ArticleCerebral cortex (New York, N.Y. : 1991)2016
Neurotensinergic Excitation of Dentate Gyrus Granule Cells via Gαq-Coupled Inhibition of TASK-3 Channels.
Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Transcriptomic analysis reveals new hippocampal gene networks induced by prolactin.Scientific reports · 2019Article
- Diverse actions of the modulatory peptide neurotensin on central synaptic transmission.The European journal of neuroscience · 2019Review
- Regulation of Memory Function by Feeding-Relevant Biological Systems: Following the Breadcrumbs to the Hippocampus.Frontiers in molecular neuroscience · 2019Review
- TWIK-1/TASK-3 heterodimeric channels contribute to the neurotensin-mediated excitation of hippocampal dentate gyrus granule cells.Experimental & molecular medicine · 2018Article
- Neurotensin speeds inhibition of dopamine neurons through temporal modulation of GABANeuropharmacology · 2018Article
- Neuropeptides Exert Neuroprotective Effects in Alzheimer's Disease.Frontiers in molecular neuroscience · 2018Review
- Emerging Roles of TWIK-1 Heterodimerization in the Brain.International journal of molecular sciences · 2017Review
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Neurotensin (NT) is a 13-amino acid peptide and serves as a neuromodulator in the brain. Whereas NT has been implicated in learning and memory, the underlying cellular and molecular mechanisms are ill-defined. Because the dentate gyrus receives profound innervation of fibers containing NT and expresses high density of NT receptors, we examined the effects of NT on the excitability of dentate gyrus granule cells (GCs). Our results showed that NT concentration dependently increased action potential (AP) firing frequency of the GCs by the activation of NTS1 receptors resulting in the depolarization of the GCs. NT-induced enhancement of AP firing frequency was not caused indirectly by releasing glutamate, GABA, acetylcholine, or dopamine, but due to the inhibition of TASK-3 K(+) channels. NT-mediated excitation of the GCs was G protein dependent, but independent of phospholipase C, intracellular Ca(2+) release, and protein kinase C. Immunoprecipitation experiment demonstrates that the activation of NTS1 receptors induced the association of Gαq/11 and TASK-3 channels suggesting a direct coupling of Gαq/11 to TASK-3 channels. Endogenously released NT facilitated the excitability of the GCs contributing to the induction of long-term potentiation at the perforant path-GC synapses. Our results provide a cellular mechanism that helps to explain the roles of NT in learning and memory.
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Registered trials
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