Kainate-type of glutamate receptors regulate development of glutamatergic synaptic circuitry in the rodent amygdala
Abstract
Perturbed information processing in the amygdala has been implicated in developmentally originating neuropsychiatric disorders. However, little is known on the mechanisms that guide formation and refinement of intrinsic connections between amygdaloid nuclei. We demonstrate that in rodents the glutamatergic connection from basolateral to central amygdala (BLA-CeA) develops rapidly during the first ten postnatal days, before external inputs underlying amygdala dependent behaviors emerge. During this restricted period of synaptic development, kainate-type of ionotropic glutamate receptors (KARs) are highly expressed in the BLA and tonically activated to regulate glutamate release via a G-protein dependent mechanism. Genetic manipulation of this endogenous KAR activity locally in the newborn LA perturbed development of glutamatergic input to CeA, identifying KARs as a physiological mechanism regulating formation of the glutamatergic circuitry in the amygdala.
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All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided for all Figures.
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Author details
Funding
Academy of Finland (SA 297211)
- Sari E Lauri
Aatos Erkko Foundation
- Sari E Lauri
Sigrid Juselius Foundation
- Sari E Lauri
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 experiments were done in accordance with the guidelines given by the ethics committee for animal research at the University of Helsinki (license numbers ESAVI/6853/04.10.07/2017 and ESAVI/29384/2019).
Copyright
© 2020, Ryazantseva 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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