Glucose-Induced Intracellular Ion Changes in Sugar-Sensitive Hypothalamic Neurons
Ian A. Silver 1 and Maria Ereci ska 2 1 Department of Anatomy, School of Veterinary Science, University of Bristol, Bristol BS2 8EJ, UK; and 2 Department of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104 Silver, Ian A. and Maria Ereci ska. Glucose-induced intracellular...
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Published in | Journal of neurophysiology Vol. 79; no. 4; pp. 1733 - 1745 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
Am Phys Soc
01.04.1998
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Subjects | |
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Abstract | Ian A. Silver 1 and
Maria Ereci ska 2
1 Department of Anatomy, School of Veterinary Science, University of Bristol, Bristol BS2 8EJ, UK; and 2 Department of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Silver, Ian A. and Maria Ereci ska. 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 -cells. |
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AbstractList | Ian A. Silver 1 and
Maria Ereci ska 2
1 Department of Anatomy, School of Veterinary Science, University of Bristol, Bristol BS2 8EJ, UK; and 2 Department of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Silver, Ian A. and Maria Ereci ska. 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 -cells. In the lateral hypothalamic area (LHA) of rat brain, similar to 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 less than or equal to 5.6 mM blood glucose but became completely silent at hyperglycemia of 10-12 mM (normoglycemia 7.6 plus or minus 0.3 mM; mean plus or minus 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, similar to 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 super(+)] sub(i) fell by 5-9 mM, [K super(+)] sub(i) rose by 6-8 mM, and plasma membrane hyperpolarized by 5 mV. [Ca super(2+)] sub(i) declined by 15-20 nM in line with membrane hyperpolarization. In VMH and type IV LHA cells, [K super(+)] sub(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 super(2+)] sub(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 super(+) 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 beta -cells. In the lateral hypothalamic area (LHA) of rat brain, approximately 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, approximately 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. [Ca2+]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 [Ca2+]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 beta-cells. In the lateral hypothalamic area (LHA) of rat brain, approximately 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, approximately 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. [Ca2+]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 [Ca2+]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 beta-cells. 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. |
Author | Silver, Ian A Erecinska, Maria |
Author_xml | – sequence: 1 fullname: Silver, Ian A – sequence: 2 fullname: Erecinska, Maria |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/9535943$$D View this record in MEDLINE/PubMed |
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Snippet | Ian A. Silver 1 and
Maria Ereci ska 2
1 Department of Anatomy, School of Veterinary Science, University of Bristol, Bristol BS2 8EJ, UK; and 2 Department of... In the lateral hypothalamic area (LHA) of rat brain, approximately 30% of cells showed sensitivity to small changes in local concentrations of glucose. These... Silver, Ian A. and Maria Erecińska. Glucose-induced intracellular ion changes in sugar-sensitive hypothalamic neurons. J. Neurophysiol. 79: 1733–1745, 1998. In... In the lateral hypothalamic area (LHA) of rat brain, similar to 30% of cells showed sensitivity to small changes in local concentrations of glucose. These... |
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SubjectTerms | Action Potentials - physiology Animals Blood Glucose - metabolism Calcium - metabolism Cations - metabolism Female Hypothalamic Area, Lateral - cytology Hypothalamic Area, Lateral - metabolism Hypothalamus, Middle - cytology Hypothalamus, Middle - metabolism Male Membrane Potentials - physiology Microelectrodes Neurons - metabolism Potassium - metabolism Rats Rats, Sprague-Dawley Sodium - metabolism |
Title | Glucose-Induced Intracellular Ion Changes in Sugar-Sensitive Hypothalamic Neurons |
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