<p>Neocortical spiking dynamics underlie voluntary behavior and are thought to emerge through synaptic plasticity during learning. However, the causal role of plasticity across cortical cell types in shaping population dynamics remains unclear. To address this, we manipulated Ca²⁺/calmodulin-dependent protein kinase II (CaMKII), a key mediator of plasticity, in mice learning a motor timing task. Transient CaMKII inactivation in the premotor cortex impaired learning without affecting execution of learned actions. Cell-type-specific manipulations revealed that CaMKII-dependent plasticity in two pyramidal tract (PT) neuron subtypes—but not intratelencephalic (IT) neurons—was required for learning. Concurrent large-scale electrophysiology showed that CaMKII activity in the two PT subtypes was necessary to shape distinct aspects of premotor cortical dynamics that jointly anticipate motor timing, whereas IT neuron plasticity was required to reduce the dimensionality of cortical activity. Together, synaptic plasticity in major cortical cell types plays specialized and complementary roles in sculpting cortical dynamics during learning.</p>