Subtype-Specific Roles of Anterior Cingulate Cortex Neurons in Pain-Induced Social Deficits in Mice - PubMed
3 days ago
- #chronic pain
- #social behavior
- #neuroscience
- Pain often leads to social behavior impairments, but the neural mechanisms are unclear.
- Study focuses on GABAergic and CaMKII+ neurons in the anterior cingulate cortex (ACC) in pain-induced social deficits.
- Mice with chronic pain showed reduced social preference and novelty.
- ACC GABAergic neuron activity decreased during social interaction in pain conditions, while CaMKII+ neuron activity increased.
- Activation of GABAergic neurons alleviated pain but did not improve social deficits; inhibition improved social deficits.
- Inhibition of CaMKII+ neurons reduced hyperalgesia; activation partially restored social preference.
- PV+ neurons regulate both pain and social preference deficits; SST+ neurons mediate social novelty deficits.
- Different ACC neuron subtypes have specialized roles in pain and social behavior, indicating a functional 'conflict'.
- Circuit- and subtype-specific interventions are needed to address pain-related social deficits.