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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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Nesfatin-1 decreased excitability of GI-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GI neurons in the DVC. Representative raw traces of spontaneous action potentials were recorded before, during, and after application of glucose (5 mM), (B) Changes in firing rate after application of glucose. (C-D) Changes in firing rate after application of nesfatin-1 (10 nM). (E) Hyperpolarizing responses to 5 mM glucose and 10 nM nesfatin-1 (horizontal bar). (F) Mean response to bath application of 5 mM glucose and 10 nM nesfatin-1.
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pone-0098967-g007: Nesfatin-1 decreased excitability of GI-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GI neurons in the DVC. Representative raw traces of spontaneous action potentials were recorded before, during, and after application of glucose (5 mM), (B) Changes in firing rate after application of glucose. (C-D) Changes in firing rate after application of nesfatin-1 (10 nM). (E) Hyperpolarizing responses to 5 mM glucose and 10 nM nesfatin-1 (horizontal bar). (F) Mean response to bath application of 5 mM glucose and 10 nM nesfatin-1.

Mentions: A total of 11 DVC neurons were identified as GI neurons, as they decreased firing frequency from 0.73±0.22 to 0.26±0.08 Hz and membrane potential from −56.27±1.78 to −62.44±1.48 mV. After perfusion with 10 nM nesfatin-1, GI neurons decreased their firing rate from 0.77±0.12 to 0.28±0.06 Hz and their membrane potential from −56.81±1.69 to −63.11±0.91 mV (Table 3, Fig. 7)


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)

Nesfatin-1 decreased excitability of GI-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GI neurons in the DVC. Representative raw traces of spontaneous action potentials were recorded before, during, and after application of glucose (5 mM), (B) Changes in firing rate after application of glucose. (C-D) Changes in firing rate after application of nesfatin-1 (10 nM). (E) Hyperpolarizing responses to 5 mM glucose and 10 nM nesfatin-1 (horizontal bar). (F) Mean response to bath application of 5 mM glucose and 10 nM nesfatin-1.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0098967-g007: Nesfatin-1 decreased excitability of GI-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GI neurons in the DVC. Representative raw traces of spontaneous action potentials were recorded before, during, and after application of glucose (5 mM), (B) Changes in firing rate after application of glucose. (C-D) Changes in firing rate after application of nesfatin-1 (10 nM). (E) Hyperpolarizing responses to 5 mM glucose and 10 nM nesfatin-1 (horizontal bar). (F) Mean response to bath application of 5 mM glucose and 10 nM nesfatin-1.
Mentions: A total of 11 DVC neurons were identified as GI neurons, as they decreased firing frequency from 0.73±0.22 to 0.26±0.08 Hz and membrane potential from −56.27±1.78 to −62.44±1.48 mV. After perfusion with 10 nM nesfatin-1, GI neurons decreased their firing rate from 0.77±0.12 to 0.28±0.06 Hz and their membrane potential from −56.81±1.69 to −63.11±0.91 mV (Table 3, Fig. 7)

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