ArticlePflugers Archiv : European journal of physiology2009
Silencing of ventromedial hypothalamic neurons by glucose-stimulated K(+) currents.
Article in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Carbohydrate and sleep: An evaluation of putative mechanisms.Frontiers in nutrition · 2022Review
- Orexin/Hypocretin and MCH Neurons: Cognitive and Motor Roles Beyond Arousal.Frontiers in neuroscience · 2021Review
- Remote control of glucose-sensing neurons to analyze glucose metabolism.American journal of physiology. Endocrinology and metabolism · 2018Review
- Neuropeptide Y cells represent a distinct glucose-sensing population in the lateral hypothalamus.Endocrinology · 2011Article
- Neuropeptide Y suppresses anorexigenic output from the ventromedial nucleus of the hypothalamus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Glucose-induced inhibition: how many ionic mechanisms?Acta physiologica (Oxford, England) · 2010Review
- Electrophysiological identification of glucose-sensing neurons in rat nodose ganglia.The Journal of physiology · 2010Article
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Authors and funding
2 authors.
Funding
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Abstract
Glucose sensing by neurons of the ventromedial hypothalamus (VMH) plays a central role in the regulation of body energy balance. Physiological rises in extracellular glucose levels hyperpolarise and inhibit a group of VMH neurons. This specialised sensing response is currently thought to involve glucose-induced activation of chloride channels, but alternative mechanisms have not been explored in detail. In this study, we converted all chloride channels from inhibitory to excitatory by filling the cytosol of VMH neurons with a high concentration of chloride. Despite this, some VMH neurons were still strongly hyperpolarised and inhibited by glucose. Voltage-clamp analysis revealed that this was due to glucose-induced activation of K(+)-selective currents of sufficient size to cause complete inhibition of whole-cell electrical activity. These K(+) currents exhibited leak-like biophysical properties and were inhibited by extracellular acidification. Our data support the idea that glucose-stimulated K(+) currents contribute to sugar-induced suppression of firing in the VMH.
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