Physical exercise rescues cocaine-evoked synaptic deficits in motor cortex.
Tong ChengXiao-Dan HuangXue-Fei HuSi-Qi WangKai ChenJi-An WeiLan YanKowk-Fai SoTi-Fei YuanLi ZhangPublished in: Molecular psychiatry (2021)
Drug exposure impairs cortical plasticity and motor learning, which underlies the reduced behavioral flexibility in drug addiction. Physical exercise has been used to prevent relapse in drug rehabilitation program. However, the potential benefits and molecular mechanisms of physical exercise on drug-evoked motor-cortical dysfunctions are unknown. Here we report that 1-week treadmill training restores cocaine-induced synaptic deficits, in the form of improved in vivo spine formation, synaptic transmission, and spontaneous activities of cortical pyramidal neurons, as well as motor-learning ability. The synaptic and behavioral benefits relied on de novo protein synthesis, which are directed by the activation of the mechanistic target of rapamycin (mTOR)-ribosomal protein S6 pathway. These findings establish synaptic functional restoration and mTOR signaling as the critical mechanism supporting physical exercise training in rehabilitating the addicted brain.
Keyphrases
- prefrontal cortex
- drug induced
- traumatic brain injury
- adverse drug
- cell proliferation
- mental health
- spinal cord
- skeletal muscle
- emergency department
- multiple sclerosis
- randomized controlled trial
- spinal cord injury
- small molecule
- resting state
- climate change
- functional connectivity
- brain injury
- study protocol
- amino acid
- electronic health record
- placebo controlled
- free survival