G-Csf Improved the Memory and Dendritic Morphology Impairments in the Hippocampal Ca1 Pyramidal Neurons After Brain Ischemia in the Male Rats Publisher Pubmed



Sarkala HB^{1, 2} ; Jahanshahi M³ ; Dolatabadi LK^{4, 5} ; Namavar MR^{1, 6, 7}
Source: Metabolic Brain Disease Published:2023

Abstract

Background: Stroke remains the leading cause of death and disability in the world. A new potential treatment for stroke is the granulocyte colony-stimulating factor (G-CSF), which exerts neuroprotective effects through multiple mechanisms. Memory impairment is the most common cognitive problem after a stroke. The suggested treatment for memory impairments is cognitive rehabilitation, which is often ineffective. The hippocampus plays an important role in memory formation. This project aimed to study the effect of G-CSF on memory and dendritic morphology of hippocampal CA1 pyramidal neurons after middle cerebral artery occlusion (MCAO)in rats. Methods: Male Sprague-Dawley rats were divided into three groups: the sham, control (MCAO + Vehicle), and treatment (MCAO + G-CSF) groups. G-CSF (50 µg/kg S.C) was administered at 6, 24, and 48 h after brain ischemia induction. The passive avoidance task to evaluate learning and memory was performed on days 6 and 7 post-ischemia. Seven days after MCAO, the brain was removed and the hippocampal slices were stained with Golgi. After that, the neurons were analyzed for dendritic morphology and maturity. Outcomes: The data showed that stroke was associated with a significant impairment in the acquisition and retention of passive avoidance tasks, while the G-CSF improved learning and memory loss. The dendritic length, arborization, spine density, and mature spines of the hippocampus CA1 neurons were significantly reduced in the control group, and treatment with G-CSF significantly increased these parameters. Conclusion: G-CSF, even with three doses, improved learning and memory deficits, and dendritic morphological changes in the CA1 hippocampal neurons resulted from brain ischemia. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.