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Abstract
Thalamocortical and corticothalamic pathways mediate bidirectional communication between
the thalamus and neocortex. These pathways are entwined, making their study challenging.
Here we used lentiviruses to express channelrhodopsin-2 (ChR2), a light-sensitive
cation channel, in either thalamocortical or corticothalamic projection cells. Infection
occurred only locally, but efferent axons and their terminals expressed ChR2 strongly,
allowing selective optical activation of each pathway. Laser stimulation of ChR2-expressing
thalamocortical axons/terminals evoked robust synaptic responses in cortical excitatory
cells and fast-spiking (FS) inhibitory interneurons, but only weak responses in somatostatin-containing
interneurons. Strong FS cell activation led to feedforward inhibition in all cortical
neuron types, including FS cells. Corticothalamic stimulation excited thalamic relay
cells and inhibitory neurons of the thalamic reticular nucleus (TRN). TRN activation
triggered inhibition in relay cells but not in TRN neurons. Thus, a major difference
between thalamocortical and corticothalamic processing was the extent to which feedforward
inhibitory neurons were themselves engaged by feedforward inhibition.
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