Anterior Cingulate Cortex Contributes to the Hyperlocomotion under Nitrogen Narcosis.
10.1007/s12264-024-01278-z
- Author:
Bin PENG
1
;
Xiao-Bo WU
1
;
Zhi-Jun ZHANG
1
;
De-Li CAO
1
;
Lin-Xia ZHAO
1
;
Hao WU
2
;
Yong-Jing GAO
3
Author Information
1. Medical School, Institute of Special Environmental Medicine, Co-innovation Center of Neuroregeneration, Nantong University, Jiangsu, 226019, China.
2. Department of Otolaryngology-Head Neck Surgery, the Affiliated Hospital of Nantong University, Jiangsu, 226001, China.
3. Medical School, Institute of Special Environmental Medicine, Co-innovation Center of Neuroregeneration, Nantong University, Jiangsu, 226019, China. gaoyongjing@ntu.edu.cn.
- Publication Type:Journal Article
- Keywords:
ACC;
DMS;
Hyperlocomotion;
Neural circuits;
Nitrogen Narcosis
- MeSH:
Animals;
Gyrus Cinguli/drug effects*;
Male;
Mice, Inbred C57BL;
Locomotion/drug effects*;
Neurons/drug effects*;
Mice;
Nitrogen/toxicity*;
Inert Gas Narcosis/physiopathology*;
Corpus Striatum/physiopathology*
- From:
Neuroscience Bulletin
2025;41(5):775-789
- CountryChina
- Language:English
-
Abstract:
Nitrogen narcosis is a neurological syndrome that manifests when humans or animals encounter hyperbaric nitrogen, resulting in a range of motor, emotional, and cognitive abnormalities. The anterior cingulate cortex (ACC) is known for its significant involvement in regulating motivation, cognition, and action. However, its specific contribution to nitrogen narcosis-induced hyperlocomotion and the underlying mechanisms remain poorly understood. Here we report that exposure to hyperbaric nitrogen notably increased the locomotor activity of mice in a pressure-dependent manner. Concurrently, this exposure induced heightened activation among neurons in both the ACC and dorsal medial striatum (DMS). Notably, chemogenetic inhibition of ACC neurons effectively suppressed hyperlocomotion. Conversely, chemogenetic excitation lowered the hyperbaric pressure threshold required to induce hyperlocomotion. Moreover, both chemogenetic inhibition and genetic ablation of activity-dependent neurons within the ACC reduced the hyperlocomotion. Further investigation revealed that ACC neurons project to the DMS, and chemogenetic inhibition of ACC-DMS projections resulted in a reduction in hyperlocomotion. Finally, nitrogen narcosis led to an increase in local field potentials in the theta frequency band and a decrease in the alpha frequency band in both the ACC and DMS. These results collectively suggest that excitatory neurons within the ACC, along with their projections to the DMS, play a pivotal role in regulating the hyperlocomotion induced by exposure to hyperbaric nitrogen.
