GluA4 Dependent Plasticity Mechanisms Contribute to Developmental Synchronization of the CA3-CA1 Circuitry in the Hippocampus

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Atanasova , T , Kharybina , Z , Kaarela , T A M , Huupponen , J T , Luchkina , N , Taira , T P & Lauri , S E 2019 , ' GluA4 Dependent Plasticity Mechanisms Contribute to Developmental Synchronization of the CA3-CA1 Circuitry in the Hippocampus ' , Neurochemical Research , vol. 44 , no. 3 , pp. 562–571 . https://doi.org/10.1007/s11064-017-2392-8

Title: GluA4 Dependent Plasticity Mechanisms Contribute to Developmental Synchronization of the CA3-CA1 Circuitry in the Hippocampus
Author: Atanasova, Tsvetomira; Kharybina, Zoya; Kaarela, Tiina Anna Marjatta; Huupponen, Johanna Tuulia; Luchkina, Natalia; Taira, Tomi Petteri; Lauri, Sari Elina
Contributor organization: Departments of Faculty of Veterinary Medicine
Neuroscience Center
Veterinary Biosciences
Biosciences
Synaptic Plasticity and Neuronal Synchronization
Tomi Taira / Principal Investigator
Syn­aptic Plas­ti­city and De­vel­op­ment
Physiology and Neuroscience (-2020)
Date: 2019-03
Language: eng
Number of pages: 10
Belongs to series: Neurochemical Research
ISSN: 0364-3190
DOI: https://doi.org/10.1007/s11064-017-2392-8
URI: http://hdl.handle.net/10138/311728
Abstract: During the course of development, molecular mechanisms underlying activity-dependent synaptic plasticity change considerably. At immature CA3-CA1 synapses in the hippocampus, PKA-driven synaptic insertion of GluA4 AMPA receptors is the predominant mechanism for synaptic strengthening. However, the physiological significance of the developmentally restricted GluA4-dependent plasticity mechanisms is poorly understood. Here we have used microelectrode array (MEA) recordings in GluA4 deficient slice cultures to study the role of GluA4 in early development of the hippocampal circuit function. We find that during the first week in culture (DIV2-6) when GluA4 expression is restricted to pyramidal neurons, loss of GluA4 has no effect on the overall excitability of the immature network, but significantly impairs synchronization of the CA3 and CA1 neuronal populations. In the absence of GluA4, the temporal correlation of the population spiking activity between CA3-CA1 neurons was significantly lower as compared to wild-types at DIV6. Our data show that synapse-level defects in transmission and plasticity mechanisms are efficiently compensated for to normalize population firing rate at the immature hippocampal network. However, lack of the plasticity mechanisms typical for the immature synapses may perturb functional coupling between neuronal sub-populations, a defect frequently implicated in the context of developmentally originating neuropsychiatric disorders.
Subject: 3112 Neurosciences
AMPA receptor
GluA4
Synaptic plasticity
Firing rate homeostasis
AMPA-RECEPTORS
FUNCTIONAL MATURATION
PHOSPHORYLATION SITE
GLUTAMATE RECEPTORS
SYNAPTIC EFFICACY
NETWORK ACTIVITY
SUBUNIT
LTP
CA1
SCHIZOPHRENIA
Peer reviewed: Yes
Usage restriction: openAccess
Self-archived version: acceptedVersion


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