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- W3157185367 abstract "Serotonin 6 receptor (5-HT6R) is a promising target for a variety of human diseases, such as Alzheimer's disease (AD) and schizophrenia. However, the detailed mechanism underlying 5-HT6R activity in the central nervous system (CNS) is not fully understood. In the present study, 5-HT6R null mutant (5-HT6R-/- ) mice were found to exhibit cognitive deficiencies and abnormal anxiety levels. 5-HT6R is considered to be specifically localized on the primary cilia. We found that the loss of 5-HT6R affected the Sonic Hedgehog signaling pathway in the primary cilia. 5-HT6R-/- mice showed remarkable alterations in neuronal morphology, including dendrite complexity and axon initial segment morphology. Neurons lacking 5-HT6R exhibited increased neuronal excitability. Our findings highlight the complexity of 5-HT6R functions in the primary ciliary and neuronal physiology, supporting the theory that this receptor modulates neuronal morphology and transmission, and contributes to cognitive deficits in a variety of human diseases, such as AD, schizophrenia, and ciliopathies." @default.
- W3157185367 created "2021-05-10" @default.
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- W3157185367 date "2021-05-07" @default.
- W3157185367 modified "2023-10-12" @default.
- W3157185367 title "5‐HT6R null mutatrion induces synaptic and cognitive defects" @default.
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- W3157185367 doi "https://doi.org/10.1111/acel.13369" @default.
- W3157185367 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8208783" @default.
- W3157185367 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33960602" @default.
- W3157185367 hasPublicationYear "2021" @default.
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