Computational modeling reveals biological mechanisms underlying the whisker-flick EEG

Abstract

Whisker flick stimulation is a commonly used protocol to investigate somatosensory processing in rodents. Neural activity in the brain evoked by whisker flicks produces a characteristic EEG waveform recorded at the skull, known as a somatosensory evoked potential. In this paper, we use in silico modeling to identify the neural populations that serve as sources and targets of the synaptic currents contributing to this signal (presynaptic and postsynaptic populations, respectively). The initial positive deflection of the EEG waveform is driven largely by direct thalamic inputs to Layer 2/3 and Layer 5 pyramidal cells, though interestingly, L5-L5 inhibition plays a modulatory role, reducing the amplitude and width of the deflection. This suggests that increasing thalamocortical connectivity and decreasing L5-L5 inhibition may be responsible for some of the changes observed in the EEG waveform over the course of development. The negative deflection is driven by a more complex mix of sources, including both thalamic and recurrent cortical connectivity. We demonstrate that small changes to the local connectivity of the circuit, particularly to perisomatic inhibitory targeting, can have an important impact on the recorded EEG, without substantially affecting firing rates, suggesting that EEG may be useful in constraining in silico neural models.