ArticleThe Journal of physiology1996
Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.
Article in The Journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 65 citations in OpenAlex.
- Neurovascular Signaling in the Perivascular Space: Biophysical Principles and Disruption in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2026Review
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Brain Capillary Ion Channels: Physiology and Channelopathies.Physiology (Bethesda, Md.) · 2026Review
- Electrocalcium coupling in brain capillaries: Rapidly traveling electrical signals ignite local calcium signals.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Electro-metabolic signaling.The Journal of general physiology · 2024Article
- Pericytes and the Control of Blood Flow in Brain and Heart.Annual review of physiology · 2023Review
- Parkinson disease and the gut: new insights into pathogenesis and clinical relevance.Nature reviews. Gastroenterology & hepatology · 2020Review
- The capillary Kir channel as sensor and amplifier of neuronal signals: Modeling insights on KProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Normal autonomic neurophysiology of postural orthostatic tachycardia and recommended physiological assessments in postural orthostatic tachycardia syndrome.Physiological reports · 2020Review
- The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020Review
- Ex Vivo Pressurized Hippocampal Capillary-Parenchymal Arteriole Preparation for Functional Study.Journal of visualized experiments : JoVE · 2019Article
- Neurophysiology of the brain stem in Parkinson's disease.Journal of neurophysiology · 2019Review
- Capillary KNature neuroscience · 2017Article
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
- Forward operation of adenine nucleotide translocase during F0F1-ATPase reversal: critical role of matrix substrate-level phosphorylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Gasping generation in developing Swiss-Webster mice in vitro and in vivo.Neurochemical research · 2008Article
- Ionic currents underlying the response of rat dorsal vagal neurones to hypoglycaemia and chemical anoxia.The Journal of physiology · 2007Article
- Neuronal responses to transient hypoglycaemia in the dorsal vagal complex of the rat brainstem.The Journal of physiology · 2006Article
- Hypoxia-induced changes in neuronal network properties.Molecular neurobiology · 2005Review
- Progesterone reverses the neuronal responses to hypoxia in rat nucleus tractus solitarius in vitro.The Journal of physiology · 2002Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Brainstem slices were taken from mature rats. In the dorsal vagal nucleus (DVNX), membrane potentials (Em) of neurons (DVNs) and glia, as well as extracellular oxygen, K+ and pH (Po2, aKo, pHo), were analysed during metabolic disturbances. 2. Postsynaptic potentials of DVNs, elicited by repetitive electrical stimulation of the solitary tract (TS), led to a secondary glial depolarization of up to 25 mV, a fall in Po2 of up to 150 mmHg, a rise in extracellular aKo of up to 9 mM, and a fall in pHo of about 0.2 pH units. 3. Hypoxic superfusates produced tissue anoxia, leading to an aKo increase of less than 2 mM and a pHo fall of 0.24 +/- 0.04 pH units (mean +/- S.D.). Glucose-free solution evoked, after a delay of more than 8 min, a slow rise in aKo of 1.9 +/- 0.8 mM, accompanied by a mean increase in pHo of 0.24 +/- 0.13 pH units. After pre-incubation in glucose-free solution, anoxia elevated aKo by up to 15 mM, whereas the anoxia-induced pHo decrease was completely blocked. 4. In 45 of 118 DVNs, anoxia elicited a persistent hyperpolarization of 15.6 +/- 5.0 mV. In the remaining DVNs, anoxic exposure either did not produce a change in Em (37%) or led to a depolarization of less than 10 mV (25%). A stable depolarization of 9 +/- 3.8 mV was detected in glial cells during anoxia. Similar responses were revealed in oxygenated glucose-free solution after a delay of 12-60 min. 5. The metabolism-related hyperpolarizations were blocked by 100-500 microM tolbutamide or 20-100 microM glibenclamide, leading to recovery of spontaneous (0.5-6 Hz) spike discharge. In these cells, 400-500 microM diazoxide evoked hyperpolarizations and blockade of spontaneous activity. 6. In DVNs and glial cells, a progressive depolarization of up to 40 mV in amplitude developed during anoxic exposure after pre-incubation in glucose-free solution. 7. The results show that oxygen or glucose depletion does not impair the viability of DVNX cells. The contribution of neuronal ATP-sensitive K+ (KATP) channels to this tolerance is discussed.
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