Neuroscience incorporates manipulating neuronal circuitry to enhance the understanding of intricate brain functions. An effective strategy to attain this objective entails utilizing viral vectors to induce varied gene expression by delivering transgenes into brain cells. Here, we combine the use of transgenic mice, neonatal transduction with adeno-associated viral constructs harboring inhibitory designer receptor exclusively activated by designer drug (DREADD) gene, and the DREADD agonist clozapine N-oxide (CNO).
View Article and Find Full Text PDFKey Points: Recovery from the potentially devastating consequences of stroke depends largely upon plastic changes occurring in the lesion periphery and its inputs. In a focal model of stroke in mouse somatosensory cortex, we found that the recovery of sensory responsiveness occurs at the level of synaptic inputs, without gross changes of the intrinsic electrical excitability of neurons, and also that recovered responses had longer than normal latencies. Under normal conditions, one somatosensory cortex inhibits the responsiveness of the other located in the opposite hemisphere (interhemispheric inhibition) via activation of GABA receptors.
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