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Involvement of the Serotonergic System of the Ventral Hippocampus (Ca3) on Amnesia Induced by Acpa in Mice Publisher Pubmed



Nasehi M1 ; Kafi F2 ; Khakpai F3 ; Zarrindast MR1, 3, 4, 5
Authors
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Authors Affiliations
  1. 1. Cognitive and Neuroscience Research Center (CNRC), Medical Genomics Research Center and School of Advanced Sciences in Medicine, Islamic Azad University, Tehran Medical Sciences Branch, Tehran, Iran
  2. 2. Department of Biology, Faculty of Basic Sciences, Tarbiat Moalem (Kharazmi) University, Tehran, Iran
  3. 3. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  4. 4. Department of Pharmacology and Iranian National Center for Addiction Studies, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), P.O. Box 13145-784, Tehran, Iran

Source: Behavioural Brain Research Published:2015


Abstract

Interactions between the cannabinoid and serotonin systems have been reported in many studies. In the present study, we investigated the influence of the serotonergic receptor agents on amnesia induced by the cannabinoid CB1 receptor agonist, arachydonilcyclopropylamide (ACPA). Bilateral guide-cannulae were implanted to allow intra-CA3 microinjection of the drugs. The results showed that the intra-peritoneal (i.p.) injection of ACPA induce amnesia but did not alter head dip latency, head dip counts, and locomotion. Moreover, intra-CA3 injection of M-Chlorophenylbiguanide (M-CHL, a 5-HT3 serotonin receptor agonist), Y-25130 (a 5-HT3 serotonin receptor antagonist), RS67333 (a 5-HT4 serotonin receptor agonist), and RS23597-190 (a 5-HT4 serotonin receptor antagonist) impaired memory but have no effect on head dip latency and locomotor activity. In addition, intra-CA3 injection of Y-25130, RS67333, and RS23597-190 heighten the ACPA-induced amnesia and head dip counts while did not alter head dip latency and locomotor activity. On the other hand, intra-CA3 microinjection of M-CHL could not modify the ACPA-induced amnesia, head dip latency and locomotor activity whereas increased head dip counts. It can be concluded that the amnesia induced by i.p. administration of ACPA is at least partly mediated through the serotonergic receptor mechanism in the CA3 area. © 2015 Elsevier B.V.
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