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CXCL12-induced rescue of cortical dendritic spines and cognitive flexibility
Journal article   Open access   Peer reviewed

CXCL12-induced rescue of cortical dendritic spines and cognitive flexibility

Lindsay K Festa, Elena Irollo, Brian J Platt, Yuzen Tian, Stan Floresco and Olimpia Meucci
eLife, v 9
23 Jan 2020
PMID: 31971513
url
https://doi.org/10.7554/eLife.49717View
Published, Version of Record (VoR) Open

Abstract

chemokine rat cognitive decline neuroHIV neuroscience prefrontal cortex
Synaptodendritic pruning is a common cause of cognitive decline in neurological disorders, including HIV-associated neurocognitive disorders (HAND). HAND persists in treated patients as a result of chronic inflammation and low-level expression of viral proteins, though the mechanisms involved in synaptic damage are unclear. Here, we report that the chemokine CXCL12 recoups both cognitive performance and synaptodendritic health in a rodent model of HAND, which recapitulates the neuroinflammatory state of virally controlled individuals and the associated structural/functional deficiencies. CXCL12 preferentially regulates plastic thin spines on layer II/III pyramidal neurons of the medial prefrontal cortex via CXCR4-dependent stimulation of the Rac1/PAK actin polymerization pathway, leading to increased spine density and improved flexible behavior. Our studies unveil a critical role of CXCL12/CXCR4 signaling in spine dynamics and cognitive flexibility, suggesting that HAND - or other diseases driven by spine loss - may be reversible and upturned by targeting Rac1-dependent processes in cortical neurons.

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27 citations in Scopus

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Web of Science research areas
Biology
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