| First Author | Grosser S | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 1 | Pages | e86250 |
| PubMed ID | 24465989 | Mgi Jnum | J:359413 |
| Mgi Id | MGI:6244801 | Doi | 10.1371/journal.pone.0086250 |
| Citation | Grosser S, et al. (2014) Hilar somatostatin interneurons contribute to synchronized GABA activity in an in vitro epilepsy model. PLoS One 9(1):e86250 |
| abstractText | Epilepsy is a disorder characterized by excessive synchronized neural activity. The hippocampus and surrounding temporal lobe structures appear particularly sensitive to epileptiform activity. Somatostatin (SST)-positive interneurons within the hilar region have been suggested to gate hippocampal activity, and therefore may play a crucial role in the dysregulation of hippocampal activity. In this study, we examined SST interneuron activity in the in vitro 4-aminopyridine (4-AP) model of epilepsy. We employed a multi-disciplinary approach, combining extracellular multi-electrode array (MEA) recordings with patch-clamp recordings and optical imaging using a genetically encoded calcium sensor. We observed that hilar SST interneurons are strongly synchronized during 4-AP-induced local field potentials (LFPs), as assayed by Ca(2+) imaging as well as juxtacellular or intracellular recording. SST interneurons were particularly responsive to GABA-mediated LFPs that occurred in the absence of ionotropic glutamatergic transmission. Our results present evidence that the extensive synchronized activity of SST-expressing interneurons contribute to the generation of GABAergic LFPs in an in vitro model of temporal lobe seizures. |
