Extended Data Fig. 10: Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states.

In the tissue injured state, an enhanced excitatory process occurs within the S1HL, which involves increased PO^Glu (Red) inputs that mediate activation of the S1HL^Glu (Orange). The alterations lead to high excitation of the S1HL^Glu neurons, and presumably cause pain. In the depression state, the circuit involves decreased PF^Glu (Blue) projection to both ACC^GABA (Green) and ACC^Glu (Orange) neurons. An increase in the ACC^Glu neurons activity is caused by inhibition of ACC^GABA local interneurons via receiving weakened PF^Glu inputs, through which depression comorbid pain is generated. PO, posterior thalamic nuclear group; S1HL, the hind limb primary somatosensory cortex; PF, parafascicular nucleus; ACC, anterior cingulate cortex; Glu, glutamate; GABA, gamma-aminobutyric acid.