Control of synaptic function by endocannabinoid-mediated retrograde signaling

Since the first reports in 2001, great advances have been made towards the understanding of endocannabinoid-mediated synaptic modulation. Electrophysiological studies have revealed that one of the two major endocannabinoids, 2-arachidonoylglycerol (2-AG), is produced from membrane lipids upon postsy...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the Japan Academy Series B, 2014/07/31, Vol.90(7), pp.235-250
Main Author: KANO, Masanobu
Format: Article
Language:English
Subjects:
2-arachidonylglycerol
anandamide
Animals
Brain
Brain - metabolism
Calcium Signaling - physiology
cannabinoid receptor
Cannabinoids
Cellular signal transduction
endocannabinoid
Endocannabinoids - metabolism
GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism
Health aspects
Humans
Long-Term Synaptic Depression - physiology
Neural transmission
Neurological research
Neurons - metabolism
Neuroses
Neurotransmitters
Receptors, G-Protein-Coupled - metabolism
retrograde signaling
Review
synapse
Synaptic Transmission - physiology
TRPV Cation Channels - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Since the first reports in 2001, great advances have been made towards the understanding of endocannabinoid-mediated synaptic modulation. Electrophysiological studies have revealed that one of the two major endocannabinoids, 2-arachidonoylglycerol (2-AG), is produced from membrane lipids upon postsynaptic Ca2+ elevation and/or activation of Gq/11-coupled receptors, and released from postsynaptic neurons. The released 2-AG then acts retrogradely onto presynaptic cannabinoid CB1 receptors and induces suppression of neurotransmitter release either transiently or persistently. These forms of 2-AG-mediated retrograde synaptic modulation are functional throughout the brain. The other major endocannabinoid, anandamide, mediates a certain form of endocannabinoid-mediated long-term depression (LTD). Anandamide also functions as an agonist for transient receptor potential vanilloid receptor type 1 (TRPV1) and mediates endocannabinoid-independent and TRPV1-dependent forms of LTD. It has also been demonstrated that the endocannabinoid system itself is plastic, which can be either up- or down-regulated by experimental or environmental conditions. In this review, I will make an overview of the mechanisms underlying endocannabinoid-mediated synaptic modulation.
ISSN:0386-2208
0021-4280
1349-2896
DOI:10.2183/pjab.90.235