ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Impairment of catecholamine systems during induction of long-term potentiation at hippocampal CA1 synapses in HPC-1/syntaxin 1A knock-out mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Alterations in brain synaptic proteins and mRNAs in mood disorders: a systematic review and meta-analysis of postmortem brain studies.Molecular psychiatry · 2022Pooled it
- Article
- Syntaxin1A in synaptopathies: From molecular mechanisms to therapeutic implications in neurological disorders (Review).Biomedical reports · 2026Review
- Genetic disorders of neurotransmitter release machinery.Frontiers in synaptic neuroscience · 2023Review
- Differential hippocampal protein expression between normal mice and mice with the perioperative neurocognitive disorder: a proteomic analysis.European journal of medical research · 2021Article
- Alterations in the Serotonin and Dopamine Pathways by Cystathionine Beta Synthase Overexpression in Murine Brain.Molecular neurobiology · 2019Article
- Molecular changes in the absence of severe pathology in the pulvinar in dementia with Lewy bodies.Movement disorders : official journal of the Movement Disorder Society · 2018Article
- Moderate decline in select synaptic markers in the prefrontal cortex (BA9) of patients with Alzheimer's disease at various cognitive stages.Scientific reports · 2018Article
- The Molecular and Neuropathological Consequences of Genetic Risk for Alzheimer's Dementia.Frontiers in neuroscience · 2018Article
- New Roles of Syntaxin-1A in Insulin Granule Exocytosis and Replenishment.The Journal of biological chemistry · 2017Article
- Synaptic plasticity and spatial working memory are impaired in the CD mouse model of Williams-Beuren syndrome.Molecular brain · 2016Article
- Conformational states of syntaxin-1 govern the necessity of N-peptide binding in exocytosis of PC12 cells and Caenorhabditis elegans.Molecular biology of the cell · 2016Article
- Targeted deletion of miR-132/-212 impairs memory and alters the hippocampal transcriptome.Learning & memory (Cold Spring Harbor, N.Y.) · 2016Article
- Different patterns of electrical activity lead to long-term potentiation by activating different intracellular pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Construction and analysis of the protein-protein interaction networks based on gene expression profiles of Parkinson's disease.PloS one · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The membrane protein HPC-1/syntaxin 1A is believed to play a key role in synaptic vesicle exocytosis, and it was recently suggested to be required for synaptic plasticity. Despite evidence for the function of HPC-1/syntaxin 1A in synaptic plasticity, the underlying cellular mechanism is unclear. We found that although fast synaptic transmission and long-term depression were unaffected, HPC-1/syntaxin 1A knock-out (STX1A(-/-)) mice showed impaired long-term potentiation (LTP) in response to theta-burst stimulation in CA1 hippocampal slices. The impairment in LTP was rescued by the application of forskolin, an adenylyl cyclase activator, or more robust stimulation, suggesting that cAMP/protein kinase A signaling was suppressed in these mice. In addition, catecholamine release from the hippocampus was significantly reduced in STX1A(-/-) mice. Because HPC-1/syntaxin 1A regulates exocytosis of dense-core synaptic vesicles, which contain neuromodulatory transmitters such as noradrenaline, dopamine and 5-HT, we examined the effect of neuromodulatory transmitters on LTP induction. Noradrenaline and dopamine enhanced LTP induction in STX1A(-/-) mice, whereas catecholamine depletion reduced LTP induction in wild-type mice. Theses results suggest that HPC-1/syntaxin 1A regulates catecholaminergic systems via exocytosis of dense-core synaptic vesicles, and that deletion of HPC-1/syntaxin 1A causes impairment of LTP induction.
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