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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 increased excitability of GE-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GE neurons in 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) Depolarizing 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-g006: Nesfatin-1 increased excitability of GE-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GE neurons in 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) Depolarizing 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 43 spontaneously firing neurons were recorded in the DVC brain slices. To identify glucosensing neurons, 5 mM glucose was applied to the bath. Of these, 20 neurons were identified as GE neurons, as they increased their firing rate from 0.46±0.12 to 1.22±0.24 Hz and depolarized the membrane potential from -61.33±1.41 to −52.32±1.79 mV (Fig. 6). These GE neurons increased their action potential frequency from 1.29±0.22 to 3.03±0.36 Hz and their membrane potential from −57.18±1.71 to −42.25±2.06 mV in response to 10 nM nesfatin-1 (Table 3, Fig. 6).


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 increased excitability of GE-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GE neurons in 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) Depolarizing 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-g006: Nesfatin-1 increased excitability of GE-neurons in DVC.Current-clamp recordings from DVC neurons in slice preparation. (A) Identification of GE neurons in 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) Depolarizing 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 43 spontaneously firing neurons were recorded in the DVC brain slices. To identify glucosensing neurons, 5 mM glucose was applied to the bath. Of these, 20 neurons were identified as GE neurons, as they increased their firing rate from 0.46±0.12 to 1.22±0.24 Hz and depolarized the membrane potential from -61.33±1.41 to −52.32±1.79 mV (Fig. 6). These GE neurons increased their action potential frequency from 1.29±0.22 to 3.03±0.36 Hz and their membrane potential from −57.18±1.71 to −42.25±2.06 mV in response to 10 nM nesfatin-1 (Table 3, Fig. 6).

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