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Nesfatin-1 influences the excitability of glucosensing neurons in the dorsal vagal complex and inhibits food intake.

Dong J, Guan HZ, Jiang ZY, Chen X - PLoS ONE (2014)

Bottom Line: Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake.Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period.Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Special Medicine, Medical College of Qingdao University, Qingdao, China; Department of Physiology, Medical College of Qingdao University, Qingdao, China.

ABSTRACT
Nesfatin-1 is a recently discovered metabolic peptide hormone that decreases food intake after lateral, third, or fourth brain ventricle; cisterna magna; or paraventricular nucleus (PVN) injection in ad libitum fed rats. Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake. We evaluated how nesfatin-1 injection into the dorsal vagal complex (DVC) modulates food intake response in rats during the dark phase. Consistent with previous observations, nesfatin-1-injected rats significantly reduced cumulative food intake over a 5-h period in rats. Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period. Because glucosensing neurons in the DVC are involved in glucoprivic feeding and homeostatic control of blood glucose, we examined the effect of nesfatin-1 on the excitability of DVC glucosensing neurons. Nesfatin-1 inhibited most of the glucose-inhibitory (GI) neurons and excited most of the glucose-excitatory (GE) neurons in the DVC. Current-clamp electrophysiology recordings from DVC glucosensing neurons in slice preparation showed that bath applied nesfatin-1(10 nM) increased the firing frequency of GE neurons and inhibited the firing rate of GI-neurons. Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons. Thus, nesfatin-1 may control food intake by modulating the excitability of glucosensing neurons in the DVC.

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Effect of nesfatin-1 on glucosensing neurons in the dorsal vagal complex (DVC).(A). A GE-neuron was excited by nesfatin-1.The first arrow indicates 5 mM glucose, the second arrow indicates nesfatin-1 (1.5×10−8 M), and the third arrow indicates 0.9% NaCl-treated control. (B). Changes in firing rate after application of nesfatin-1 (n = 20, **P<0.01). (C). A GI-neuron was inhibited by nesfatin-1. (D). Changes in firing rate after application of nesfatin-1 (n = 33, **P<0.01).
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pone-0098967-g004: Effect of nesfatin-1 on glucosensing neurons in the dorsal vagal complex (DVC).(A). A GE-neuron was excited by nesfatin-1.The first arrow indicates 5 mM glucose, the second arrow indicates nesfatin-1 (1.5×10−8 M), and the third arrow indicates 0.9% NaCl-treated control. (B). Changes in firing rate after application of nesfatin-1 (n = 20, **P<0.01). (C). A GI-neuron was inhibited by nesfatin-1. (D). Changes in firing rate after application of nesfatin-1 (n = 33, **P<0.01).

Mentions: After glucose was applied to the surface of 97 spontaneously active neurons recorded in 56 rats, 39 were identified as GI neurons and 26 as GE neurons. A control injection of 0.9% NaCl was used to rule out any neurons that responded to Na+ or Cl− applications. Of 39 GI neurons in the DVC examined, 33 were depressed, 1 was activated, and 5 failed to respond to nesfatin-1 (Table 1). Administration of nesfatin-1 significantly decreased the firing rate of GI neurons from 8.3±2.2 Hz to 4.9±2.1 Hz (n = 33, P<0.01, Fig. 4). Of the 26 GE neurons, 20 were excited, 3 were inhibited, and 3 show no response to nesfatin-1. Micro-injection of nesfatin-1 significantly increased the spontaneous firing rate of GE neurons from 9.1±2.0 Hz to 13.1±2.3 Hz (n = 20, P<0.01).


Nesfatin-1 influences the excitability of glucosensing neurons in the dorsal vagal complex and inhibits food intake.

Dong J, Guan HZ, Jiang ZY, Chen X - PLoS ONE (2014)

Effect of nesfatin-1 on glucosensing neurons in the dorsal vagal complex (DVC).(A). A GE-neuron was excited by nesfatin-1.The first arrow indicates 5 mM glucose, the second arrow indicates nesfatin-1 (1.5×10−8 M), and the third arrow indicates 0.9% NaCl-treated control. (B). Changes in firing rate after application of nesfatin-1 (n = 20, **P<0.01). (C). A GI-neuron was inhibited by nesfatin-1. (D). Changes in firing rate after application of nesfatin-1 (n = 33, **P<0.01).
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4048226&req=5

pone-0098967-g004: Effect of nesfatin-1 on glucosensing neurons in the dorsal vagal complex (DVC).(A). A GE-neuron was excited by nesfatin-1.The first arrow indicates 5 mM glucose, the second arrow indicates nesfatin-1 (1.5×10−8 M), and the third arrow indicates 0.9% NaCl-treated control. (B). Changes in firing rate after application of nesfatin-1 (n = 20, **P<0.01). (C). A GI-neuron was inhibited by nesfatin-1. (D). Changes in firing rate after application of nesfatin-1 (n = 33, **P<0.01).
Mentions: After glucose was applied to the surface of 97 spontaneously active neurons recorded in 56 rats, 39 were identified as GI neurons and 26 as GE neurons. A control injection of 0.9% NaCl was used to rule out any neurons that responded to Na+ or Cl− applications. Of 39 GI neurons in the DVC examined, 33 were depressed, 1 was activated, and 5 failed to respond to nesfatin-1 (Table 1). Administration of nesfatin-1 significantly decreased the firing rate of GI neurons from 8.3±2.2 Hz to 4.9±2.1 Hz (n = 33, P<0.01, Fig. 4). Of the 26 GE neurons, 20 were excited, 3 were inhibited, and 3 show no response to nesfatin-1. Micro-injection of nesfatin-1 significantly increased the spontaneous firing rate of GE neurons from 9.1±2.0 Hz to 13.1±2.3 Hz (n = 20, P<0.01).

Bottom Line: Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake.Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period.Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Special Medicine, Medical College of Qingdao University, Qingdao, China; Department of Physiology, Medical College of Qingdao University, Qingdao, China.

ABSTRACT
Nesfatin-1 is a recently discovered metabolic peptide hormone that decreases food intake after lateral, third, or fourth brain ventricle; cisterna magna; or paraventricular nucleus (PVN) injection in ad libitum fed rats. Additional micro-injection studies will improve the understanding of how nesfatin-1 acts on the brain and define specific nuclei responsive to nesfatin-1, which will provide insight on its effects on food intake. We evaluated how nesfatin-1 injection into the dorsal vagal complex (DVC) modulates food intake response in rats during the dark phase. Consistent with previous observations, nesfatin-1-injected rats significantly reduced cumulative food intake over a 5-h period in rats. Chronic administration of nesfatin-1 into the DVC reduced body weight gain over a 10-day period. Because glucosensing neurons in the DVC are involved in glucoprivic feeding and homeostatic control of blood glucose, we examined the effect of nesfatin-1 on the excitability of DVC glucosensing neurons. Nesfatin-1 inhibited most of the glucose-inhibitory (GI) neurons and excited most of the glucose-excitatory (GE) neurons in the DVC. Current-clamp electrophysiology recordings from DVC glucosensing neurons in slice preparation showed that bath applied nesfatin-1(10 nM) increased the firing frequency of GE neurons and inhibited the firing rate of GI-neurons. Nesfatin-1 inhibited 88.9% (16/18) of gastric distension inhibitory (GD-INH) neurons and excited 76.2% (32/42) of gastric distension excitatory (GD-EXC) neurons. Thus, nesfatin-1 may control food intake by modulating the excitability of glucosensing neurons in the DVC.

Show MeSH
Related in: MedlinePlus