ArticleCell2016
Near-Perfect Synaptic Integration by Nav1.7 in Hypothalamic Neurons Regulates Body Weight.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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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
56 citing papers in PubMed, 98 citations in OpenAlex.
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- Thermally induced neuronal plasticity in the hypothalamus mediates heat tolerance.Nature neuroscience · 2025Article
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- Competition between stochastic neuropeptide signals calibrates the rate of satiation.Research square · 2023Article
- Increased intrinsic and synaptic excitability of hypothalamic POMC neurons underlies chronic stress-induced behavioral deficits.Molecular psychiatry · 2023Article
- Nav1.7 is required for normal C-low threshold mechanoreceptor function in humans and mice.Brain : a journal of neurology · 2022Article
- CX3CL1 Action on Microglia Protects from Diet-Induced Obesity by Restoring POMC Neuronal Excitability and Melanocortin System Activity Impaired by High-Fat Diet Feeding.International journal of molecular sciences · 2022Article
- The HumanFrontiers in molecular neuroscience · 2022Article
- AMPA Receptor Function in Hypothalamic Synapses.Frontiers in synaptic neuroscience · 2022Review
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- Cancer as a homeostatic challenge: the role of the hypothalamus.Trends in neurosciences · 2021Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Neurons are well suited for computations on millisecond timescales, but some neuronal circuits set behavioral states over long time periods, such as those involved in energy homeostasis. We found that multiple types of hypothalamic neurons, including those that oppositely regulate body weight, are specialized as near-perfect synaptic integrators that summate inputs over extended timescales. Excitatory postsynaptic potentials (EPSPs) are greatly prolonged, outlasting the neuronal membrane time-constant up to 10-fold. This is due to the voltage-gated sodium channel Nav1.7 (Scn9a), previously associated with pain-sensation but not synaptic integration. Scn9a deletion in AGRP, POMC, or paraventricular hypothalamic neurons reduced EPSP duration, synaptic integration, and altered body weight in mice. In vivo whole-cell recordings in the hypothalamus confirmed near-perfect synaptic integration. These experiments show that integration of synaptic inputs over time by Nav1.7 is critical for body weight regulation and reveal a mechanism for synaptic control of circuits regulating long term homeostatic functions.
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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.