ArticleNeuroscience2016
Characterization of cognitive impairments and neurotransmitter changes in a novel transgenic mouse lacking Slc10a4.
Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Serotonergic SLC10A4 regulates extracellular serotonin levels and antidepressant responsiveness.Molecular psychiatry · 2026Article
- Frequency and duration of sensory flicker control transcriptional profiles in 5xFAD mice.APL bioengineering · 2025Article
- Integrative multiomics reveals common endotypes across PSEN1, PSEN2, and APP mutations in familial Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Role of the Sodium-Dependent Organic Anion Transporter (SOAT/SLC10A6) in Physiology and Pathophysiology.International journal of molecular sciences · 2023Review
- Tsc1-mTORC1 signaling controls striatal dopamine release and cognitive flexibility.Nature communications · 2019Article
- Icariside II affects hippocampal neuron axon regeneration and improves learning and memory in a chronic cerebral hypoperfusion rat model.International journal of clinical and experimental pathology · 2019Article
- Sigmoid colon mucosal gene expression supports alterations of neuronal signaling in irritable bowel syndrome with constipation.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Recent advances in understanding hepatic drug transport.F1000Research · 2016Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
An orphan member of the solute carrier (SLC) family SLC10, SLC10A4 has been found to be enriched in midbrain and brainstem neurons and has been found to co-localize with and to affect dopamine (DA) homeostasis. We generated an SLC10A4 knockout mouse (Slc10a4(Δ/Δ)) using Cre-targeted recombination, and characterized behavioral measures of motor and cognitive function as well as DA and acetylcholine (ACh) levels in midbrain and brainstem. In agreement with previous studies, Slc10a4 mRNA was preferentially expressed in neurons in the brains of wild-type (Slc10a4(+/+)) mice and was enriched in dopaminergic and cholinergic regions. Slc10a4(Δ/Δ) mice had no impairment in motor function or novelty-induced exploratory behaviors but performed significantly worse in measures of spatial memory and cognitive flexibility. Slc10a4(Δ/Δ) mice also did not differ from Slc10a4(+/+) in measures of anxiety. High-performance liquid chromatography (HPLC) measures on tissue punches taken from the dorsal and ventral striatum reveal a decrease in DA content and a corresponding increase in the metabolite 3,4-dihydroxyphenylacetic acid (DOPAC), indicating an increase in DA turnover. Punches taken from the brainstem revealed a decrease in ACh as compared with Slc10a4(+/+) littermates. Together, these data indicate that loss of SLC10A4 protein results in neurotransmitter imbalance and cognitive impairment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.