scholarly journals Gastric Vagal Efferent Inhibition Evoked by Intravenous CRF Is Unrelated to Simultaneously Recorded Vagal Afferent Activity in Urethane-Anesthetized Rats

2007 ◽  
Vol 97 (4) ◽  
pp. 3004-3014 ◽  
Author(s):  
David W. Adelson ◽  
Hovsep P. Kosoyan ◽  
Yuhua Wang ◽  
Justin Z. Steinberg ◽  
Yvette Taché
Keyword(s):  
Impulse Activity ◽  
Simultaneous Recording ◽  
Corticotropin Releasing Factor ◽  
Inhibitory Influence ◽  
Afferent Activity ◽  
Nerve Branch ◽  
Gastric Tone ◽  
Gastric Distention ◽  
Anesthetized Rats ◽  
Vagal Afferent

Corticotropin-releasing factor (CRF) injected peripherally or released in response to stressful challenges to the organism reduces gastric tone and contractility, in part by vagal pathways. However, information on the changes in gastric vagal impulse activity evoked by peripheral CRF administration is entirely lacking. Using a novel “dual recording” method in urethane-anesthetized rats, vagal efferent (VE) and afferent (VA) impulse activities were recorded simultaneously from separate, fine bundles dissected from the ventral gastric vagus nerve branch innervating the glandular stomach. Activity records for 38 VA single units (SUs) and 33 VE SUs were sorted from multiunit records obtained from 13 preparations. Intravenous (iv) administration of saline had no effect on multiunit VE activity, whereas CRF (1 μg/kg, iv) immediately inhibited VE activity, reaching a nadir of 54 ± 8.0% of preinjection levels at 3.0 min postinjection. CRF (1 μg/kg, iv) inhibited 25/33 (75.8%) VE SUs and excited three of 33 (9.1%) VE SUs. In contrast to potent effects on VE activity, iv CRF did not alter multiunit VA activity. Single-unit analysis, however, revealed five of 38 (13.1%) VA SUs excited by iv CRF at widely varying latencies (suggesting an indirect mode of action) and one inhibited VA SU. VA SUs excited after iv CRF did not respond during gastric distention and vice versa. These experiments are the first to use simultaneous recording of gastric VA and VE units. The data demonstrate a predominantly inhibitory influence of iv CRF on VE outflow to the hindstomach, not driven by gastric vagovagal reflex activity.

scholarly journals Urocortins and Cholecystokinin-8 Act Synergistically to Increase Satiation in Lean But Not Obese Mice: Involvement of Corticotropin-Releasing Factor Receptor-2 Pathway

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 6115-6123 ◽  
Author(s):  
G. Gourcerol ◽  
L. Wang ◽  
Y. H. Wang ◽  
M. Million ◽  
Y. Taché
Keyword(s):  
Corticotropin Releasing Factor ◽  
Vehicle Group ◽  
Afferent Activity ◽  
Wild Type ◽  
Rat Stomach ◽  
Urocortin 1 ◽  
Crf2 Receptor ◽  
Vagal Afferent ◽  
Deficient Mice

Interactions between gastrointestinal signals are a part of integrated systems regulating food intake (FI). We investigated whether cholecystokinin (CCK)-8 and urocortin systems potentiate each other to inhibit FI and gastric emptying (GE) in fasted mice. Urocortin 1 and urocortin 2 (1 μg/kg) were injected ip alone or with CCK (3 μg/kg) in lean, diet-induced obese (DIO) or corticotropin-releasing factor receptor-2 (CRF2)-deficient mice. Gastric vagal afferent activity was recorded from a rat stomach-vagus in vitro preparation. When injected separately, urocortin 1, urocortin 2, or CCK did not modify the 4-h cumulative FI in lean mice. However, CCK plus urocortin 1 or CCK plus urocortin 2 decreased significantly the 4-h FI by 39 and 27%, respectively, compared with the vehicle + vehicle group in lean mice but not in DIO mice. Likewise, CCK-urocortin-1 delayed GE in lean but not DIO mice, whereas either peptide injected alone at the same dose had no effect. CCK-urocortin 2 suppression of FI was observed in wild-type but not CRF2-deficient mice. Gastric vagal afferent activity was increased by intragastric artery injection of urocortin 2 after CCK at a subthreshold dose, and the response was reversed by devazepide. These data establish a peripheral synergistic interaction between CCK and urocortin 1 or urocortin 2 to suppress FI and GE through CRF2 receptor in lean mice that may involve CCK modulation of gastric vagal afferent responsiveness to urocortin 2. Such synergy is lost in DIO mice, suggesting a resistance to the satiety signaling that may contribute to maintain obesity.

Peripheral bombesin decreases gastric vagal efferent activity in part through vagal pathways in rats

1994 ◽  
Vol 266 (6) ◽  
pp. R1868-R1875
Author(s):  
E. Yoshida-Yoneda ◽  
Y. Tache ◽  
H. P. Kosoyan ◽  
J. Y. Wei
Keyword(s):  
Saline Injection ◽  
Afferent Activity ◽  
Recording Site ◽  
Systemic Injection ◽  
Efferent Activity ◽  
Anesthetized Rats ◽  
Cervical Vagotomy ◽  
Vagal Afferent

The influence of intravenous (iv) bombesin on multiunit activities recorded from the ventral gastric branch of the vagus was investigated in urethan-anesthetized rats. Consecutive injections of bombesin (0.062, 0.62, 6.2, 62, and 620 pmol iv) decreased dose dependently gastric vagal efferent discharges to 79.8 +/- 4.9, 68.3 +/- 10.2, 47.0 +/- 6.7, 41.6 +/- 4.7, and 36.5 +/- 8.9%, respectively, from preinjection levels. Saline injection had no effect. Bombesin (62 pmol iv) reduced cervical vagal efferent discharges to 25 +/- 6% before and 67 +/- 5% after bilateral cervical vagotomy distal to the recording site. Bombesin (62 and 620 pmol iv) increased gastric vagal afferent discharges by 45 and 93%, respectively. These data show that systemic injection of bombesin potently decreases gastric and cervical vagal efferent activity in part through vagal-dependent mechanisms that may involve the increase in gastric vagal afferent activity.

Jejunal or portal vein infusions of lipids increase hepatic vagal afferent activity

Neuroreport ◽  
2001 ◽  
Vol 12 (14) ◽  
pp. 3101-3105 ◽  
Author(s):  
Alan Randich ◽  
D. Seth Spraggins ◽  
James E. Cox ◽  
Stephen T. Meller ◽  
Gary R. Kelm
Keyword(s):  
Portal Vein ◽  
Afferent Activity ◽  
Vagal Afferent

scholarly journals High-Sugar, but Not High-Fat, Food Activates Supraoptic Nucleus Neurons in the Male Rat

Endocrinology ◽  
2017 ◽  
Vol 158 (7) ◽  
pp. 2200-2211 ◽  
Author(s):  
Catherine Hume ◽  
Nancy Sabatier ◽  
John Menzies
Keyword(s):  
Firing Rate ◽  
Supraoptic Nucleus ◽  
Male Rat ◽  
Plasma Sodium ◽  
Neural Activation ◽  
High Fat ◽  
Gastric Distention ◽  
High Sugar ◽  
Anesthetized Rats

Abstract Oxytocin is a potent anorexigen and is believed to have a role in satiety signaling. We developed rat models to study the activity of oxytocin neurons in response to voluntary consumption or oral gavage of foods using c-Fos immunohistochemistry and in vivo electrophysiology. Using c-Fos expression as an indirect marker of neural activation, we showed that the percentage of magnocellular oxytocin neurons expressing c-Fos increased with voluntary consumption of sweetened condensed milk (SCM). To model the effect of food in the stomach, we gavaged anesthetized rats with SCM. The percentage of supraoptic nucleus and paraventricular nucleus magnocellular oxytocin-immunoreactive neurons expressing c-Fos increased with SCM gavage but not with gastric distention. To further examine the activity of the supraoptic nucleus, we made in vivo electrophysiological recordings from SON neurons, where anesthetized rats were gavaged with SCM or single cream. Pharmacologically identified oxytocin neurons responded to SCM gavage with a linear, proportional, and sustained increase in firing rate, but cream gavage resulted in a transient reduction in firing rate. Blood glucose increased after SCM gavage but not cream gavage. Plasma osmolarity and plasma sodium were unchanged throughout. We show that in response to high-sugar, but not high-fat, food in the stomach, there is an increase in the activity of oxytocin neurons. This does not appear to be a consequence of stomach distention or changes in osmotic pressure. Our data suggest that the presence of specific foods with different macronutrient profiles in the stomach differentially regulates the activity of oxytocin neurons.

Selective potentiating effect of RS14203 on a serotoninergic pathway in anesthetized rats

2000 ◽  
Vol 78 (9) ◽  
pp. 708-713
Author(s):  
Chantal Savoie ◽  
Chi-Chung Chan ◽  
Ian W Rodger ◽  
Annette Robichaud
Keyword(s):  
Electrical Stimulation ◽  
Side Effects ◽  
Vagal Nerve ◽  
Nausea And Vomiting ◽  
Pulmonary Diseases ◽  
Selective Inhibitors ◽  
Anesthetized Rats ◽  
Afferent Fibers ◽  
Vagal Afferent

The usefulness of selective inhibitors of type 4 phosphodiesterase (PDE4) in the treatment of inflammation and pulmonary diseases is limited by their side effects: nausea and vomiting. We studied the effect of three structurally diverse PDE4 inhibitors on the vagal nerve afferent and efferent fibers in anesthetized rats. The effects of RS14203, (R)-rolipram, and CT-2450 were evaluated on the von Bezold-Jarisch reflex (vagal afferent fibers) and in a model of vagal electrical stimulation (vagal efferent fibers). All three PDE4 inhibitors were administered at 1, 10, or 100 µg/kg (iv) 15 min prior to the induction of bradycardia by an iv injection of 2-methyl-5-HT (von Bezold-Jarisch reflex) or by vagal electrical stimulation. At 100 µg/kg, RS14203 significantly potentiated the 2-methyl-5-HT response. No statistically significant effects were observed with (R)-rolipram or CT-2450 at the doses studied. RS14203, (R)-rolipram, or CT-2450 (1-100 µg/kg iv) did not affect the bradycardia induced by vagal electrical stimulation. Consequently, our results show that RS14203 selectively facilitates serotoninergic neurotransmission in vagal afferent fibers. The emetic action of RS14203 may be mediated by this mechanism.Key words: PDE4 inhibitors, von Bezold-Jarisch reflex, emesis, vagal afferent and efferent fibres, bradycardia.

Responses of celiac and cervical vagal afferents to infusions of lipids in the jejunum or ileum of the rat

2000 ◽  
Vol 278 (1) ◽  
pp. R34-R43 ◽  
Author(s):  
Alan Randich ◽  
William J. Tyler ◽  
James E. Cox ◽  
Stephen T. Meller ◽  
Gary R. Kelm ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Linoleic Acid ◽  
Single Unit ◽  
Corn Oil ◽  
Body Weight Gain ◽  
Vagal Afferents ◽  
Afferent Activity ◽  
Inhibitory Effects ◽  
Vagal Afferent ◽  
Increased Activity

Multiunit celiac and single-unit cervical recordings of vagal afferents were performed before and during infusions of fatty acids, triglycerides, or saline into either the ileum or jejunum of the rat. In multiunit recordings, lipids increased activity of vagal afferents to a greater extent than saline. The greatest increases in vagal afferent activity resulted from infusions of linoleic acid, conjugated linoleic acid, or oleic acid. The triglycerides, corn oil or Intralipid, were less effective than the fatty acids in affecting vagal afferent activity. Ileal pretreatment with the hydrophobic surfactant Pluronic L-81 significantly attenuated the response of celiac vagal afferents to ileal infusion of linoleic acid. Single-unit recordings of cervical vagal afferents supported the multiunit data in showing lipid-induced increased vagal afferent activity in ∼50% of ileal units sampled and 100% of a limited number of jejunal units sampled. These data demonstrate that free fatty acids can activate ileal and jejunal vagal afferents in the rat, and this effect can be attenuated by pretreatment with a chylomicron inhibitor. These data are consistent with the view that lipid-induced activation of vagal afferents could be a potential substrate for the inhibitory effects of intestinal lipids on gastrointestinal function, food intake, and body weight gain.

Integration of vagal afferent responses to gastric loads and cholecystokinin in rats

1991 ◽  
Vol 261 (1) ◽  
pp. R64-R69 ◽  
Author(s):  
G. J. Schwartz ◽  
P. R. McHugh ◽  
T. H. Moran
Keyword(s):  
Discharge Rate ◽  
Celiac Artery ◽  
Gastric Volume ◽  
Afferent Activity ◽  
Rapid Adaptation ◽  
Discharge Rates ◽  
Group I ◽  
Afferent Fibers ◽  
Vagal Afferent ◽  
Contrast Group

The neurophysiological responses to 2-ml intragastric saline loads and 100-pmol celiac artery infusions of cholecystokinin (CCK) were obtained from 20 vagal afferent fibers in 14 rats. Two groups of fibers were identified. Discharge rates of group I fibers (n = 16) were significantly increased by gastric loading, adapted slowly to maintained gastric volume, and were inhibited by load withdrawal. CCK elicited a significant increase in the discharge rate of these group I fibers. Prior exposure to CCK nearly doubled the response of these fibers to a subsequent gastric load. In contrast, group II fibers (n = 4) increased firing rate only during infusion of a gastric load and showed rapid adaptation and no response to CCK. CCK failed to alter subsequent responses to gastric loads in these fibers. These results 1) demonstrate an integration of signals elicited by exogenous CCK and gastric loads at the level of vagal afferent fibers and 2) imply that aspects of CCK's inhibition of food intake may derive from CCK's ability to mimic and amplify vagal afferent activity provoked by meal-related gastric events.

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