NDLI: Knockdown of Myo-Inositol Transporter SMIT1 Normalizes Cholinergic and Glutamatergic Function in an Immortalized Cell Line Established from the Cerebral Cortex of a Trisomy 16 Fetal Mouse, an Animal Model of Human Trisomy 21 (Down Syndrome)

Content Provider	Springer Nature Link
Author	Cárdenas, Ana María Fernández Olivares, Paola Díaz Franulic, Ignacio González Jamett, Arlek M. Shimahara, Takeshi Segura Aguilar, Juan Caviedes, Raúl Caviedes, Pablo
Copyright Year	2017
Abstract	The Na$^{+}$/myo-inositol cotransporter (SMIT1) is overexpressed in human Down syndrome (DS) and in trisomy 16 fetal mice (Ts16), an animal model of the human condition. SMIT1 overexpression determines increased levels of intracellular myo-inositol, a precursor of phophoinositide synthesis. SMIT1 is overexpressed in CTb cells, an immortalized cell line established from the cerebral cortex of a Ts16 mouse fetus. CTb cells exhibit impaired cytosolic Ca$^{2+}$ signals in response to glutamatergic and cholinergic stimuli (increased amplitude and delayed time-dependent kinetics in the decay post-stimulation), compared to our CNh cell line, derived from the cerebral cortex of a euploid animal. Considering the role of myo-inositol in intracellular signaling, we normalized SMIT1 expression in CTb cells using specific mRNA antisenses. Forty-eight hours post-transfection, SMIT1 levels in CTb cells reached values comparable to those of CNh cells. At this time, decay kinetics of Ca$^{2+}$ signals induced by either glutamate, nicotine, or muscarine were accelerated in transfected CTb cells, to values similar to those of CNh cells. The amplitude of glutamate-induced cytosolic Ca$^{2+}$ signals in CTb cells was also normalized. The results suggest that SMIT1 overexpression contributes to abnormal cholinergic and glutamatergic Ca$^{2+}$ signals in the trisomic condition, and knockdown of DS-related genes in our Ts16-derived cell line could constitute a relevant tool to study DS-related neuronal dysfunction.
Starting Page	614
Ending Page	623
Page Count	10
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	32
Issue Number	4
e-ISSN	14763524
Language	English
Publisher	Springer US
Publisher Date	2017-07-10
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Down syndrome SMIT1 Myo-inositol Calcium Glutamate Cholinergic Neurosciences Neurology Neurochemistry Pharmacology/Toxicology Neurobiology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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