The interplay between inflammatory cytokines and the endocannabinoid system in the regulation of synaptic transmission

Research output: Contribution to journalArticle

Abstract

Abstract Excessive glutamate-mediated synaptic transmission and secondary excitotoxicity have been proposed as key determinants of neurodegeneration in many neurological diseases. Soluble mediators of inflammation have recently gained attention owing to their ability to enhance glutamate transmission and affect synaptic sensitivity to neurotransmitters. In the complex crosstalk between soluble immunoactive molecules and synapses, the endocannabinoid system (ECS) plays a central role, exerting an indirect neuroprotective action by inhibiting cytokine-dependent synaptic alterations, and a direct neuroprotective effect by limiting glutamate transmission and excitotoxic damage. On the other hand, the endocannabinoid (eCB)-mediated control of synaptic transmission is altered by proinflammatory cytokines with consequent effects in central nervous system (CNS) disorders. In this review, we summarize the interactions, at the pre- and postsynaptic level, between major inflammatory cytokines and the ECS. In addition, the behavioral and clinical consequences of the modulation of synaptic transmission during neuroinflammation are discussed. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.

Original languageEnglish
Article number5610
Pages (from-to)105-112
Number of pages8
JournalNeuropharmacology
Volume96
Issue numberPA
DOIs
Publication statusPublished - Jun 16 2015

Fingerprint

Endocannabinoids
Synaptic Transmission
Cytokines
Glutamic Acid
Inflammation Mediators
Central Nervous System Diseases
Neuroprotective Agents
Synapses
Neurotransmitter Agents

Keywords

  • CB1 receptor
  • GABA
  • Glutamate
  • IL-1β
  • Multiple sclerosis
  • TNF
  • TRPV1

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

@article{fca05261bfaa42dc8b682120a1153c19,
title = "The interplay between inflammatory cytokines and the endocannabinoid system in the regulation of synaptic transmission",
abstract = "Abstract Excessive glutamate-mediated synaptic transmission and secondary excitotoxicity have been proposed as key determinants of neurodegeneration in many neurological diseases. Soluble mediators of inflammation have recently gained attention owing to their ability to enhance glutamate transmission and affect synaptic sensitivity to neurotransmitters. In the complex crosstalk between soluble immunoactive molecules and synapses, the endocannabinoid system (ECS) plays a central role, exerting an indirect neuroprotective action by inhibiting cytokine-dependent synaptic alterations, and a direct neuroprotective effect by limiting glutamate transmission and excitotoxic damage. On the other hand, the endocannabinoid (eCB)-mediated control of synaptic transmission is altered by proinflammatory cytokines with consequent effects in central nervous system (CNS) disorders. In this review, we summarize the interactions, at the pre- and postsynaptic level, between major inflammatory cytokines and the ECS. In addition, the behavioral and clinical consequences of the modulation of synaptic transmission during neuroinflammation are discussed. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.",
keywords = "CB1 receptor, GABA, Glutamate, IL-1β, Multiple sclerosis, TNF, TRPV1",
author = "Silvia Rossi and Caterina Motta and Alessandra Musella and Diego Centonze",
year = "2015",
month = "6",
day = "16",
doi = "10.1016/j.neuropharm.2014.09.022",
language = "English",
volume = "96",
pages = "105--112",
journal = "Neuropharmacology",
issn = "0028-3908",
publisher = "Elsevier Limited",
number = "PA",

}

TY - JOUR

T1 - The interplay between inflammatory cytokines and the endocannabinoid system in the regulation of synaptic transmission

AU - Rossi, Silvia

AU - Motta, Caterina

AU - Musella, Alessandra

AU - Centonze, Diego

PY - 2015/6/16

Y1 - 2015/6/16

N2 - Abstract Excessive glutamate-mediated synaptic transmission and secondary excitotoxicity have been proposed as key determinants of neurodegeneration in many neurological diseases. Soluble mediators of inflammation have recently gained attention owing to their ability to enhance glutamate transmission and affect synaptic sensitivity to neurotransmitters. In the complex crosstalk between soluble immunoactive molecules and synapses, the endocannabinoid system (ECS) plays a central role, exerting an indirect neuroprotective action by inhibiting cytokine-dependent synaptic alterations, and a direct neuroprotective effect by limiting glutamate transmission and excitotoxic damage. On the other hand, the endocannabinoid (eCB)-mediated control of synaptic transmission is altered by proinflammatory cytokines with consequent effects in central nervous system (CNS) disorders. In this review, we summarize the interactions, at the pre- and postsynaptic level, between major inflammatory cytokines and the ECS. In addition, the behavioral and clinical consequences of the modulation of synaptic transmission during neuroinflammation are discussed. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.

AB - Abstract Excessive glutamate-mediated synaptic transmission and secondary excitotoxicity have been proposed as key determinants of neurodegeneration in many neurological diseases. Soluble mediators of inflammation have recently gained attention owing to their ability to enhance glutamate transmission and affect synaptic sensitivity to neurotransmitters. In the complex crosstalk between soluble immunoactive molecules and synapses, the endocannabinoid system (ECS) plays a central role, exerting an indirect neuroprotective action by inhibiting cytokine-dependent synaptic alterations, and a direct neuroprotective effect by limiting glutamate transmission and excitotoxic damage. On the other hand, the endocannabinoid (eCB)-mediated control of synaptic transmission is altered by proinflammatory cytokines with consequent effects in central nervous system (CNS) disorders. In this review, we summarize the interactions, at the pre- and postsynaptic level, between major inflammatory cytokines and the ECS. In addition, the behavioral and clinical consequences of the modulation of synaptic transmission during neuroinflammation are discussed. This article is part of a Special Issue entitled 'Neuroimmunology and Synaptic Function'.

KW - CB1 receptor

KW - GABA

KW - Glutamate

KW - IL-1β

KW - Multiple sclerosis

KW - TNF

KW - TRPV1

UR - http://www.scopus.com/inward/record.url?scp=84930930081&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84930930081&partnerID=8YFLogxK

U2 - 10.1016/j.neuropharm.2014.09.022

DO - 10.1016/j.neuropharm.2014.09.022

M3 - Article

C2 - 25268960

AN - SCOPUS:84930930081

VL - 96

SP - 105

EP - 112

JO - Neuropharmacology

JF - Neuropharmacology

SN - 0028-3908

IS - PA

M1 - 5610

ER -