PV and SST neurons in the anterior cingulate cortex regulate social disorders in adulthood induced by sensory abnormalities in childhood

• Published in: CNS neuroscience & therapeutics 2024-07, Vol.30 (7), p.e14863-n/a
• Main Authors: Wan, Xiang‐Dong, Cai, Guo‐Hong, Yan, Zi‐Qian, Liu, Xue‐Qing, Yang, Ding‐Ding, Lu, Yi‐Fan, An, Lei‐Ting, Wu, Sheng‐Xi, Zhang, Fan
• Format: Article
• Language: English
• Subjects: Adverse childhood experiences; Animal models; Animals; anterior cingulate cortex; Antibodies; Behavior; Brain research; Childhood; Children; Chronic pain; Cortex (cingulate); Fiber optics; Freund's adjuvant; Freund's Adjuvant - toxicity; Functional anatomy; GABAergic Neurons - physiology; Gyrus Cinguli; Immunofluorescence; Lasers; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Neurological diseases; Neurons; Neurosciences; Novelty; Original; Pain; Parvalbumin; Parvalbumins - metabolism; PV neurons; Sensory neurons; Social Behavior Disorders - etiology; social disorder; Somatosensory cortex; Somatostatin; Somatostatin - metabolism; SST neurons; Structure-function relationships; Vibrissae - innervation; Vibrissae - physiology; γ-Aminobutyric acid
• ISSN: 1755-5930; 1755-5949; 1755-5949
• DOI: 10.1111/cns.14863

Objective Childhood sensory abnormalities experience has a crucial influence on the structure and function of the adult brain. The underlying mechanism of neurological function induced by childhood sensory abnormalities experience is still unclear. Our study was to investigate whether the GABAergic neurons in the anterior cingulate cortex (ACC) regulate social disorders caused by childhood sensory abnormalities experience. Methods We used two mouse models, complete Freund's adjuvant (CFA) injection mice and bilateral whisker trimming (BWT) mice in childhood. We applied immunofluorescence, chemogenetic and optogenetic to study the mechanism of parvalbumin (PV) neurons and somatostatin (SST) neurons in ACC in regulating social disorders induced by sensory abnormalities in childhood. Results Inflammatory pain in childhood leads to social preference disorders, while BWT in childhood leads to social novelty disorders in adult mice. Inflammatory pain and BWT in childhood caused an increase in the number of PV and SST neurons, respectively, in adult mice ACC. Inhibiting PV neurons in ACC improved social preference disorders in adult mice that experienced inflammatory pain during childhood. Inhibiting SST neurons in ACC improved social novelty disorders in adult mice that experienced BWT in childhood. Conclusions Our study reveals that PV and SST neurons of the ACC may play a critical role in regulating social disorders induced by sensory abnormalities in childhood. Inflammatory pain in childhood leads to social preference disorders, while BWT in childhood leads to social novelty disorders in adult mice. Inflammatory pain and BWT in childhood caused an increase in the number of PV and SST neurons, respectively, in adult mice ACC. Inhibiting PV neurons in ACC improved social preference disorders in adult mice that experienced inflammatory pain during childhood. Inhibiting SST neurons in ACC improved social novelty disorders in adult mice that experienced BWT in childhood. PV and SST neurons of the ACC may play a critical role in regulating social disorders induced by sensory abnormalities in childhood.