Layer-specific modulation of neuronal excitability by 660-nm laser irradiation in mouse neocortex.

It has been reported that laser light irradiation (LLI) could regulate neuronal activities in the forebrain, but little is known if and how LLI in the red wavelength range affects neuronal excitability. Here, we investigated the effects of a continuous diode laser at 660 nm on intrinsic membrane properties and excitability of presumed pyramidal neurons in the thalamocortical input layer (layer 3/4) and in layer 5 of mouse primary auditory cortex using the whole-cell patch-clamp recording technique. In layer 3/4 neurons, 660-nm laser irradiation (LLI-660) at 20 mW for 5 min gradually increased resting membrane potentials, which reached a plateau after irradiation. Concomitantly, LLI-660 decreased onset latency of first action potentials (spikes) without changing spike threshold or peak amplitude, but increased inter-spike interval of initial bursting spike doublets and their peak amplitude ratio. None of these changes was observed in layer 5 neurons. Instead, LLI-660 at 20 mW rapidly reduced spike width ~5 % within 1 min of irradiation onset. The magnitude of this reduction did not change during 5 or 10 min irradiation, and returned quickly to at least baseline levels after turning the LLI off. Decreasing laser power to 10 mW reduced spike width to a lesser extent, suggesting laser power dependence of this phenomenon. These data suggest that LLI-660 regulates different aspects of neuronal excitability in cortical neurons in a layer-dependent manner possibly by affecting different voltage-gated ion channels.