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Endocannabinoids affect neurological and cognitive function in thioacetamide-induced hepatic encephalopathy in mice.

Abstract：

:Endocannabinoids function as neurotransmitters and neuromodulators in the central nervous system via specific receptors and apparently have a neuroprotective role. We assumed that the endocannabinoid system could be involved in the pathogenesis of hepatic encephalopathy (HE), a neuropsychiatric syndrome due to liver disease. We used a mouse model of a thioacetamide induced fulminant hepatic failure. We found that the levels of the endocannabinoid 2-arachidonoyl-glycerol (2-AG) were elevated in the brain. Treatment with either 2-AG or with the CB1 receptor antagonist, SR141716A, improved a neurological score, activity and cognitive function. Activation of the CB2 receptor by a selective agonist, HU308, also improved the neurological score. 2-AG activity could be blocked with the specific CB2 receptor antagonist SR144528A. The CB1 receptor agonist noladin ether was inactive. We conclude that the endocannabinoid system may play an important role in the pathogenesis of HE. Modulation of this system either by exogenous agonists specific for the CB2 receptors or possibly also by antagonists to the CB1 receptors may have therapeutic potential.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Avraham Y,Israeli E,Gabbay E,Okun A,Zolotarev O,Silberman I,Ganzburg V,Dagon Y,Magen I,Vorobia L,Pappo O,Mechoulam R,Ilan Y,Berry EM

doi

10.1016/j.nbd.2005.07.008

keywords:

subject

Has Abstract

pub_date

2006-01-01 00:00:00

pages

237-45

issue

1

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(05)00206-8

journal_volume

21

pub_type

杂志文章

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