| First Author | Royero P | Year | 2022 |
| Journal | Cell Rep | Volume | 41 |
| Issue | 10 | Pages | 111757 |
| PubMed ID | 36476865 | Mgi Jnum | J:333432 |
| Mgi Id | MGI:7410740 | Doi | 10.1016/j.celrep.2022.111757 |
| Citation | Royero P, et al. (2022) Circuit-selective cell-autonomous regulation of inhibition in pyramidal neurons by Ste20-like kinase. Cell Rep 41(10):111757 |
| abstractText | Maintaining an appropriate balance between excitation and inhibition is critical for neuronal information processing. Cortical neurons can cell-autonomously adjust the inhibition they receive to individual levels of excitatory input, but the underlying mechanisms are unclear. We describe that Ste20-like kinase (SLK) mediates cell-autonomous regulation of excitation-inhibition balance in the thalamocortical feedforward circuit, but not in the feedback circuit. This effect is due to regulation of inhibition originating from parvalbumin-expressing interneurons, while inhibition via somatostatin-expressing interneurons is unaffected. Computational modeling shows that this mechanism promotes stable excitatory-inhibitory ratios across pyramidal cells and ensures robust and sparse coding. Patch-clamp RNA sequencing yields genes differentially regulated by SLK knockdown, as well as genes associated with excitation-inhibition balance participating in transsynaptic communication and cytoskeletal dynamics. These data identify a mechanism for cell-autonomous regulation of a specific inhibitory circuit that is critical to ensure that a majority of cortical pyramidal cells participate in information coding. |
