Intracisternal sauvagine is more potent than corticotropin-releasing factor to decrease gastric vagal efferent activity in rats☆

Kosoyan, Hovsep P.; Wei, Jiann-Wu; Taché, Yvette

doi:10.1016/s0196-9781(99)00072-8

Cited by 23 publications

(12 citation statements)

References 34 publications

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“…In addition, CRF injected intracisternally or into the DMN inhibits gastric motility stimulated by vagal-dependent thyrotropin releasing hormone (TRH) excitatory action on DMN neurons (10,19). In support of vagal inhibitory pathways are also the observations that intracisternal CRF decreased gastric vagal efferent discharge (23) and that intracerebroventricular CRF blocked the activation of DMN neurons and gastric function induced by endogenous TRH released by acute cold exposure (47). In contrast, an in vitro patch-clamp study performed on coronal sections containing the dorsal vagal complex of 25-day-old rats showed that superfusion of CRF increases discharge rate and membrane depolarization of gastric projecting DMN neurons (26).…”

Section: Discussionmentioning

confidence: 99%

Urocortin 2 acts centrally to delay gastric emptying through sympathetic pathways while CRF and urocortin 1 inhibitory actions are vagal dependent in rats

Czimmer¹,

Million²,

Taché³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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We characterized the influence of the selective corticotropin-releasing factor 2 (CRF(2)) receptor agonist human urocortin 2 (Ucn 2), injected intracisternally, on gastric emptying and its mechanism of action compared with intracisternal CRF or urocortin (Ucn 1) in conscious rats. The methylcellulose phenol red solution was gavaged 20 min after peptide injection, and gastric emptying was measured 20 min later. The intracisternal injection of Ucn 2 (0.1 and 1 microg) and Ucn 1 (1 microg) decreased gastric emptying to 37.8 +/- 6.9%, 23.1 +/- 8.6%, and 21.6 +/- 5.9%, respectively, compared with 58.4 +/- 3.8% after intracisternal vehicle. At lower doses, Ucn 2 (0.03 microg) and Ucn 1 (0.1 microg) had no effect. The CRF(2) antagonist astressin(2)-B (3 microg ic) antagonized intracisternal Ucn 2 (0.1 microg) and CRF (0.3 microg)-induced inhibition of gastric emptying. Vagotomy enhanced intracisternal Ucn 2 (0.1 or 1 microg)-induced inhibition of gastric emptying compared with sham-operated group, whereas it blocked intracisternal CRF (1 microg) inhibitory action (45.5 +/- 8.4% vs. 9.7 +/- 9.7%). Sympathetic blockade by bretylium prevented intracisternal and intracerebroventricular Ucn 2-induced delayed gastric emptying, whereas it did not influence intravenous Ucn 2-, intracisternal CRF-, and intracisternal Ucn 1-induced inhibition of gastric emptying. Prazosin abolished the intracisternal Ucn 2 inhibitory effect, whereas yohimbine and propranolol did not. None of the pretreatments modified basal gastric emptying. These data indicate that intracisternal Ucn 2 induced a central CRF(2)-mediated inhibition of gastric emptying involving sympathetic alpha(1)-adrenergic mechanisms independent from the vagus contrasting with the vagal-dependent inhibitory actions of CRF and Ucn 1.

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Section: Discussionmentioning

confidence: 99%

Urocortin 2 acts centrally to delay gastric emptying through sympathetic pathways while CRF and urocortin 1 inhibitory actions are vagal dependent in rats

Czimmer¹,

Million²,

Taché³

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…administration of CRF was found to inhibit Fos expression in the dorsal motor nucleus of the vagus nerve in rats (Wang et al, 1996). Also, intracisternal injections of CRF or sauvagine inhibit basal gastric vagal efferent discharge (Kosoyan et al, 1999) and i.c.v. CRF alters cardiac baroreflex function predominantly through inhibition of cardiac vagal outflow (Fisher, 1989).…”

Section: Introductionmentioning

confidence: 93%

Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

Wood

Verhoeven

Savit

et al. 2006

Neuropsychopharmacol

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Exposure to stressors that elicit fear and feelings of hopelessness can cause severe vagal activation leading to bradycardia, syncope, and sudden death. These phenomena though documented, are difficult to diagnose, treat clinically, and prevent. Therefore, an animal model incorporating these cardiovascular conditions could be useful. The present study examined 'sinking' during a 2-h swim stress, a phenomenon that occurs in 50% of rats during 251C water exposure. Concurrent measurements of body temperature, immobility, heart rate (HR), and PR interval (a measure of vagal activity) were made. Neither decreases in immobility nor variations in hypothermia during swim were correlated with sinking. Bradycardia was more severe in sinking rats (average minimum HR7SEM; 143713 vs 247714; po0.01), and PR interval was elevated (po0.0001). To examine potential modulation of vagal activity during stress, corticotropinrelasing factor (CRF) receptor antagonists (antalarmin, R121919 and astressin B), a glucocorticoid receptor antagonist (RU486), and a peripherally acting cholinergic antagonist (methylatropine nitrate) were administered. The centrally acting CRF antagonist, antalarmin (32 mg/kg), produced elongation of the PR interval (po0.0001), robust bradycardia (135718; po0.001), and increased sinking (92%; po0.05), and methylatropine nitrate (3.2 mg/kg) blocked these effects. Corroborating these data, two different CRF antagonists, R121919 (30 mg/kg) and astressin B (intracerebroventricular (i.c.v.), 0.03 mg/rat) increased sinking to 100%. RU486 (20 mg/kg) blocked HPA axis negative feedback and decreased percent sinking to 25%. From these studies, we concluded that sinking during a 2-h water exposure was a result of extreme vagal hyperactivity. Furthermore, stress-induced CRF release may serve to protect against elevated cardiac vagal activity.

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“…There is evidence that abdominal surgery performed under similar conditions activates brain stress-related circuitries, including CRF signaling pathway [1,4,5,9,28]. Activation of brain CRF circuitry is known to inhibit RX-77368 excitatory input to the prevagal motor neurons [11,21,26] leading to decreased vagal excitatory discharges [13] directed to gastric myenteric neurons [12]. On the other hand, abdominal surgery may also recruit peripheral inhibitory mechanisms at presynaptic levels to modulate the cholinergic vagal efferent output conveyed to gastric myenteric neurons or directly on myenteric neurons.…”

Section: Discussionmentioning

confidence: 99%

Brain–gut interactions between central vagal activation and abdominal surgery to influence gastric myenteric ganglia Fos expression in rats

2011

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We previously showed that medullary thyrotropin-releasing hormone (TRH) or the stable TRH agonist, RX-77368 administered intracisternally induces vagal-dependent activation of gastric myenteric neurons and prevents post surgery-induced delayed gastric emptying in rats. We investigated whether abdominal surgery alters intracisternal (ic) RX-77368 (50 ng)-induced gastric myenteric neuron activation. Under 10 min enflurane anesthesia, rats underwent an ic injection of saline or RX-77368 followed by a laparotomy and a 1-min cecal palpation, or no surgery and were euthanized 90 min later. Longitudinal muscle/myenteric plexus whole-mount preparations of gastric corpus and antrum were processed for immunohistochemical detection of Fos alone or double labeled with protein gene-product 9.5 (PGP 9.5) and vesicular acetylcholine transporter (VAChT). In the non surgery groups, ic RX-77368 induced a 17 fold increase in Fos-expression in both gastric antrum and corpus myenteric neurons compared to saline injected rats. PGP 9.5 ascertained the neuronal identity of myenteric cells expressing Fos. In the abdominal surgery groups, ic RX-77368 induced a significant increase in Fos-expression in both the corpus and antrum myenteric ganglia compared with ic saline injected rats which has no Fos in the gastric myenteric ganglia. However, the response was reduced by 73–78% compared with that induced by ic RX 77368 without surgery. Abundant VAChT positive nerve fibers were present around Fos positive neurons. These results indicate a bidirectional interaction between central vagal stimulation of gastric myenteric neurons and abdominal surgery. The modulation of gastric vagus-myenteric neuron activity could play an important role in the recovery phase of postoperative gastric ileus.

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Intracisternal sauvagine is more potent than corticotropin-releasing factor to decrease gastric vagal efferent activity in rats☆

Cited by 23 publications

References 34 publications

Urocortin 2 acts centrally to delay gastric emptying through sympathetic pathways while CRF and urocortin 1 inhibitory actions are vagal dependent in rats

Urocortin 2 acts centrally to delay gastric emptying through sympathetic pathways while CRF and urocortin 1 inhibitory actions are vagal dependent in rats

Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

Brain–gut interactions between central vagal activation and abdominal surgery to influence gastric myenteric ganglia Fos expression in rats

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