| First Author | Scheyltjens I | Year | 2018 |
| Journal | Brain Struct Funct | Volume | 223 |
| Issue | 5 | Pages | 2073-2095 |
| PubMed ID | 29372324 | Mgi Jnum | J:313221 |
| Mgi Id | MGI:6791671 | Doi | 10.1007/s00429-018-1611-7 |
| Citation | Scheyltjens I, et al. (2018) Transient and localized optogenetic activation of somatostatin-interneurons in mouse visual cortex abolishes long-term cortical plasticity due to vision loss. Brain Struct Funct 223(5):2073-2095 |
| abstractText | Unilateral vision loss through monocular enucleation (ME) results in partial reallocation of visual cortical territory to another sense in adult mice. The functional recovery of the visual cortex occurs through a combination of spared-eye potentiation and cross-modal reactivation driven by whisker-related, somatosensory inputs. Brain region-specific intracortical inhibition was recently recognized as a crucial regulator of the cross-modal component, yet the contribution of specific inhibitory neuron subpopulations remains poorly understood. Somatostatin (SST)-interneurons are ideally located within the cortical circuit to modulate sensory integration. Here we demonstrate that optogenetic stimulation of visual cortex SST-interneurons prior to eye removal decreases ME-induced cross-modal recovery at the stimulation site. Our results suggest that SST-interneurons act as local hubs, which are able to control the influx and extent of cortical cross-modal inputs into the deprived cortex. These insights critically expand our understanding of SST-interneuron-specific regulation of cortical plasticity induced by sensory loss. |
