Somatostatin interneurons activated by 5-HT2A receptor suppress slow oscillations in medial entorhinal cortex
Year: 2021
Type: article
Abstract: Serotonin (5-HT) is one of the major neuromodulators present in the mammalian brain and has been shown to play a role in multiple physiological processes. The mechanisms by which 5-HT modulates cortical network activity, however, are not yet fully understood. We investigated the effects of 5-HT on slow oscillations (SOs), a synchronized cortical network activity universally present across species. SOs are observed during anesthesia and are considered to be the default cortical activity pattern. We discovered that (±)3,4-methylenedioxymethamphetamine (MDMA) and fenfluramine, two potent 5-HT releasers, inhibit SOs within the entorhinal cortex (EC) in anesthetized mice. Combining opto- and pharmacogenetic manipulations with in vitro electrophysiological recordings, we uncovered that somatostatin-expressing (Sst) interneurons activated by the 5-HT 2A receptor (5-HT 2A R) play an important role in the suppression of SOs. Since 5-HT 2A R signaling is involved in the etiology of different psychiatric disorders and mediates the psychological effects of many psychoactive serotonergic drugs, we propose that the newly discovered link between Sst interneurons and 5-HT will contribute to our understanding of these complex topics.
Source: eLife
DOI: 10.7554/elife.66960
Authors: Roberto De Filippo, Benjamin R. Rost, Alexander Stumpf, Claire Cooper, John J. Tukker, Christoph Harms, Prateep Beed, Dietmar Schmitz
Institutions: Humboldt-Universität zu Berlin, Berlin Institute of Health at Charité - Universitätsmedizin Berlin, NeuroCure Cluster of Excellence, Freie Universität Berlin, Charité - Universitätsmedizin Berlin, German Center for Neurodegenerative Diseases, Einstein Center for Neurosciences Berlin, Center for Stroke Research Berlin
Language: English
Subfield: Cognitive Neuroscience
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,500
OpenAlex ID: W3151129275
