Abstract
Synaptic plasticity is the mechanistic basis of development, aging, learning and memory, both in the healthy and pathological brain. 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. In our current study, we characterized the time course of neural activity, neural morphology, and the expression of synaptic proteins 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 h after stimulation. Stimulus-induced cortical hyperactivity persisted up to 1.5 h and decayed to baseline after 24 h, indicated by c-Fos expression. The synaptic proteins VGLUT1 and PSD-95, in contrast, were upregulated at 24 h and downregulated at 48 h, respectively. Spine density and spine head volume were also increased at 24 h and decreased at 48 h. This specific sequence of events reflects a continuous joint evolution of activity and connectivity that is typical of homeostatic structural plasticity. In this computational model, the turnover of dendritic spines and axonal boutons is regulated via firing rate homeostasis of individual neurons.
Competing Interest Statement
The authors have declared no competing interest.