Optimization of intracerebroventricular streptozotocin dose for the induction of neuroinflammation and memory impairment
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ORIGINAL ARTICLE
Optimization of intracerebroventricular streptozotocin dose for the induction of neuroinflammation and memory impairments in rats Rupsa Ghosh 1 & Susmita Sil 1,2 & Pritha Gupta 1 & Tusharkanti Ghosh 1 Received: 17 June 2019 / Accepted: 12 June 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Intracerebroventricular (ICV) injection of streptozotocin (STZ) is a well established procedure to induce neuroinflammation leading to dementia in experimental animals. However, the optimal dose of STZ has not been determined. In the present study, rats were ICV injected with 1.5, 3 and 6 mg of STZ per kg of body weight. After 21 days, neuroinflammatory markers i.e. TNF-α, IL-1β, ROS and nitrite were quantified in the hippocampus. Memory function was assessed by the radial arm maze test after 9, 12, 15, 18, 21 days following STZ injection. STZ treatment significantly increased neuroinflammatory markers and decreased memory functions in a dose dependent manner showing optimum effects at the dose of 3 mg/kg. Keywords Streptozotocin . Neuroinflammation . Memory . Intracerebroventricular injection . Doses
Abbreviations AD Alzheimer’s Disease sAD sporadic Alzheimer’s Disease ICV intracerebroventricular STZ streptozotocin STZ-ER intracerebroventricular streptozotocin injected experimental rats TNF – α Tumor Necrosis Factor – α IL-1β Interleukin − 1β ROS Reactive oxygen species WME Working Memory Error RME Referrence Memory Error
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11011-020-00588-1) contains supplementary material, which is available to authorized users. * Tusharkanti Ghosh [email protected] 1
Neurophysiology Laboratory, Department of Physiology, University College of Science and Technology, University of Calcutta, 92, Acharya Prafulla Chandra Road, West Bengal 700 009 Kolkata, India
2
Present address: Department of Pharmacology and Experimental, Neuroscience, University of Nebraska Medical Center, Omaha, NE, USA
Introduction Rodent models have notably contributed to elucidate the underlying mechanisms of Alzheimer’s disease (AD), the leading causes of dementia in the world (Neha et al. 2014). The pathogenesis of AD is complex and the mechanism of neurodegeneration is disparate in different AD patients (Chetelat 2013). In comparison to the familial AD type (2–5% of total AD patients), sporadic AD (sAD) constitutes over 90% of total AD population (Blennow et al. 2006). Very little is known about the mechanism of neurodegeneration in sAD (Kamat et al. 2016). Although the “Amyloid cascade” hypothesis supports the neurodegeneration process in familial AD but it fails to explain the pathophysiological mechanisms in the sporadic type (Chetelat 2013). The sporadic AD has been explained by different investigators on the basis of oxidativenitrosative stress (Reeta et al. 2017), neuroinflammation (Nazem et al. 2015) and impaired energy metabolism (Grieb 2016). The decreased ability of brain tissue to metabolize glucos
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