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VTA DA neuron excitatory synapses in Shank3 Δex4-9 mouse line

Published in Synapse. 2017, vol. 71, no. 6
Abstract Several mutations within SHANK3 gene have been identified in Autism Spectrum Disorder patients and several studies have now started to show that those mutations could impact different brain circuits leading to the heterogeneity of the disease. Here we show that, compared to a mouse model lacking SHANK3 proline-rich containing isoforms, in a mouse model lacking SHANK3 ANK(yrin)-domain containing isoforms, the excitatory synaptic transmission within the Ventral Tegmental Area is not affected. We discuss about the possibility that different domains of SHANK3 are involved in regulating the synapses in a circuit-specific manner resulting in different behavioral and synaptic phenotypes.
Keywords AnimalsAutism Spectrum Disorder/genetics/physiopathologyDopaminergic Neurons/metabolism/physiologyExcitatory Postsynaptic PotentialsGene DeletionMiceNerve Tissue Proteins/chemistry/genetics/metabolismPhenotypeProtein DomainsProtein Isoforms/chemistry/genetics/metabolismReceptorsAMPA/chemistry/genetics/metabolismReceptorsN-Methyl-D-Aspartate/chemistry/genetics/metabolismVentral Tegmental Area/cytology/metabolism/physiology
PMID: 28002633
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Research group Les dysfonctions synaptiques du cerveau (971)
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BARISELLI, Sebastiano, BELLONE, Camilla. VTA DA neuron excitatory synapses in Shank3 Δex4-9 mouse line. In: Synapse, 2017, vol. 71, n° 6. doi: 10.1002/syn.21955 https://archive-ouverte.unige.ch/unige:111208

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Deposited on : 2018-11-21

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