ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Sympathoexcitation and pressor responses induced by ethanol in the central nucleus of amygdala involves activation of NMDA receptors in rats.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Morning sympathetic activity after evening binge alcohol consumption.American journal of physiology. Heart and circulatory physiology · 2021Trial
- Small-Conductance CaNeuroscience bulletin · 2026Review
- Central Sympathetic Nerve Activation-Mediated Hypertension: Target Mechanisms and Multimodal Interventions-From Basic Research to Clinical Translation.International journal of molecular sciences · 2026Review
- Peripheral alcohol metabolism dictates ethanol consumption and drinking microstructure in mice.Alcohol, clinical & experimental research · 2025Article
- The Gut Microbiota and the Nerve-Bone Axis: Insights from a Mendelian Randomization and Mediation Analysis.Journal of multidisciplinary healthcare · 2025Article
- Physiological acetic acid concentrations from ethanol metabolism stimulate accumbens shell medium spiny neurons via NMDAR activation in a sex-dependent manner.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Acetic Acid: An Underestimated Metabolite in Ethanol-Induced Changes in Regulating Cardiovascular Function.Antioxidants (Basel, Switzerland) · 2024Review
- Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption.Antioxidants (Basel, Switzerland) · 2023Review
- Ethanol Metabolite, Acetate, Increases Excitability of the Central Nucleus of Amygdala Neurons through Activation of NMDA Receptors.ACS chemical neuroscience · 2023Article
- Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension.Cardiovascular research · 2022Article
- A Brain-Spleen Axis Regulates Humoral Immunity.Neuroscience bulletin · 2021Article
- The ethanol metabolite acetic acid activates mouse nucleus accumbens shell medium spiny neurons.Journal of neurophysiology · 2021Article
- Gut Microbiota and Short Chain Fatty Acids: Influence on the Autonomic Nervous System.Neuroscience bulletin · 2020Review
- Acetate Mediates Alcohol Excitotoxicity in Dopaminergic-like PC12 Cells.ACS chemical neuroscience · 2019Article
- Measurement of cations, anions, and acetate in serum, urine, cerebrospinal fluid, and tissue by ion chromatography.Physiological reports · 2018Article
- Role of neuronal nitric oxide synthase (nNOS) at medulla in tachycardia induced by repeated administration of ethanol in conscious rats.Journal of biomedical science · 2018Article
- Central GPR109A Activation Mediates Glutamate-Dependent Pressor Response in Conscious Rats.The Journal of pharmacology and experimental therapeutics · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The central nervous system plays an important role in regulating sympathetic outflow and arterial pressure in response to ethanol exposure. However, the underlying neural mechanisms have not been fully understood. In the present study, we tested the hypothesis that injection of ethanol in the central nucleus of the amygdala (CeA) increases sympathetic outflow, which may require the activation of local ionotropic excitatory amino acid receptors. In anesthetized rats, CeA injection of ethanol (0, 0.17, and 1.7 μmol) increased splanchnic sympathetic nerve activity (SSNA), lumbar sympathetic nerve activity (LSNA), and mean arterial pressure (MAP) in a dose-dependent manner. A cocktail containing ethanol (1.7 μmol) and kynurenate (KYN), an ionotropic excitatory amino acid receptor blocker, showed significantly blunted sympathoexcitatory and pressor responses compared with those elicited by CeA-injected ethanol alone (P < 0.01). A cocktail containing ethanol and d-2-amino-5-phosphonovalerate, an N-methyl-d-aspartate (NMDA) receptor antagonist, elicited attenuated sympathoexcitatory and pressor responses that were significantly less than ethanol alone (P < 0.01). In addition, CeA injection of acetate (0.20 μmol, n = 7), an ethanol metabolite, consistently elicited sympathoexcitatory and pressor responses, which were effectively blocked by d-2-amino-5-phosphonovalerate (n = 9, P < 0.05). Inhibition of neuronal activity of the rostral ventrolateral medulla (RVLM) with KYN significantly (P < 0.01) attenuated sympathoexcitatory responses elicited by CeA-injected ethanol. Double labeling of immune fluorescence showed NMDA NR1 receptor expression in CeA neurons projecting to the RVLM. We conclude that ethanol and acetate increase sympathetic outflow and arterial pressure, which may involve the activation of NMDA receptors in CeA neurons projecting to the RVLM.
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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.