40-Hz optogenetic stimulation rescues functional synaptic plasticity after stroke
Cong Wang,
Caixia Lin,
Yue Zhao,
Montana Samantzis,
Petra Sedlak,
Pankaj Sah,
Matilde Balbi
Affiliations
Cong Wang
Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4067, Australia; Engineering Research Centre of Traditional Chinese Medicine Intelligent Rehabilitation, Ministry of Education, Shanghai 201203, China
Caixia Lin
Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4067, Australia
Yue Zhao
Departments of Thoracic Surgery and State Key Laboratory of Genetic Engineering, Fudan University Shanghai Cancer Centre, Shanghai 200032, China; Institute of Thoracic Oncology, Fudan University, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China
Montana Samantzis
Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4067, Australia
Petra Sedlak
Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4067, Australia
Pankaj Sah
Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4067, Australia
Matilde Balbi
Queensland Brain Institute, The University of Queensland, Brisbane, QLD 4067, Australia; Corresponding author
Summary: Evoked brain oscillations in the gamma range have been shown to assist in stroke recovery. However, the causal relationship between evoked oscillations and neuroprotection is not well understood. We have used optogenetic stimulation to investigate how evoked gamma oscillations modulate cortical dynamics in the acute phase after stroke. Our results reveal that stimulation at 40 Hz drives activity in interneurons at the stimulation frequency and phase-locked activity in principal neurons at a lower frequency, leading to increased cross-frequency coupling. In addition, 40-Hz stimulation after stroke enhances interregional communication. These effects are observed up to 24 h after stimulation. Our stimulation protocol also rescues functional synaptic plasticity 24 h after stroke and leads to an upregulation of plasticity genes and a downregulation of cell death genes. Together these results suggest that restoration of cortical dynamics may confer neuroprotection after stroke.
