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Effects of Precondition Α2-Adrenoceptor Agents on Memory- and Anxiety-Related Processes in the Transient Cerebral Ischemic Rats Publisher Pubmed



Nasehi M1 ; Imani E2 ; Ebrahimighiri M3 ; Sabourikhanghah V2 ; Zarrindast MR2, 4, 5, 6
Authors
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Authors Affiliations
  1. 1. Cognitive and Neuroscience Research Center (CNRC), Amir-Almomenin Hospital, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
  2. 2. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  3. 3. Department of Biology, Faculty of Sciences, University of Zanjan, Zanjan, Iran
  4. 4. Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, P.O.Box 13145-784, Tehran, Iran
  5. 5. Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Neuroendocrinology, Endocrinology, and Metabolism Research Institute, Tehran University of Medical Sciences, Tehran, Iran

Source: Naunyn-Schmiedeberg's Archives of Pharmacology Published:2020


Abstract

Neurological evidence for the neuroprotective function of α2-adrenoceptors in the cerebral ischemia is inconsistent. It is not examined how pretreatment with a single dose of α2-adrenoceptor agents can affect motor function and anxiety- and memory-related responses in the cerebral ischemic animals. The transient forebrain ischemia model was provided, using a bilateral common carotid arterial occlusion (two-vessel occlusion, 2VO) in male Wistar rats. The 2VO rats impaired motor functions in the Rota-rod and wire grip tests and also decreased the step-through latency and the percentage of time spent on the open arms (%OAT), the percentage of entries into the open arms (%OAE) as well as locomotion in the elevated plus maze (EPM), indicating a memory deficit and anxiety-like behavior. Intraperitoneal single administration of yohimbine (0, 0.001, 0.01, and 0.1 mg/kg) before the 2VO did not alter these parameters while the higher and middle doses of clonidine (0.01 and 0.1 mg/kg) prevented the memory deficit and hypo-locomotion and its middle dose abrogated Rota-rod dysfunction and anxiety-like response. Meanwhile, both drugs did not influence on the measured behaviors in the sham groups by themselves. Moreover, yohimbine (0.001 mg/kg) abolished the beneficial effects of clonidine (0.01 and 0.1 mg/kg) on motor function in the Rota-rod and memory retention and also at its middle dose on the %OAT and locomotion in the 2VO rats. Our findings show a neuroprotective role for clonidine in motor function and memory- and anxiety-related behaviors of 2VO rats and the importance of α2-adrenoceptors in these processes. © 2019, Springer-Verlag GmbH Germany, part of Springer Nature.