Hosseini Sayed Masoud, Gholami Pourbadie Hamid, Naderi Nima, Sayyah Mohammad, Zibaii Mohammad Ismail
Department of Pharmacology and Toxicology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran; Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
J Pharmacol Toxicol Methods. 2018 Nov-Dec;94(Pt 1):77-86. doi: 10.1016/j.vascn.2018.06.003. Epub 2018 Jun 12.
The vulnerability of hippocampal formation to ischemic insult has been documented in both humans and animal models. Ischemic injury induction through photothrombosis is an invasive and reproducible model of ischemic stroke which provides the ability to induce ischemia selectively in any desired area. In this study, we describe a method to induce selective unilateral hippocampal ischemia in rat through modified photothrombotic model.
Male wistar rats (n = 66) were subjected to stereotaxic surgery to insert a guide cannula just above the ascending part of hippocampal fissure. After recovery femoral vein was cannulated and rats were mounted in stereotaxic frame to optical fiber insertion in guide cannula and illumination of hippocampal fissure for 25 min. Rose Bengal dye was slowly injected through femoral vein during the first two-minute of illumination. Twenty-four hours later, infarct volume and histological change were evaluated in rat hippocampus. Cognitive function was also evaluated 48 h after ischemia induction.
This procedure caused significant neuronal necrosis and infarct formation in the right hemisphere hippocampus. The infarct size was consisted in different subjects and was paralleled to cognitive impairment. The mean volume of infarction was 6.5% which affected whole right hippocampus and caused significant cognitive impairment compared to sham group (P < 0.001).
The method described in this study provides the ability of selective hippocampal ischemia induction and study of hippocampal injury consequences following ischemia or other neurodegenerative disease that affect hippocampus.
在人类和动物模型中均已证实海马结构对缺血性损伤具有易损性。通过光血栓形成诱导缺血性损伤是一种侵入性且可重复的缺血性中风模型，它能够在任何期望的区域选择性地诱导缺血。在本研究中，我们描述了一种通过改良光血栓形成模型在大鼠中诱导选择性单侧海马缺血的方法。
雄性Wistar大鼠（n = 66）接受立体定向手术，在海马裂上升部分上方插入一根引导套管。恢复后，对股静脉进行插管，将大鼠固定在立体定向框架上，将光纤插入引导套管并对海马裂进行光照25分钟。在光照的前两分钟通过股静脉缓慢注射孟加拉玫瑰红染料。24小时后，评估大鼠海马的梗死体积和组织学变化。在缺血诱导后48小时也评估认知功能。
该操作导致右侧半球海马出现明显的神经元坏死和梗死形成。不同个体的梗死大小有所不同，且与认知障碍平行。梗死的平均体积为6.5%，影响了整个右侧海马，与假手术组相比导致了明显的认知障碍（P < 0.001）。
本研究中描述的方法提供了选择性诱导海马缺血以及研究缺血或其他影响海马的神经退行性疾病后海马损伤后果的能力。
