Abstract
Focal cooling is a powerful technique to temporally scale neural dynamics. However, the underlying cellular mechanisms causing this scaling remain unresolved. Here, using targeted focal cooling (with a spatial resolution of 100 micrometers), dual somato-dendritic patch clamp recordings, two-photon calcium imaging, transmitter uncaging, and modeling we reveal that a 5°C drop can enhance synaptic transmission, plasticity, and input-output transformations in the distal apical tuft, but not in the basal dendrites of intrinsically bursting L5 pyramidal neurons. This enhancement depends on N-methyl-D-aspartate (NMDA) and Kv4.2, suggesting electrical structure modulation. Paradoxically, and despite the increase in tuft excitability, we observe a reduced rate of recovery from inactivation for apical Na+ channels, thereby regulating back-propagating action potential invasion, coincidence detection, and overall burst probability, resulting in an "apparent" slowing of somatic spike output. Our findings reveal a differential temperature sensitivity along the basal-tuft axis of L5 neurons analog modulates cortical output.