ArticleEndocrinology2007
Rapid inhibition of neurons in the dorsal motor nucleus of the vagus by leptin.
Article in Endocrinology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 76 citations in OpenAlex.
- Molecular cell types as functional units of the efferent vagus nerve.Seminars in cell & developmental biology · 2024Review
- Leptin excites basolateral amygdala principal neurons and reduces food intake by LepRb-JAK2-PI3K-dependent depression of GIRK channels.Journal of cellular physiology · 2024Article
- Systemic Glucose Regulation by a Hindbrain Inhibitory Circuit in a Mouse Model of Type 1 Diabetes.Neuroendocrinology · 2024Article
- GABAergic leptin receptor-expressing neurons in the dorsomedial hypothalamus project to brown adipose tissue-related neurons in the paraventricular nucleus of mice.Autonomic neuroscience : basic & clinical · 2023Article
- Autonomic control of energy balance and glucose homeostasis.Experimental & molecular medicine · 2022Review
- Brain-gut communication: vagovagal reflexes interconnect the two "brains".American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- FGF19 in the Hindbrain Lowers Blood Glucose and Alters Excitability of Vagal Motor Neurons in Hyperglycemic Mice.Endocrinology · 2021Article
- Central Neurocircuits Regulating Food Intake in Response to Gut Inputs-Preclinical Evidence.Nutrients · 2021Review
- Musings on the wanderer: What's new in our understanding of vago-vagal reflexes? VI. Central vagal circuits that control glucose metabolism.American journal of physiology. Gastrointestinal and liver physiology · 2021Review
- Fibroblast Growth Factor 19 Increases the Excitability of Pre-Motor Glutamatergic Dorsal Vagal Complex Neurons From Hyperglycemic Mice.Frontiers in endocrinology · 2021Article
- Sex-steroid-dependent plasticity of brain-stem autonomic circuits.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Review
- Review
- Neurochemical Characterization of Brainstem Pro-Opiomelanocortin Cells.Endocrinology · 2020Article
- Identification of Leptin Receptor-Expressing Cells in the Nodose Ganglion of Male Mice.Endocrinology · 2019Article
- A hindbrain inhibitory microcircuit mediates vagally-coordinated glucose regulation.Scientific reports · 2019Article
- Acute high-fat diet upregulates glutamatergic signaling in the dorsal motor nucleus of the vagus.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Functional and molecular plasticity of γ and α1 GABAJournal of neurophysiology · 2017Article
- Lipid Processing in the Brain: A Key Regulator of Systemic Metabolism.Frontiers in endocrinology · 2017Review
- Adiponectin potentiates the acute effects of leptin in arcuate Pomc neurons.Molecular metabolism · 2016Article
- Glutamatergic drive facilitates synaptic inhibition of dorsal vagal motor neurons after experimentally induced diabetes in mice.Journal of neurophysiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The peptide leptin conveys the availability of adipose energy stores to the brain. Increasing evidence implicates a significant role for extrahypothalamic sites of leptin action, including the dorsal vagal complex, a region critical for regulating visceral parasympathetic function. The hypothesis that leptin suppresses cellular activity in the dorsal motor nucleus of the vagus nerve (DMV) was tested using whole-cell patch-clamp recordings in brainstem slices. Leptin caused a rapid membrane hyperpolarization in 50% of rat DMV neurons. Leptin also hyperpolarized a subset of gastric-related neurons (62%), identified after gastric inoculation with a transneuronal retrograde viral tracer. The hyperpolarization was associated with a decrease in input resistance and cellular responsiveness and displayed characteristics consistent with an increased K+ conductance. Perfusion of tolbutamide (200 microM) reversed the leptin-induced hyperpolarization, and tolbutamide or wortmannin (10-100 nM) prevented the hyperpolarization, indicating that leptin activated an ATP-sensitive K+ channel via a phosphoinositide-3-kinase-dependent mechanism. Leptin reduced the frequency of spontaneous and miniature excitatory postsynaptic currents (EPSCs), whereas inhibitory postsynaptic currents (IPSCs) were largely unaffected. Electrical stimulation of the nucleus tractus solitarii (NTS) resulted in constant-latency EPSCs, which were decreased in amplitude by leptin. The paired-pulse ratio was increased, suggesting leptin effects involved activation of receptors presynaptic to the recorded neuron. A leptin-induced suppression of EPSCs, but not IPSCs, evoked by focal photolytic uncaging of glutamate within the NTS was also observed, supportive of leptin effects on the glutamatergic NTS projection to the DMV. Therefore, leptin directly hyperpolarized and indirectly suppressed excitatory synaptic activity to DMV neurons involved in visceral regulation, including gastric-related neurons.
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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.