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Research discovers the neural mechanism that exercise promotes drug rehabilitation |
With the support of Su Guohui, academician of the Chinese Academy of Sciences, the Zhang Li team, an associate researcher of the Guangdong-Hong Kong-Macao Central Nervous Regeneration Institute of Jinan University, and the team of Professor Yuan Tifei from the Shanghai Mental Health Center elaborated on the molecular-cell loop mechanism of exercise to promote neurological rehabilitation after detoxification
.
A related study was recently published in Molecular Psychiatry under the title "Exercise Improves Cortical Synapse Defects Caused by Cocaine"
Drug addiction is accompanied by synaptic remodeling and functional changes in the cortex, leading to a decline in learning and memory functions
.
The Zhang Zhang team used the technique of transcranial in vivo two-photon imaging to dynamically map the dendritic spine remodeling of the fifth layer of pyramidal neurons in the primary motor cortex of mice after cocaine exposure; it was found that cocaine caused a reduction in the formation of dendritic spine, thereby mediating it.
The researchers further adopted the treadmill aerobic training mode and found that one week of exercise training can effectively enhance the remodeling of cortical pyramidal neuron dendritic spines and synaptic plasticity, reverse the loss of dendritic spines, and improve learning ability
.
In order to clarify the relevant neural circuit mechanism, the researchers found through in vivo two-photon calcium imaging technology that continuous cocaine exposure caused a significant decrease in the newborn rate of apical dendritic spines of the fifth layer of pyramidal neurons in the primary motor cortex of mice, accompanied by excitatory synapses.
The enhancement of transmission and the excessive activity of presynaptic somatostatin-positive interneurons (SST-IN) eventually lead to the imbalance of local excitation-inhibition balance (E/I balance)
.
These processes participate in the process of animal cognitive behavior impairment (such as the decline of motor learning ability)
In order to further analyze the molecular mechanism of the remodeling of cortical synaptic function caused by exercise, the researchers explored the changes in different molecular signaling pathways in the cortex and found that exercise can activate the target of rapamycin (mTOR) signaling pathway in the cortex
.
By pharmacological intervention or DOX-ON-mediated gene expression knockdown, inhibiting the mTOR pathway, or blocking the de novo protein synthesis pathway, can eliminate the remodeling of cortical synaptic function caused by exercise
This study reveals the mechanism of dendritic structure remodeling and synaptic function alteration of cognitive impairment caused by addictive drugs, and further analyzes the cellular and molecular mechanisms of exercise promoting cognitive function recovery, and provides more theoretical support for the field of exercise and brain health
.
The non-invasive measurement of synaptic function and neural activity in the motor cortex is expected to provide objective physiological indicators for the improvement of brain function in sports training; the development and research of drugs targeting exercise to regulate molecular signaling pathways in the brain will help to further optimize the brain function of exercise The effectiveness of regulation
It is reported that the experimental work was mainly completed by Cheng Tong, a neurobiology graduate of Jinan University.
Dr.
Huang Xiaodan of Jinan University, doctoral student Hu Xuefei, and undergraduate student Wang Siqi from the School of Life Science and Technology also participated in the project work
.
(Source: Zhu Hanbin, China Science News)
Related paper information: https://doi.
https://doi.
org/10.
1038/s41380-021-01336-2