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Jahanmahin A, Abbasnejad Z, Haghparast A, Ahmadiani A, Ghasemi R. Intrahippocampal insulin injection does not prevent against scopolamine-induced spatial memory impairment and ERK alteration. BCN. 2017;
URL: http://bcn.iums.ac.ir/article-1-1096-en.html
1- Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2- Department of Physiology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3- PhD Department of Physiology and neurophysiology research center, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abstract:  
It is well documented that insulin has neuroprotective and neuromodulator effects and could protect against different models of memory loss. Furthermore, cholinergic activity plays a significant role in memory and scopolamine induced memory loss is widely used as an experimental model of dementia. In current study we investigated the possible effects of insulin against scopolamine induced memory impairment in wistar rat and its underlying molecular mechanisms. Accordingly, animals were bilaterally cannulated in CA1, hippocampus. Intra-hippocampal administration of insulin 6MU and 12MU CA1/day was done during first 6days after surgery. During next four days animal’s spatial learning and memory was assessed in Morris water maze test (three days of learning and one day of retention test). The animals received scopolamine (1 mg/kg/ip) 30min before the onset of behavioural tests in each day. In the last day, the hippocampi were dissected and the levels of MAPK and Caspase-3 activation were analyzed by western blot. Our behavioural results showed that scopolamine impaired spatial learning and memory without activating casapase-3, P38 and JNK, but chronic pre-treatment by both doses of insulin was unable to restore this spatial memory impairment. In addition, scopolamine caused a significant reduction in ERK activity and insulin was unable to restore this reduction. Results disclosed that scopolamine mediated memory loss is not associated with hippocampal damage. Therefore, insulin as a neuroprotective agent could not restore memory when there is no hippocampal damage, in addition, the neuromodulator effects of insulin is not potent enough to overwhelm scopolamine-mediated disruptions of synaptic neurotransmission.
 
Type of Study: Original | Subject: Behavioral Neuroscience
Received: 2017/12/19 | Accepted: 2018/03/6 | Published: 2018/05/13

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