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Posted On: 03/23/2025 4:00:30 AM
Post# of 155754
Jan 10th, 2011 -- A new window of opportunity for stroke rehabilitation?
In a mouse stroke model, Tom Carmichael and his colleagues at the University of California, Los Angeles demonstrated increased γ-aminobutyric acid (GABA)-mediated tonic inhibition in the peri-infarct zone, and showed that an inverse agonist of extrasynaptic GABAA receptors could promote recovery of motor function in the animals.
https://www.nature.com/articles/nrneurol.2010.194
June 2018 publication:
CREB controls cortical circuit plasticity and functional recovery after stroke
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.
https://www.researchgate.net/publication/3256...ter_stroke
Thx Ohm !!
In a mouse stroke model, Tom Carmichael and his colleagues at the University of California, Los Angeles demonstrated increased γ-aminobutyric acid (GABA)-mediated tonic inhibition in the peri-infarct zone, and showed that an inverse agonist of extrasynaptic GABAA receptors could promote recovery of motor function in the animals.
https://www.nature.com/articles/nrneurol.2010.194
June 2018 publication:
CREB controls cortical circuit plasticity and functional recovery after stroke
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.
https://www.researchgate.net/publication/3256...ter_stroke
Thx Ohm !!
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