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Cited by 210Regulation of Appetite and ObesityNeuroscience of respiration and sleepPancreatic function and diabetes

Glucose-Induced Intracellular Ion Changes in Sugar-Sensitive Hypothalamic Neurons

Silver, Ian A., Erecinska, Maria·1998·Journal of Neurophysiology
DOI 10.1152/jn.1998.79.4.1733
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Abstract

Silver, Ian A. and Maria Erecińska. Glucose-induced intracellular ion changes in sugar-sensitive hypothalamic neurons. J. Neurophysiol. 79: 1733–1745, 1998. In the lateral hypothalamic area (LHA) of rat brain, ∼30% of cells showed sensitivity to small changes in local concentrations of glucose. These “glucose-sensitive” neurons demonstrated four types of behavior, three of which probably represent segments of a continuous spectrum of recruitment in response to ever more severe changes in blood sugar. Type I cells showed maximum activity ≤5.6 mM blood glucose but became completely silent at hyperglycemia of 10–12 mM (normoglycemia 7.6 ± 0.3 mM; mean ± SD). Type II and III neurons exhibited a wider range of response. Type IV cells (5–7% of glucose-sensitive neurons) paralleled the behavior of sugar-sensitive cells in ventromedial hypothalamic nucleus (VMH). In VMH, ∼40% of cells responded to changes in blood glucose over a range of concentrations from 3.6 to 17 mM, by increasing their firing rate as sugar level rose and vice versa. Ionic shifts during increases in blood (brain) glucose levels were similar in LHA types I–III but fastest in I and slowest in III. [Na+]i fell by 5–9 mM, [K+]i rose by 6–8 mM, and plasma membrane hyperpolarized by 5 mV. [Ca 2+]i declined by 15–20 nM in line with membrane hyperpolarization. In VMH and type IV LHA cells, [K+]i fell 3–8 mM and plasma membrane depolarized −3 to −5 mV as blood/brain glucose concentration increased from 7.6/2.4 to 17.6/4.2 mM, whereas [Ca 2+]i increased from 125 to 180 nM as a consequence of falling membrane potential. During falls in blood/brain sugar concentration the effects in both VMH and LHA cells were reversed. The findings are consistent with the ionic shifts in types I–III LHA cells being dependent on alterations in Na/K-ATPase activity, whereas those in VMH and type IV LHA cells could be caused by modulation of ATP-dependent K+channels. A possible mechanism for linking the effects of small changes in glucose to ATP generation, which could bring about the above phenomena, is the interposition of a “glucokinase-type” enzyme in a role similar to that which it has in glucose-sensing pancreatic β-cells.

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  • In rats, an increase of 50 mg/dl in blood glucose from baseline causes only 10 mg/dl increase in brain glucose.

    “In rats, an increase of 50 mg/dl in blood glucose level from baseline value only caused 10 mg/dl increase in brain glucose level [14].”

    From A mathematical model of brain glucose homeostasis (2009) · cites this paper as [14]

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Authors
Silver, I. A., & Erecinska, M.
Affiliations
  • University of Bristol (GB)
  • Department of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104
ORCID
Silver, Ian A.
Venue
Journal of Neurophysiology
Publisher
American Physiological Society
Published
1998-04-01
Volume
79
Issue
4
Pages
1733-1745
ISSN
  • 0022-3077 (ISSN-L)
  • 1522-1598
DOI
10.1152/jn.1998.79.4.1733
OpenAlex
W2143915327
Cited by
210
References
57
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 6 · 2021: 13 · 2020: 10 · 2019: 6 · 2018: 8 · 2017: 7 · 2016: 6 · 2015: 11 · 2014: 5 · 2013: 8 · 2012: 8
FWCI
2.30
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurophysiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns028329-05)
  • National Institute of Neurological Disorders and Stroke (NS 28329)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
glucose detection, lateral hypothalamus, ventromedial hypothalamus, hypothalamic neurons, hyperglycemia, hypoglycemia, membrane hyperpolarization, intracellular calcium, intracellular potassium, intracellular sodium, Na+/K+-ATPase, ATP-sensitive potassium channels, glucokinase, neuronal firing rate
MeSH terms
Action Potentials, Animals, Blood Glucose, Calcium, Cations, Female, Hypothalamic Area, Lateral, Hypothalamus, Middle, Male, Membrane Potentials, Microelectrodes, Neurons, Potassium, Sodium, Rats, Sprague-Dawley, Rats

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