학술논문

CREB controls cortical circuit plasticity and functional recovery after stroke.
Document Type
article
Source
Nature communications. 9(1)
Subject
Motor Cortex
Motor Neurons
Animals
Mice
Inbred C57BL
Brain Mapping
Patch-Clamp Techniques
Gene Expression Profiling
Recovery of Function
Neuronal Plasticity
Male
Cyclic AMP Response Element-Binding Protein
Stroke
Language
Abstract
Treatments that stimulate neuronal excitability enhance motor performance after stroke. cAMP-response-element binding protein (CREB) is a transcription factor that plays a key role in neuronal excitability. Increasing the levels of CREB with a viral vector in a small pool of motor neurons enhances motor recovery after stroke, while blocking CREB signaling prevents stroke recovery. Silencing CREB-transfected neurons in the peri-infarct region with the hM4Di-DREADD blocks motor recovery. Reversing this inhibition allows recovery to continue, demonstrating that by manipulating the activity of CREB-transfected neurons it is possible to turn off and on stroke recovery. CREB transfection enhances remapping of injured somatosensory and motor circuits, and induces the formation of new connections within these circuits. CREB is a central molecular node in the circuit responses after stroke that lead to recovery from motor deficits.