The article examines thalamic activation of the visual cortex at the level of the single synapse through electrical stimulation of the lateral geniculate nucleus (LGN) and recording of monosynaptic responses in layer 4 neurons of the visual cortex.[2] At low to medium currents, the stimulations elicit cortical spikes of low to medium probability that are modulated by continuous visual input.[2] Repetitive stimulation at 8–12 Hz strongly inhibits cortical activity, allowing mapping of the receptive field of summed thalamic input to single cells.[2] At higher currents (50–500 μA), the probability of monosynaptic spikes increases and the inhibition lasts 50–200 ms.[2] Monocular deprivation reduces the intrinsic excitability of dLGN cells, changes the latency of the first spike (from −39.6 ± 0.9 mV to −42.8 ± 1.1 mV, n=15, P<0.001) and lowers the threshold.[1] These changes are caused by the down-regulation of Kv1 channels, which is confirmed by the blockers DTx-I and DTx-K, which increase the number of action potentials 3-fold and shorten the latency.[1] Thalamo-cortical synapses on L2/3 pyramidal neurons are sparse, heterogeneous in number and density on dendrites, and are smaller than cortical synapses.[4]