| First Author | Stevens SR | Year | 2021 |
| Journal | Elife | Volume | 10 |
| PubMed ID | 34180393 | Mgi Jnum | J:310189 |
| Mgi Id | MGI:6727693 | Doi | 10.7554/eLife.66491 |
| Citation | Stevens SR, et al. (2021) Ankyrin-R regulates fast-spiking interneuron excitability through perineuronal nets and Kv3.1b K(+) channels. Elife 10:e66491 |
| abstractText | Neuronal ankyrins cluster and link membrane proteins to the actin and spectrin-based cytoskeleton. Among the three vertebrate ankyrins, little is known about neuronal Ankyrin-R (AnkR). We report AnkR is highly enriched in Pv(+) fast-spiking interneurons in mouse and human. We identify AnkR-associated protein complexes including cytoskeletal proteins, cell adhesion molecules (CAMs), and perineuronal nets (PNNs). We show that loss of AnkR from forebrain interneurons reduces and disrupts PNNs, decreases anxiety-like behaviors, and changes the intrinsic excitability and firing properties of Pv(+) fast-spiking interneurons. These changes are accompanied by a dramatic reduction in Kv3.1b K(+) channels. We identify a novel AnkR-binding motif in Kv3.1b, and show that AnkR is both necessary and sufficient for Kv3.1b membrane localization in interneurons and at nodes of Ranvier. Thus, AnkR regulates Pv(+) fast-spiking interneuron function by organizing ion channels, CAMs, and PNNs, and linking these to the underlying beta1 spectrin-based cytoskeleton. |
