad, Iran.
Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran.
Avicenna J Phytomed. 2021 May-Jun;11(3):247-257.
This study intended to evaluate if central administration of abscisic acid (ABA) alone or in combination with GW9662, a peroxisome proliferator-activated receptor γ (PPAR-γ) antagonist, could modulate learning and memory as well as hippocampal synaptic plasticity in a rat model of streptozotocin (STZ)-induced diabetes.
Intraperitoneal injection of STZ (65 mg/kg) was used to induce diabetes. Diabetic rats were than treated with intracerebroventricular (i.c.v.) administration of ABA (10, 15 and 20 µg/rat), GW9662 (3 µg/rat) or GW9662 (3 µg/rat) plus ABA (20 µg/rat). Animals' spatial and passive avoidance learning and memory performances were assessed by Morris water maze (MWM) and shuttle box tasks, respectively. Further, electrophysiological field recordings were assessed in the CA1 region.
STZ diabetic rats showed diminished learning and memory in both MWM and shuttle box tasks. The STZ-induced memory deficits were attenuated by central infusion of ABA (10 and 20 µg/rat). Besides, STZ injection impaired long-term potentiation induction in CA1 neurons that was attenuated by ABA at 20 μg/rat. Central administration of GW9662 (3 µg/rat) alone did not modify STZ-induced spatial and passive avoidance learning and memory performances of rats. Further, GW9662 prevented ABA capacity to restore learning and memory in behavioral and electrophysiology trials.
Altogether, ABA ameliorates cognitive deficits in rats via activation of PPAR-γ receptor in diabetic rats.
本研究旨在评估单独脑室内注射脱落酸（ABA）或联合过氧化物酶体增殖物激活受体γ（PPAR-γ）拮抗剂GW9662，是否能调节链脲佐菌素（STZ）诱导的糖尿病大鼠模型的学习记忆及海马突触可塑性。
腹腔注射STZ（65mg/kg）诱导糖尿病。糖尿病大鼠随后接受脑室内注射ABA（10、15和20μg/只）、GW9662（3μg/只）或GW9662（3μg/只）加ABA（20μg/只）治疗。分别通过莫里斯水迷宫（MWM）和穿梭箱任务评估动物的空间及被动回避学习记忆能力。此外，在CA1区进行电生理场记录评估。
STZ糖尿病大鼠在MWM和穿梭箱任务中的学习记忆能力均下降。脑室内注射ABA（10和20μg/只）可减轻STZ诱导的记忆缺陷。此外，STZ注射损害了CA1神经元的长时程增强诱导，而20μg/只的ABA可减轻这种损害。单独脑室内注射GW9662（3μg/只）未改变STZ诱导的大鼠空间及被动回避学习记忆能力。此外，在行为学和电生理学实验中，GW9662阻止了ABA恢复学习记忆的能力。
总之，ABA通过激活糖尿病大鼠的PPAR-γ受体改善大鼠的认知缺陷。
