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Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states
Ist Teil von
Nature neuroscience, 2021-04, Vol.24 (4), p.542
Ort / Verlag
United States
Erscheinungsjahr
2021
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
In humans, tissue injury and depression can both cause pain hypersensitivity, but whether this involves distinct circuits remains unknown. Here, we identify two discrete glutamatergic neuronal circuits in male mice: a projection from the posterior thalamic nucleus (PO
) to primary somatosensory cortex glutamatergic neurons (S1
) mediates allodynia from tissue injury, whereas a pathway from the parafascicular thalamic nucleus (PF
) to anterior cingulate cortex GABA-containing neurons to glutamatergic neurons (ACC
) mediates allodynia associated with a depression-like state. In vivo calcium imaging and multi-tetrode electrophysiological recordings reveal that PO
and PF
populations undergo different adaptations in the two conditions. Artificial manipulation of each circuit affects allodynia resulting from either tissue injury or depression-like states, but not both. Our study demonstrates that the distinct thalamocortical circuits PO
→S1
and PF
→ACC
subserve allodynia associated with tissue injury and depression-like states, respectively, thus providing insights into the circuit basis of pathological pain resulting from different etiologies.