Endocannabinoid-mediated metaplasticity in the hippocampus

Vivien Chevaleyre; Pablo E. Castillo

doi:10.1016/j.neuron.2004.08.036

Endocannabinoid-mediated metaplasticity in the hippocampus

Vivien Chevaleyre, Pablo E. Castillo

Neuroscience

Research output: Contribution to journal › Article › peer-review

248 Scopus citations

Abstract

Repetitive activation of glutamatergic fibers that normally induces long-term potentiation (LTP) at excitatory synapses in the hippocampus also triggers long-term depression at inhibitory synapses (I-LTD) via retrograde endocannabinoid signaling. Little is known, however, about the physiological significance of I-LTD. Here, we show that synaptic-driven release of endocannabinoids is a highly localized and efficient process that strongly depresses cannabinoid-sensitive inhibitory inputs within the dendritic compartment of CA1 pyramidal cells. By removing synaptic inhibition in a restricted area of the dendritic tree, endocannabinoids selectively "primed" nearby excitatory synapses, thereby facilitating subsequent induction of LTP. This induction of local metaplasticity is a novel mechanism by which endocannabinoids can contribute to the storage of information in the brain.

Original language	English (US)
Pages (from-to)	871-881
Number of pages	11
Journal	Neuron
Volume	43
Issue number	6
DOIs	https://doi.org/10.1016/j.neuron.2004.08.036
State	Published - Sep 16 2004

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/j.neuron.2004.08.036

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title = "Endocannabinoid-mediated metaplasticity in the hippocampus",

abstract = "Repetitive activation of glutamatergic fibers that normally induces long-term potentiation (LTP) at excitatory synapses in the hippocampus also triggers long-term depression at inhibitory synapses (I-LTD) via retrograde endocannabinoid signaling. Little is known, however, about the physiological significance of I-LTD. Here, we show that synaptic-driven release of endocannabinoids is a highly localized and efficient process that strongly depresses cannabinoid-sensitive inhibitory inputs within the dendritic compartment of CA1 pyramidal cells. By removing synaptic inhibition in a restricted area of the dendritic tree, endocannabinoids selectively {"}primed{"} nearby excitatory synapses, thereby facilitating subsequent induction of LTP. This induction of local metaplasticity is a novel mechanism by which endocannabinoids can contribute to the storage of information in the brain.",

author = "Vivien Chevaleyre and Castillo, {Pablo E.}",

note = "Funding Information: We thank R.C. Carroll and Donald Faber for helpful discussions. We also thank K. Takahashi, K. Khodakhah, M. Frerking, and G.O. Hjelmstad for their constructive comments on the manuscript. CB1R knockout mice animals were kindly provided by Dr. George Kunos (NIAAA/NIH). Supported by NIH/NIDA. P.E.C. is a Pew Biomedical Scholar.",

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doi = "10.1016/j.neuron.2004.08.036",

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AU - Chevaleyre, Vivien

AU - Castillo, Pablo E.

N1 - Funding Information: We thank R.C. Carroll and Donald Faber for helpful discussions. We also thank K. Takahashi, K. Khodakhah, M. Frerking, and G.O. Hjelmstad for their constructive comments on the manuscript. CB1R knockout mice animals were kindly provided by Dr. George Kunos (NIAAA/NIH). Supported by NIH/NIDA. P.E.C. is a Pew Biomedical Scholar.

PY - 2004/9/16

Y1 - 2004/9/16

N2 - Repetitive activation of glutamatergic fibers that normally induces long-term potentiation (LTP) at excitatory synapses in the hippocampus also triggers long-term depression at inhibitory synapses (I-LTD) via retrograde endocannabinoid signaling. Little is known, however, about the physiological significance of I-LTD. Here, we show that synaptic-driven release of endocannabinoids is a highly localized and efficient process that strongly depresses cannabinoid-sensitive inhibitory inputs within the dendritic compartment of CA1 pyramidal cells. By removing synaptic inhibition in a restricted area of the dendritic tree, endocannabinoids selectively "primed" nearby excitatory synapses, thereby facilitating subsequent induction of LTP. This induction of local metaplasticity is a novel mechanism by which endocannabinoids can contribute to the storage of information in the brain.

AB - Repetitive activation of glutamatergic fibers that normally induces long-term potentiation (LTP) at excitatory synapses in the hippocampus also triggers long-term depression at inhibitory synapses (I-LTD) via retrograde endocannabinoid signaling. Little is known, however, about the physiological significance of I-LTD. Here, we show that synaptic-driven release of endocannabinoids is a highly localized and efficient process that strongly depresses cannabinoid-sensitive inhibitory inputs within the dendritic compartment of CA1 pyramidal cells. By removing synaptic inhibition in a restricted area of the dendritic tree, endocannabinoids selectively "primed" nearby excitatory synapses, thereby facilitating subsequent induction of LTP. This induction of local metaplasticity is a novel mechanism by which endocannabinoids can contribute to the storage of information in the brain.

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Endocannabinoid-mediated metaplasticity in the hippocampus

Abstract

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