Fiche publication
Date publication
avril 2022
Journal
Cerebral cortex (New York, N.Y. : 1991)
Auteurs
Membres identifiés du Cancéropôle Est :
Dr YALCIN CHRISTMANN Ipek
Tous les auteurs :
Lu H, Gallinaro JV, Normann C, Rotter S, Yalcin I
Lien Pubmed
Résumé
Plasticity is the mechanistic basis of development, aging, learning, and memory, both in healthy and pathological brains. Structural plasticity is rarely accounted for in computational network models due to a lack of insight into the underlying neuronal mechanisms and processes. Little is known about how the rewiring of networks is dynamically regulated. To inform such models, we characterized the time course of neural activity, the expression of synaptic proteins, and neural morphology employing an in vivo optogenetic mouse model. We stimulated pyramidal neurons in the anterior cingulate cortex of mice and harvested their brains at 1.5 h, 24 h, and $48\,\mathrm{h}$ after stimulation. Stimulus-induced cortical hyperactivity persisted up to 1.5 h and decayed to baseline after $24\,\mathrm{h}$ indicated by c-Fos expression. The synaptic proteins VGLUT1 and PSD-95, in contrast, were upregulated at $24\,\mathrm{h}$ and downregulated at $48\,\mathrm{h}$, respectively. Spine density and spine head volume were also increased at $24\,\mathrm{h}$ and decreased at $48\,\mathrm{h}$. This specific sequence of events reflects a continuous joint evolution of activity and connectivity that is characteristic of the model of homeostatic structural plasticity. Our computer simulations thus corroborate the observed empirical evidence from our animal experiments.
Mots clés
ACC, dendritic morphology, depressive disorder, network remodeling, spiking network model
Référence
Cereb Cortex. 2022 04 5;32(8):1574-1592
