Somatostatin-positive interneurons in the dentate gyrus of mice provide local- and long-range septal synaptic inhibition
Abstract
Somatostatin-expressing-interneurons (SOMIs) in the dentate gyrus (DG) control formation of granule cell (GC) assemblies during memory acquisition. Hilar-perforant-path-associated interneurons (HIPP cells) have been considered to be synonymous for DG-SOMIs. Deviating from this assumption, we show two functionally contrasting DG-SOMI-types. The classical feedback-inhibitory HIPPs distribute axon fibers in the molecular layer. They are engaged by converging GC-inputs and provide dendritic inhibition to the DG circuitry. In contrast, SOMIs with axon in the hilus, termed hilar interneurons (HILs), provide perisomatic inhibition onto GABAergic cells in the DG and project to the medial septum. Repetitive activation of glutamatergic inputs onto HIPP cells induces long-lasting-depression (LTD) of synaptic transmission but long-term-potentiation (LTP) of synaptic signals in HIL cells. Thus, LTD in HIPPs may assist flow of spatial information from the entorhinal cortex to the DG, whereas LTP in HILs may facilitate the temporal coordination of GCs with activity patterns governed by the medial septum.
Article and author information
Author details
Funding
Deutsche Forschungsgemeinschaft (FOR2143)
- Marlene Bartos
Volkswagen Foundation (Lichtenberg Award)
- Marlene Bartos
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Animal experimentation: All animal procedures were performed in accordance to national and european legislations (license no.: G-11/53; X-12/20D).
Reviewing Editor
- Gary L Westbrook, Vollum Institute, United States
Publication history
- Received: August 31, 2016
- Accepted: April 1, 2017
- Accepted Manuscript published: April 3, 2017 (version 1)
- Version of Record published: April 18, 2017 (version 2)
Copyright
© 2017, Yuan et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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