Faculty Collaboration Database

Electroconvulsive shock treatment differentially modulates cortical and subcortical endocannabinoid activity. J Neurochem 2007 Oct;103(1):47-56

Date

06/15/2007

Pubmed ID

17561935

DOI

10.1111/j.1471-4159.2007.04688.x

Scopus ID

2-s2.0-34548648818 (requires institutional sign-in at Scopus site)   45 Citations

Abstract

Previous studies indicate that the endocannabinoid system is a potential target for the treatment of depression. To further examine this question we assessed the effects of electroconvulsive shock (ECS) treatment, both a single session and 10 daily sessions, on endocannabinoid content, CB(1) receptor binding parameters and CB(1) receptor-mediated [(35)S]GTPgammaS binding in the prefrontal cortex, hippocampus, hypothalamus and amygdala. A single ECS session resulted in a general reduction in the binding affinity of the CB(1) receptor in all brain regions examined, as well as reductions in N-arachidonylethanolamine (anandamide) content in the prefrontal cortex and the hippocampus, reduced hydrolysis of anandamide by fatty acid amide hydrolase (FAAH) in the prefrontal cortex and an increase in the binding site density of the CB(1) receptor in the amygdala. Following 10 ECS sessions, all these effects subsided except for the reductions in anandamide content in the prefrontal cortex, which increased in magnitude, as well as the reductions in FAAH activity in the prefrontal cortex. Additionally, repeated ECS treatment resulted in a significant reduction in the binding site density of the CB(1) receptor in the prefrontal cortex, but did not alter CB(1) receptor-mediated [(35)S]GTPgammaS binding. Repeated ECS treatment also significantly enhanced the sensitivity of CB(1) receptor-mediated [(35)S]GTPgammaS binding in the amygdala. Collectively, these data demonstrate that ECS treatment results in a down-regulation of cortical and an up-regulation of subcortical endocannabinoid activity, illustrating the possibility that the role of the endocannabinoid system in affective illness may be both complex and regionally specific.

Author List

Hill MN, Barr AM, Ho WS, Carrier EJ, Gorzalka BB, Hillard CJ

Author

Cecilia J. Hillard PhD Associate Dean, Center Director, Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Amidohydrolases
Amygdala
Animals
Arachidonic Acids
Binding Sites
Cannabinoid Receptor Modulators
Cerebral Cortex
Down-Regulation
Electroshock
Endocannabinoids
Enzyme Activation
Guanosine 5'-O-(3-Thiotriphosphate)
Hippocampus
Hypothalamus
Male
Polyunsaturated Alkamides
Prefrontal Cortex
Rats
Rats, Sprague-Dawley
Receptor, Cannabinoid, CB1
Up-Regulation