ArticleMolecular brain2018
Reduced synaptic function of Kainate receptors in the insular cortex of Fmr1 Knock-out mice.
Article in Molecular brain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 9 citations in OpenAlex.
- Aberrant hippocampal gamma oscillations in a mouse model of fragile X syndrome: insights from in vitro slice models.Molecular autism · 2025Article
- Increased degradation of FMRP contributes to neuronal hyperexcitability in tuberous sclerosis complex.Cell reports · 2023Article
- An intellectual-disability-associated mutation of the transcriptional regulatorFrontiers in molecular neuroscience · 2023Review
- Multiple synaptic connections into a single cortical pyramidal cell or interneuron in the anterior cingulate cortex of adult mice.Molecular brain · 2021Article
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Authors and funding
6 authors at 5 institutions in 2 countries.
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Abstract
Fragile X syndrome is caused by the loss of fragile X mental retardation protein (FMRP). Kainate receptor (KAR) is a subfamily of ionotropic glutamate receptors (iGluR) that acts mainly as a neuromodulator of synaptic transmission and neuronal excitability. However, little is known about the changes of synaptic KAR in the cortical area of Fmr1 KO mice. In this study, we performed whole-cell patch-clamp recordings from layer II/III pyramidal neurons in the insular cortex of Fmr1 KO mice. We found that KARs mediated currents were reduced in Fmr1 KO mice. KARs were mainly located in the synaptosomal fraction of the insular cortex. The abundance of KAR subunit GluK1 and GluK2/3 in the synaptosome was reduced in Fmr1 KO mice, whereas the total expressions of these KARs subunits were not changed. Finally, lack of FMRP impairs subsequent internalization of surface GluK2 after KAR activation, while having no effect on the surface GluK2 expression. Our studies provide evidence indicating that loss of FMRP leads to the abnormal function and localization of KARs. This finding implies a new molecular mechanism for Fragile X syndrome.
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