ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Synapsin II Regulation of GABAergic Synaptic Transmission Is Dependent on Interneuron Subtype.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Early endocannabinoid-mediated depolarization-induced suppression of excitation delays the appearance of the epileptic phenotype in synapsin II knockout mice.Cellular and molecular life sciences : CMLS · 2024Article
- Preferential expression of SCN1A in GABAergic neurons improves survival and epileptic phenotype in a mouse model of Dravet syndrome.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Early Alterations in Structural and Functional Properties in the Neuromuscular Junctions of Mutant FUS Mice.International journal of molecular sciences · 2023Article
- Neonatal Oxidative Stress Impairs Cortical Synapse Formation and GABA Homeostasis in Parvalbumin-Expressing Interneurons.Oxidative medicine and cellular longevity · 2022Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 4 countries.
Funding
Abstract
Synapsins are epilepsy susceptibility genes that encode phosphoproteins reversibly associated with synaptic vesicles. Synapsin II (SynII) gene deletion produces a deficit in inhibitory synaptic transmission, and this defect is thought to cause epileptic activity. We systematically investigated how SynII affects synchronous and asynchronous release components of inhibitory transmission in the CA1 region of the mouse hippocampus. We found that the asynchronous GABAergic release component is diminished in SynII-deleted (SynII(-)) slices. To investigate this defect at different interneuron subtypes, we selectively blocked either N-type or P/Q-type Ca
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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.