NDLI: Alterations of endocannabinoid signaling, synaptic plasticity, learning and memory in monoacylglycerol lipase knockout mice

Content Provider	PubMed Central
Author	Pan, Bin Wang, Wei Zhong, Peng Blankman, Jacqueline L. Cravatt, Benjamin F. Liu, Qing-song
Abstract	Endocannabinoid (eCB) signaling is tightly regulated by eCB biosynthetic and degradative enzymes. The eCB 2-arachidonoylglycerol (2-AG) is hydrolyzed primarily by monoacylglycerol lipase (MAGL). Here, we investigated whether eCB signaling, synaptic function and behavior were altered in MAGL knockout mice. We report that MAGL−/− mice exhibited prolonged depolarization-induced suppression of inhibition (DSI) in hippocampal CA1 pyramidal neurons, providing genetic evidence that the inactivation of 2-AG by MAGL determines the time course of the eCB-mediated retrograde synaptic depression. CB1 receptor antagonists enhanced basal inhibitory postsynaptic currents (IPSCs) in CA1 pyramidal neurons in MAGL−/− mice, while the magnitude of DSI or CB1 receptor agonist-induced depression of IPSCs was decreased in MAGL−/− mice. These results suggest that 2-AG elevations in MAGL−/− mice cause tonic activation of and partial desensitization of CB1 receptors. Genetic deletion of MAGL selectively enhanced theta burst stimulation (TBS)-induced long-term potentiation (LTP) in the CA1 region of hippocampal slices but had no significant effect on LTP induced by high-frequency stimulation or long-term depression induced by low-frequency stimulation. The enhancement of TBS-LTP in MAGL−/− mice appears to be mediated by 2-AG-induced suppression of GABAA receptor-mediated inhibition. MAGL−/− mice exhibited enhanced learning as shown by improved performance in novel object recognition and Morris water maze. These results indicate that genetic deletion of MAGL causes profound changes in eCB signaling, long-term synaptic plasticity and learning behavior.
Related Links	http://dx.doi.org/10.1523/jneurosci.2075-11.2011
Ending Page	13430
Page Count	11
Starting Page	13420
File Format	PDF
ISSN	02706474
e-ISSN	15292401
Journal	The Journal of Neuroscience
Issue Number	38
Volume Number	31
Language	English
Publisher Date	2011-09-21
Access Restriction	Open
Subject Keyword	Neuroscience(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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