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The Effect of Ca1 Α2 Adrenergic Receptors on Memory Retention Deficit Induced by Total Sleep Deprivation and the Reversal of Circadian Rhythm in a Rat Model Publisher Pubmed



Norozpour Y1, 2 ; Nasehi M3 ; Sabourikhanghah V1 ; Torabinami M4, 5 ; Zarrindast MR1, 3, 6, 7, 8, 9
Authors
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Authors Affiliations
  1. 1. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  2. 2. Sadra Cognitive Science Institute, Tehran, Iran
  3. 3. Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
  4. 4. Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran
  5. 5. Shiraz Neuroscience Research Center (SNRC), Shiraz University of Medical Sciences, Shiraz, Iran
  6. 6. Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran
  7. 7. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran
  8. 8. Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  9. 9. Medical Genomics Research Center, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran

Source: Neurobiology of Learning and Memory Published:2016


Abstract

The α2 adrenergic receptors which abundantly express in the CA1 region of the hippocampus play an important role in the regulation of sleep and memory retention processes. Based on the available evidence, the aim of our study was to investigate consequences of the activation and deactivation of CA1 α2 adrenergic receptors (by clonidine and yohimbine, respectively) on the impairment of memory retention induced by total sleep deprivation (TSD) and the reversal of circadian rhythm (RCR) in a rat model. To this end, the water box apparatus and passive avoidance task were in turn used to induce sleep deprivation and assess memory retention. Our findings suggested that TSD (for 24 and 36, but not 12 h) and RCR (12 h/day for 3 consecutive days) impair memory function. The post-training intra-CA1 administration of yohimbine (α2 adrenergic receptor antagonist) on its own, at the dose of 0.1 μg/rat, decreased the step-through latency and locomotor activity in the TSD- sham treated but not undisturbed sleep rats. Unlike yohimbine, clonidine (α2 adrenergic receptor agonist), in all applied doses (0.001, 0.01 and 0.1 μg/rat), failed to induce such an effect. While the subthreshold dose of yohimbine (0.001 μg/rat) abrogated the impairment of memory retention induced by the 24-h TSD, it could potentiate the impairment of memory retention induced by 36-h TSD, suggesting the modulatory effect of yohimbine. Moreover, the subthreshold dose of clonidine (0.1 μg/rat) restored the memory retention deficit in TSD rats (24 and 36 h). On the other hand, the subthreshold dose of clonidine (0.1 μg/rat), but not yohimbine (0.001 μg/rat) restored the memory retention deficit in RCR rats. Such interventions however did not alter the locomotor activity. The above observations proposed that CA1 α2 adrenergic receptors play a potential role in memory retention deficits induced by TSD and RCR. © 2016 .
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