Relapse-Associated Transient Synaptic Potentiation Requires Integrin-Mediated Activation of Focal Adhesion Kinase and Cofilin in D1-Expressing Neurons.
Actin Depolymerizing Factors
/ metabolism
Animals
Cocaine-Related Disorders
/ physiopathology
Cues
Dendritic Spines
/ drug effects
Dopaminergic Neurons
/ metabolism
Drug-Seeking Behavior
Enzyme Activation
Focal Adhesion Kinase 1
/ metabolism
Humans
Integrin beta3
/ metabolism
Male
Rats
Rats, Long-Evans
Rats, Sprague-Dawley
Rats, Transgenic
Receptors, Dopamine D1
/ metabolism
Recurrence
Synapses
cocaine
cofilin
cued relapse
focal adhesion kinase
integrins
medium spine neurons
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN: 1529-2401
Titre abrégé: J Neurosci
Pays: United States
ID NLM: 8102140
Informations de publication
Date de publication:
28 10 2020
28 10 2020
Historique:
received:
11
11
2019
revised:
17
07
2020
accepted:
21
07
2020
pubmed:
15
10
2020
medline:
2
2
2021
entrez:
14
10
2020
Statut:
ppublish
Résumé
Relapse to drug use can be initiated by drug-associated cues. The intensity of cue-induced drug seeking in rodent models correlates with the induction of transient synaptic potentiation (t-SP) at glutamatergic synapses in the nucleus accumbens core (NAcore). Matrix metalloproteinases (MMPs) are inducible endopeptidases that degrade extracellular matrix (ECM) proteins, and reveal tripeptide Arginine-Glycine-Aspartate (RGD) domains that bind and signal through integrins. Integrins are heterodimeric receptors composed of αβ subunits, and a primary signaling kinase is focal adhesion kinase (FAK). We previously showed that MMP activation is necessary for and potentiates cued reinstatement of cocaine seeking, and MMP-induced catalysis stimulates β3-integrins to induce t-SP. Here, we determined whether β3-integrin signaling through FAK and cofilin (actin depolymerization factor) is necessary to promote synaptic growth during t-SP. Using a small molecule inhibitor to prevent FAK activation, we blocked cued-induced cocaine reinstatement and increased spine head diameter (d
Identifiants
pubmed: 33051346
pii: JNEUROSCI.2666-19.2020
doi: 10.1523/JNEUROSCI.2666-19.2020
pmc: PMC7605418
doi:
Substances chimiques
Actin Depolymerizing Factors
0
Integrin beta3
0
Receptors, Dopamine D1
0
Focal Adhesion Kinase 1
EC 2.7.10.2
Ptk2 protein, rat
EC 2.7.10.2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
8463-8477Subventions
Organisme : NIDA NIH HHS
ID : K99 DA047426
Pays : United States
Organisme : NIDA NIH HHS
ID : R00 DA040004
Pays : United States
Informations de copyright
Copyright © 2020 the authors.
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