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Peer-reviewedCC BY-NC-NDNature Communications

Complementary roles of cell-type-specific plasticity in shaping neocortical dynamics for learning action timing

  • Shouvik Majumder1,2,3
  • Koichi Hirokawa1,2,3
  • Zidan Yang1,2,3
  • Anant Jain3
  • Ronald F. Paletzki4
  • Charles R. Gerfen4
  • Lorenzo Fontolan5,6
  • Sandro Romani5
  • Ryohei Yasuda3
  • H. Inagaki7
7 affiliations
  1. 1Florida Atlantic University, Boca Raton, FL, USA
  2. 2IMPRS for Synapses and Circuits, Jupiter, FL, USA
  3. 3Max Planck Florida Institute for Neuroscience, Jupiter, FL, USA
  4. 4National Institute of Mental Health, Bethesda, MD, USA
  5. 5Janelia Research Campus, HHMI, Ashburn, VA, USA
  6. 6Turing Centre for Living Systems, Aix-Marseille University, Marseille, France
  7. 7Max Planck Florida Institute for Neuroscience, Jupiter, FL, USA. [email protected]
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Abstract

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. During motor learning, population spiking dynamics reconfigure in motor cortex. Here, the authors show that synaptic plasticity in distinct pyramidal cell types plays complementary and specific roles in shaping neural dynamics during learning.

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Cite

BibTeXRIS
BibTeX
@article{majumder2026complementary,
  title = {{Complementary roles of cell-type-specific plasticity in shaping neocortical dynamics for learning action timing}},
  author = {Shouvik Majumder and Koichi Hirokawa and Zidan Yang and Anant Jain and Ronald F. Paletzki and Charles R. Gerfen and Lorenzo Fontolan and Sandro Romani and Ryohei Yasuda and H. Inagaki},
  journal = {Nature Communications},
  year = {2026},
  month = jul,
  doi = {10.1038/s41467-026-74869-1},
  url = {https://doi.org/10.1038/s41467-026-74869-1},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Complementary roles of cell-type-specific plasticity in shaping neocortical dynamics for learning action timing
AU  - Shouvik Majumder
AU  - Koichi Hirokawa
AU  - Zidan Yang
AU  - Anant Jain
AU  - Ronald F. Paletzki
AU  - Charles R. Gerfen
AU  - Lorenzo Fontolan
AU  - Sandro Romani
AU  - Ryohei Yasuda
AU  - H. Inagaki
PY  - 2026
DA  - 2026/07/06
JO  - Nature Communications
DO  - 10.1038/s41467-026-74869-1
UR  - https://doi.org/10.1038/s41467-026-74869-1
AB  - 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. During motor learning, population spiking dynamics reconfigure in motor cortex. Here, the authors show that synaptic plasticity in distinct pyramidal cell types plays complementary and specific roles in shaping neural dynamics during learning.
SN  - 2041-1723
ER  -