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Behav Brain Res. 2015 Jun 1;286:356-63. doi: 10.1016/j.bbr.2015.03.011. Epub 2015 Mar 11.

Involvement of the serotonergic system of the ventral hippocampus (CA3) on amnesia induced by ACPA in mice.

Author information

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. Electronic address: Nasehi@iricss.org.
2
Department of Biology, Faculty of Basic Sciences, Tarbiat Moalem (Kharazmi) University, Tehran, Iran.
3
Institute for Cognitive Science Studies (ICSS), Tehran, Iran.
4
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; Institute for Cognitive Science Studies (ICSS), Tehran, Iran; Department of Pharmacology and Iranian National Center for Addiction Studies, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), P.O. Box 13145-784, Tehran, Iran. Electronic address: zarinmr@ams.ac.ir.

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.

KEYWORDS:

ACPA; CA3; Memory; Mice; Serotonin

PMID:
25771207
DOI:
10.1016/j.bbr.2015.03.011
[Indexed for MEDLINE]

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