Endocannabinoid mediated long-term depression at inhibitory synapses

Chiayu Q. Chiu, Pablo E. Castillo

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Long-lasting activity-dependent changes in synaptic strength, in the form of long-term potentiation (LTP) or depression (LTD), are thought to be the cellular basis of learning and memory. Although inhibitory synapses are critical for proper functioning of neural circuits, most of the studies investigating synaptic plasticity have concentrated on excitatory glutamatergic synapses. The idea that inhibitory synapses are plastic like excitatory synapses is gradually being accepted. Different forms of GABAergic synaptic plasticity have recently been reported. Among them, one of the most intensely studied is a form of LTD mediated by a group of retrograde messengers, collectively called endocannabinoids (eCBs). eCB-mediated LTD at inhibitory synapses (I-LTD) is a heterosynaptic form of plasticity, whose induction typically requires the activation of metabotropic glutamatergic receptors by nearby excitatory inputs and the resulting eCB mobilization from the postsynaptic cell. By activating presynaptic type 1 cannabinoid receptors (CB1Rs), eCBs can cause a long-lasting reduction in GABA release. I-LTD has been identified in several brain structures and may serve as a mechanism by which neurons adjust the strength of the inhibition they receive in response to excitatory afferent stimulation. In light of the wide-ranging effects of inhibition on synaptic transmission, from shaping the input-output relationship and excitability of neurons to modulating the inducibility of excitatory synaptic plasticity, I-LTD is expected to have significant impact on the excitatory/inhibitory balance within circuits and on neural network function. In this chapter, we review the main properties of eCB-mediated LTD at GABAergic synapses with the aim of understanding its physiological role.

Original languageEnglish (US)
Title of host publicationInhibitory Synaptic Plasticity
PublisherSpringer New York
Pages149-166
Number of pages18
ISBN (Print)9781441969781, 9781441969774
DOIs
StatePublished - 2011

Fingerprint

Endocannabinoids
Synapses
Depression
Neuronal Plasticity
Neurons
Cannabinoid Receptors
Long-Term Potentiation
Synaptic Transmission
gamma-Aminobutyric Acid
Plastics
Learning
Brain

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)

Cite this

Chiu, C. Q., & Castillo, P. E. (2011). Endocannabinoid mediated long-term depression at inhibitory synapses. In Inhibitory Synaptic Plasticity (pp. 149-166). Springer New York. https://doi.org/10.1007/978-1-4419-6978-1_11

Endocannabinoid mediated long-term depression at inhibitory synapses. / Chiu, Chiayu Q.; Castillo, Pablo E.

Inhibitory Synaptic Plasticity. Springer New York, 2011. p. 149-166.

Research output: Chapter in Book/Report/Conference proceedingChapter

Chiu, Chiayu Q. ; Castillo, Pablo E. / Endocannabinoid mediated long-term depression at inhibitory synapses. Inhibitory Synaptic Plasticity. Springer New York, 2011. pp. 149-166
@inbook{16a93c2c478443c7801df013e32cf181,
title = "Endocannabinoid mediated long-term depression at inhibitory synapses",
abstract = "Long-lasting activity-dependent changes in synaptic strength, in the form of long-term potentiation (LTP) or depression (LTD), are thought to be the cellular basis of learning and memory. Although inhibitory synapses are critical for proper functioning of neural circuits, most of the studies investigating synaptic plasticity have concentrated on excitatory glutamatergic synapses. The idea that inhibitory synapses are plastic like excitatory synapses is gradually being accepted. Different forms of GABAergic synaptic plasticity have recently been reported. Among them, one of the most intensely studied is a form of LTD mediated by a group of retrograde messengers, collectively called endocannabinoids (eCBs). eCB-mediated LTD at inhibitory synapses (I-LTD) is a heterosynaptic form of plasticity, whose induction typically requires the activation of metabotropic glutamatergic receptors by nearby excitatory inputs and the resulting eCB mobilization from the postsynaptic cell. By activating presynaptic type 1 cannabinoid receptors (CB1Rs), eCBs can cause a long-lasting reduction in GABA release. I-LTD has been identified in several brain structures and may serve as a mechanism by which neurons adjust the strength of the inhibition they receive in response to excitatory afferent stimulation. In light of the wide-ranging effects of inhibition on synaptic transmission, from shaping the input-output relationship and excitability of neurons to modulating the inducibility of excitatory synaptic plasticity, I-LTD is expected to have significant impact on the excitatory/inhibitory balance within circuits and on neural network function. In this chapter, we review the main properties of eCB-mediated LTD at GABAergic synapses with the aim of understanding its physiological role.",
author = "Chiu, {Chiayu Q.} and Castillo, {Pablo E.}",
year = "2011",
doi = "10.1007/978-1-4419-6978-1_11",
language = "English (US)",
isbn = "9781441969781",
pages = "149--166",
booktitle = "Inhibitory Synaptic Plasticity",
publisher = "Springer New York",

}

TY - CHAP

T1 - Endocannabinoid mediated long-term depression at inhibitory synapses

AU - Chiu, Chiayu Q.

AU - Castillo, Pablo E.

PY - 2011

Y1 - 2011

N2 - Long-lasting activity-dependent changes in synaptic strength, in the form of long-term potentiation (LTP) or depression (LTD), are thought to be the cellular basis of learning and memory. Although inhibitory synapses are critical for proper functioning of neural circuits, most of the studies investigating synaptic plasticity have concentrated on excitatory glutamatergic synapses. The idea that inhibitory synapses are plastic like excitatory synapses is gradually being accepted. Different forms of GABAergic synaptic plasticity have recently been reported. Among them, one of the most intensely studied is a form of LTD mediated by a group of retrograde messengers, collectively called endocannabinoids (eCBs). eCB-mediated LTD at inhibitory synapses (I-LTD) is a heterosynaptic form of plasticity, whose induction typically requires the activation of metabotropic glutamatergic receptors by nearby excitatory inputs and the resulting eCB mobilization from the postsynaptic cell. By activating presynaptic type 1 cannabinoid receptors (CB1Rs), eCBs can cause a long-lasting reduction in GABA release. I-LTD has been identified in several brain structures and may serve as a mechanism by which neurons adjust the strength of the inhibition they receive in response to excitatory afferent stimulation. In light of the wide-ranging effects of inhibition on synaptic transmission, from shaping the input-output relationship and excitability of neurons to modulating the inducibility of excitatory synaptic plasticity, I-LTD is expected to have significant impact on the excitatory/inhibitory balance within circuits and on neural network function. In this chapter, we review the main properties of eCB-mediated LTD at GABAergic synapses with the aim of understanding its physiological role.

AB - Long-lasting activity-dependent changes in synaptic strength, in the form of long-term potentiation (LTP) or depression (LTD), are thought to be the cellular basis of learning and memory. Although inhibitory synapses are critical for proper functioning of neural circuits, most of the studies investigating synaptic plasticity have concentrated on excitatory glutamatergic synapses. The idea that inhibitory synapses are plastic like excitatory synapses is gradually being accepted. Different forms of GABAergic synaptic plasticity have recently been reported. Among them, one of the most intensely studied is a form of LTD mediated by a group of retrograde messengers, collectively called endocannabinoids (eCBs). eCB-mediated LTD at inhibitory synapses (I-LTD) is a heterosynaptic form of plasticity, whose induction typically requires the activation of metabotropic glutamatergic receptors by nearby excitatory inputs and the resulting eCB mobilization from the postsynaptic cell. By activating presynaptic type 1 cannabinoid receptors (CB1Rs), eCBs can cause a long-lasting reduction in GABA release. I-LTD has been identified in several brain structures and may serve as a mechanism by which neurons adjust the strength of the inhibition they receive in response to excitatory afferent stimulation. In light of the wide-ranging effects of inhibition on synaptic transmission, from shaping the input-output relationship and excitability of neurons to modulating the inducibility of excitatory synaptic plasticity, I-LTD is expected to have significant impact on the excitatory/inhibitory balance within circuits and on neural network function. In this chapter, we review the main properties of eCB-mediated LTD at GABAergic synapses with the aim of understanding its physiological role.

UR - http://www.scopus.com/inward/record.url?scp=84919841525&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84919841525&partnerID=8YFLogxK

U2 - 10.1007/978-1-4419-6978-1_11

DO - 10.1007/978-1-4419-6978-1_11

M3 - Chapter

AN - SCOPUS:84919841525

SN - 9781441969781

SN - 9781441969774

SP - 149

EP - 166

BT - Inhibitory Synaptic Plasticity

PB - Springer New York

ER -