Journal
NATURE NEUROSCIENCE
Volume 16, Issue 1, Pages 64-U98Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.3269
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Funding
- US National Institute of Neurological Disorders and Stroke [K99NS078118-01, 5R01NS006477, 5R01NS034774]
- Epilepsy Foundation
- Berry Foundation
- Howard Hughes Medical Institute
- California Institute for Regenerative Medicine
- US National Institutes of Health
- Defence Advanced Research Projects Agency (DARPA) Reorganization and Plasticity to Accelerate Injury Recovery (REPAIR) Program
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS006477, K99NS078118, R01NS034774] Funding Source: NIH RePORTER
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Cerebrocortical injuries such as stroke are a major source of disability. Maladaptive consequences can result from post-injury local reorganization of cortical circuits. For example, epilepsy is a common sequela of cortical stroke, but the mechanisms responsible for seizures following cortical injuries remain unknown. In addition to local reorganization, long-range, extra-cortical connections might be critical for seizure maintenance. In rats, we found that the thalamus, a structure that is remote from, but connected to, the injured cortex, was required to maintain cortical seizures. Thalamocortical neurons connected to the injured epileptic cortex underwent changes in HCN channel expression and became hyperexcitable. Targeting these neurons with a closed-loop optogenetic strategy revealed that reducing their activity in real-time was sufficient to immediately interrupt electrographic and behavioral seizures. This approach is of therapeutic interest for intractable epilepsy, as it spares cortical function between seizures, in contrast with existing treatments, such as surgical lesioning or drugs.
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