Optogenetic Neuronal Stimulation Promotes Functional Recovery Of Lateral Amygdala After Endothelin-1-induced Mini-stroke

Occlusions in the blood supply to brain lead to a debilitating neurological symptoms termed ischemia stroke[1]. Focal stroke is associated with abnormal synaptic activity, morphologic plasticity and neurologic impairments [2, 3]. Clinical and research efforts have focused on promoting functional recovery after stroke. Functional recovery has been observed and is currently attributed to both brain remodeling and plasticity. Structural and functional remodeling of areas next to an infarct regions can alter signaling within bilateral neuronal networks and thus contribute to functional recovery [4- 7].Brain stimulation is a promising tool of research because it allows direct activation of the target area’s excitability. This techniques is limited by indiscriminate activation or inhibition of all cell types near the stimulated point[4, 7, 8].The latest study shows that the activation of upstream neurons in the neuronal network is important in the recovery after stroke[11].We tried to use optogenetics[9, 10] to selectively stimulate the neurons of AuV(the ventral part of the secondary auditory cortex), in order to promoting the recovery of LA.Based on the updated literature search, the neural circuit that begin from AuV to LA is a critical circuit of fear conditioning[12, 13]. Virus system that carried the protein channelrhodopsin-2(ChR-2) was injected into AuV. How does Optical stimulation activated neurons of AuV contribute to the endothelin-1-induced mini-stroke in the LA? This is exactly the point we are interested in.These findings suggest that ET-1-induced mini-infarct in deep brain area leads to functional deficits in learning and memory associated with these regions. Virus systems have successful expressions and excellent electrophysiological characteristics in vitro or in vivo.