Huge thanks to Haruo Kasai, Siqi Zhou, and all our wonderful collaborators who made this work possible!

It also induced a unique, intermittent non-wake/non-sleep “State-C,” marked by behavioral arrest and reduced γ-power, without major δ changes.

Together, these findings suggest that associative spine enlargement is critical for sustaining cortical processing and wakefulness.

Interestingly, broad induction of SynC in the frontoparietal cortex caused acute deficits in goal-directed behaviors (e.g., laser-dot chasing).
The firing rates of cortical neurons were largely unchanged, but pairwise correlations between neurons decreased.

Induction of SynC in the primary motor cortex impaired motor learning.

Prefrontal synaptic regulation of homeostatic sleep pressure revealed through synaptic chemogenetics Sleep is regulated by homeostatic processes, yet the biological basis of sleep pressure that accumulates during wakefulness, triggers sleep, and dissipates during sleep remains elusive. We explored a ...

Following our synaptic-potentiation tool SYNCit-K published last year (www.science.org/doi/10.1126/...), we have now developed SYNCit-C (SynC), which selectively and reversibly blocks associative dendritic-spine enlargement while leaving basal synaptic transmission and neuronal excitability intact.

Excited to share our new preprint:
Blockade of associative spine enlargement impairs awake cortical function
biorxiv.org/content/10.1...

Blockade of associative spine enlargement impairs awake cortical function www.biorxiv.org/content/10.1101/2025.11....