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Changes in the cannabinoids receptors in rats following treatment with antidepressants.

Authors :
Smaga I
Zaniewska M
Gawliński D
Faron-Górecka A
Szafrański P
Cegła M
Filip M
Source :
Neurotoxicology [Neurotoxicology] 2017 Dec; Vol. 63, pp. 13-20. Date of Electronic Publication: 2017 Sep 01.
Publication Year :
2017

Abstract

The endocannabinoid (eCB) system plays a significant role in the pathophysiology of depression. The potential participation of this system in the mechanism of action of antidepressants has been highlighted in recent years. The aim of this study was to investigate the expression of cannabinoid (CB) receptors using Western blot and CB <subscript>1</subscript> receptor density using autoradiography after acute or chronic administration of antidepressant drugs [imipramine (IMI, 15mg/kg), escitalopram (ESC, 10mg/kg) and tianeptine (TIA, 10mg/kg)]. Antidepressants given chronically elevated CB <subscript>1</subscript> receptor density in the cortical structures and hippocampal areas, while a decrease of CB <subscript>1</subscript> receptor density was observed in the striatum after IMI and ESC treatment. The CB <subscript>1</subscript> receptor expression decreases in the dorsal striatum after chronic administration of IMI and ESC or the receptor rise in the hippocampus after chronic ESC and TIA treatment were confirmed using Western blot analyses. An increase in the CB <subscript>2</subscript> receptor expression was observed in the cortical structures and hippocampus after chronic administration of ESC and TIA, while a decrease in this expression was noted in the striatum and cerebellum after chronic IMI treatment. Our results provide clear evidence that the antidepressant exposures provoke some modulations within the eCB system through CB receptors.<br /> (Copyright © 2017 Elsevier B.V. All rights reserved.)

Details

Language :
English
ISSN :
1872-9711
Volume :
63
Database :
MEDLINE
Journal :
Neurotoxicology
Publication Type :
Academic Journal
Accession number :
28866072
Full Text :
https://doi.org/10.1016/j.neuro.2017.08.012