Kainate receptors regulate development of glutamatergic synaptic circuitry in the rodent amygdala

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http://hdl.handle.net/10138/314212

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Ryazantseva , M , Englund , J , Shintyapina , A , Huupponen , J , Shteinikov , V , Pitkänen , A , Partanen , J M & Lauri , S E 2020 , ' Kainate receptors regulate development of glutamatergic synaptic circuitry in the rodent amygdala ' , eLife , vol. 9 , 52798 . https://doi.org/10.7554/eLife.52798

Title: Kainate receptors regulate development of glutamatergic synaptic circuitry in the rodent amygdala
Author: Ryazantseva, Maria; Englund, Jonas; Shintyapina, Alexandra; Huupponen, Johanna; Shteinikov, Vasilii; Pitkänen, Asla; Partanen, Juha M; Lauri, Sari E
Contributor: University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Neuroscience Center
University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Molecular and Integrative Biosciences Research Programme
University of Helsinki, Molecular and Integrative Biosciences Research Programme
Date: 2020-03-23
Language: eng
Number of pages: 25
Belongs to series: eLife
ISSN: 2050-084X
URI: http://hdl.handle.net/10138/314212
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 10 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.
Subject: 3112 Neurosciences
glutamate receptor
amygdala
synaptic transmission
circuit development
SYSTEM
ACTIVATION
BASOLATERAL AMYGDALA
POSTNATAL MATURATION
HIPPOCAMPAL
ACQUISITION
FACILITATION
FEAR
TRANSMISSION
EXPRESSION
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