Early postnatal inhibition of GLAST causes abnormalities of psychobehaviors and neuronal morphology in adult mice

Mizuki Uchida, Yukihiro Noda, Sho Hasegawa, Hirotake Hida, Masayuki Taniguchi, Akihiro Mouri, Akira Yoshimi, Toshitaka Nabeshima, Kiyofumi Yamada, Tomomi Aida, Kohichi Tanaka, Norio Ozaki

Research output: Contribution to journalArticlepeer-review

Abstract

The importance of glutamate transporters in learning, memory, and emotion remains poorly understood; hence, in the present study, we investigated whether deficiency of pharmacological GLAST in neurodevelopmental processes affects cognitive and/or emotional behaviors in mice. The mice were injected with a glutamate transporter inhibitor, DL-threo-β-benzyloxyaspartate (DL-TBOA), during the early postnatal period. At 8 weeks of age, they showed impairments in cognitive or emotional behaviors; dysfunction of glutamatergic neurotransmission (increased expressions of GLAST, GLT-1, or GFAP protein, and decreased ability of glutamate release) in the cortex or hippocampus; morphological changes (decreased cell size in the cortex and thickness of the pyramidal neuronal layer of the CA1 area in the hippocampus). Such behavioral and morphological changes were not observed in adult mice injected with DL-TBOA. These results suggest that GLAST plays an important role in the regulation of cognitive and emotional behaviors. Early postnatal glutamatergic facilitation by GLAST dysfunction leads to cognitive and emotional abnormalities due to neurodevelopmental abnormalities such as morphological changes.

Original languageEnglish
Article number105177
JournalNeurochemistry International
Volume150
DOIs
Publication statusPublished - 11-2021
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cell Biology

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