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Deletion of CB 2 cannabinoid receptors reduces synaptic transmission and long‐term potentiation in the mouse hippocampus
Author(s) -
Li Yong,
Kim Jimok
Publication year - 2016
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.22558
Subject(s) - long term potentiation , neuroscience , cannabinoid receptor , synaptic plasticity , long term depression , cannabinoid receptor type 2 , neurotransmission , cannabinoid , receptor , gpr18 , hippocampus , dendritic spine , endocannabinoid system , biology , chemistry , hippocampal formation , ampa receptor , agonist , glutamate receptor , biochemistry
The effects of cannabinoids are mostly mediated by two types of cannabinoid receptors—CB1 receptors in the nervous system and CB2 receptors in the immune system. However, CB2 cannabinoid receptors have recently been discovered in the brain and also implicated in neurophysiological functions. The deletion of CB2 receptors in mice induces long‐term memory deficits and schizophrenia‐like behaviors, implying that endogenous activity of CB2 receptors might be involved in neuropsychiatric effects. Little is known about the cellular mechanisms by which physiological activation of CB2 receptors modulates neuronal functions. We aimed to determine how deletion of CB2 receptors in mice affects synaptic transmission and plasticity. Electrophysiological and morphological studies indicated that CB2 receptor knockout resulted in decreases in excitatory synaptic transmission, long‐term potentiation, and dendritic spine density in the hippocampus. Our data imply that endogenous activity of CB2 receptors might contribute to the maintenance of synaptic functions and the expression of normal long‐term potentiation. This study provides insights into the role of CB2 cannabinoid receptors in regulating cognitive functions such as long‐term memory. © 2016 Wiley Periodicals, Inc.