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. Author manuscript; available in PMC: 2015 Sep 7.
Published in final edited form as: Nat Neurosci. 2015 Mar;18(3):351–359. doi: 10.1038/nn.3950

Figure 2. Feed-forward inhibition in cortical and thalamic microcircuits.

Figure 2

(a) Extrinsic excitatory projections from regions outside of local cortical networks recruit feed-forward inhibition. Cortical inter-areal or thalamic inputs to the cortex result in stronger activation of FS parv cells than excitatory stellate and pyramidal cells, thus causing a robust feed-forward inhibition of excitatory cells. In case of a loss of this feed-forward inhibition (eraser*), thalamic inputs to the cortex recruit epileptiform activity in a neocortical microgyrus model of focal neocortical epilepsy (bottom multi-unit and local field recordings7). (b) Excitatory inputs from the cortex to the thalamus results in stronger activation of the inhibitory interneurons, which causes a strong feed-forward inhibition of relay excitatory neurons. Loss of feed-forward inhibition (eraser*) has been implicated in the gria4−/− mouse model of absence epilepsy (multi-unit recordings21) Black circle: electrical stimulation of excitatory afferents. Cx, cortex; parv, parvalbumin-positive interneuron; Pyr, pyramidal neuron; RT, reticular thalamic neuron; St, stellate; TC, thalamocortical neuron.