Impaired hippocampal NMDAR-LTP in a transgenic model of NSUN2-deficiency

Harry George, Zafar Bashir, Shobbir Hussain

Research output: Contribution to journalArticlepeer-review

1 Citation (SciVal)

Abstract

Biallelic loss-of-function NSUN2 mutations have recently been associated with cases of Autism Spectrum Condition (ASC), and NSun2-deficiency was also previously shown to cause a severe autosomal recessive intellectually disability disorder syndrome in which patients can sometimes display autistic behaviour. It has been demonstrated that NSUN2 can control protein synthesis rates via direct regulation of RNA methylation, and it is therefore of interest that other studies have suggested protein synthesis-dependent synaptic plasticity dysregulation as a mechanism for learning difficulties in various other autism-expressing conditions and disorders. Here we investigated NMDAR-LTP in a murine transgenic model harbouring loss-of-function mutation in the NSun2 gene and find an impairment of a protein synthesis-dependent form of this synaptic plasticity pathway. Our findings support the idea that NMDAR-LTP mis-regulation may represent a previously underappreciated mechanism associated with autism phenotypes.
Original languageEnglish
Article number105597
JournalNeurobiology of Disease
Volume163
Early online date23 Dec 2021
DOIs
Publication statusPublished - 28 Feb 2022

Keywords

  • ASC
  • ASD
  • Autism
  • Intellectual disability
  • NMDAR-LTP
  • NSun2
  • Synaptic plasticity

ASJC Scopus subject areas

  • Neurology

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