The thalamus controls transmission of sensory signals from periphery to cortex, ultimately shaping perception. Despite this significant role, dynamic thalamic gating and the consequences for downstream cortical sensory representations have not been well studied in the awake brain. We optogenetically modulated the ventro-posterior medial thalamus in the vibrissa pathway of the awake mouse, and measured spiking activity in the thalamus, and activity in primary somatosensory cortex (S1) using extracellular electrophysiology and genetically encoded voltage imaging. Thalamic hyperpolarization significantly enhanced thalamic sensory-evoked bursting, yet surprisingly the S1 cortical response was not amplified, but instead timing precision was significantly increased, spatial activation more focused, and there was an increased synchronization of cortical inhibitory neurons. A thalamocortical network model implicates the modulation of precise timing of feedforward thalamic population spiking, presenting a highly sensitive, timing-based gating of sensory signaling to cortex.

These data were collected from the ventral posteromedial (VPm) nucleus and/or primary somatosensory (S1) cortex in the vibrissa system of isoflurane-anesthetized and awake mice.  In some cases (where noted below), the data are saved results from a model thalamocortical network.  Electrophysiological data was acquired using silicon microelectrode arrays (NeuroNexus).  Spike-sorting was performed using KiloSort2, and clustering performed using Phy2.  Mesoscale voltage activity was recorded using the genetically-encoded voltage indicator (GEVI) ArcLight.

For more information, please see the detailed Methods section of the associated publication.

Matlab is required to access the data files and create all figures, except for Figure 4 E, F and Figure 8, which require Python.