Vagus nerve participates in CCK-induced Fos expression in hindbrain but not myenteric plexus

Sayegh, Ayman I.; Ritter, Robert C.

doi:10.1016/s0006-8993(00)02731-1

Cited by 50 publications

(28 citation statements)

References 28 publications

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“…Although apparently at odds with previous studies conducted on vagotomized or capsaicin-treated animals (53), one should consider the technical differences between our study and the studies of Sayegh and Ritter (53), foremost the deafferentation procedures. In fact, Sayegh and Ritter did their experiments 8 wk after conducting a complete subdiaphragmatic vagotomy or after systemic administration of capsaicin; conversely, we conducted our experimental procedures 5-10 days after afferent rhizotomy and subdiaphragmatic vagotomy.…”

Section: Discussioncontrasting

confidence: 73%

“…The longer postsurgical recovery period allowed by these colleagues (i.e., 8 wk) before the experimentation may well have induced a degeneration of vagal afferent fibers, as well as NTS and DMV neurons, whereas our selective surgery and relatively short recovery period are likely to have affected only vagal afferent terminals. Sayegh and Ritter (53) reported that the c-Fos expression elicited by CCK-8s was decreased in vagotomized vs. control rats [see, for example, columns 1 (control saline), vs. column 2 (control CCK-8s), vs. column 5 (vagotomized CCK-8s), in Table 1 Indeed, similar to our data, systemic CCK-8s administration induced a (possibly significant) increase in cFos expression also in the vagotomized rats reported in their study (53).…”

Section: Discussionmentioning

confidence: 99%

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Effects of cholecystokinin-8s in the nucleus tractus solitarius of vagally deafferented rats

Baptista¹,

Browning²,

Travagli³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Baptista V, Browning KN, Travagli RA. Effects of cholecystokinin-8s in the nucleus tractus solitarius of vagally deafferented rats. Am J Physiol Regul Integr Comp Physiol 292: R1092-R1100, 2007. First published November 22, 2006; doi:10.1152/ajpregu.00517.2006.-We have shown recently that cholecystokinin octapeptide (CCK-8s) increases glutamate release from nerve terminals onto neurons of the nucleus tractus solitarius pars centralis (cNTS). The effects of CCK on gastrointestinal-related functions have, however, been attributed almost exclusively to its paracrine action on vagal afferent fibers. Because it has been reported that systemic or perivagal capsaicin pretreatment abolishes the effects of CCK, the aim of the present work was to investigate the response of cNTS neurons to CCK-8s in vagally deafferented rats. In surgically deafferented rats, intraperitoneal administration of 1 or 3 g/kg CCK-8s increased c-Fos expression in cNTS neurons (139 and 251% of control, respectively), suggesting that CCK-8s' effects are partially independent of vagal afferent fibers. Using whole cell patch-clamp techniques in thin brain stem slices, we observed that CCK-8s increased the frequency of spontaneous and miniature excitatory postsynaptic currents in 43% of the cNTS neurons via a presynaptic mechanism. In slices from deafferented rats, the percentage of cNTS neurons receiving glutamatergic inputs responding to CCK-8s decreased by ϳ50%, further suggesting that central terminals of vagal afferent fibers are not the sole site for the action of CCK-8s in the brain stem. Taken together, our data suggest that the sites of action of CCK-8s include the brain stem, and in cNTS, the actions of CCK-8s are not restricted to vagal central terminals but that nonvagal synapses are also involved. brain stem; electrophysiology; c-fos CHOLECYSTOKININ, WHICH IS released from intestinal cells following ingestion of nutrients (34,37,47), has profound effects on gastrointestinal functions. In fact, it is well known that cholecystokinin, and, in particular, the cleaved octapeptide cholecystokinin-8s (CCK-8s), induces vagally mediated gastric relaxation, increases pancreatic exocrine secretion, and induces short-term satiety (36,38,41,42,48,62).Many studies have proposed that the vagally mediated effects of CCK-8s are almost exclusively due to a paracrine action of CCK-8s on peripheral, capsaicin-sensitive vagal afferent fibers (8,14,41). This postulate stems mainly from the observations that C-fiber ablation induced by perivagal capsaicin treatment greatly attenuates, or abolishes altogether, the effects of systemic administration of CCK-8s on gastric motility, gastric acid secretion, and pancreatic exocrine secretion (32,33,41,58). One must keep in mind, however, that the localized perineural application involves the use of very high concentrations of capsaicin, usually 33 mM (i.e., 1% solution) (9,23,25,41,56,63,67). Such a high concentration of capsaicin raises the possibility that its observed effects are due to the toxic effects of massiv...

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Section: Discussioncontrasting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Effects of cholecystokinin-8s in the nucleus tractus solitarius of vagally deafferented rats

Baptista¹,

Browning²,

Travagli³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…There are several similarities between CCK and apoA-IV. Secretion of each is induced by fat absorption, and this lipid-induced stimulation is dependent on chylomicron formation ( 54,120,128 ). In addition, both act peripherally (after either ip or iv administration) as well as centrally to reduce food intake ( 82,129,130 ).…”

Section: Apoa-iv As a Satiety Factormentioning

confidence: 99%

Apolipoprotein A-IV: a protein intimately involved in metabolism

Wang

Kohan

et al. 2015

Journal of Lipid Research

132

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“…Vagal afferent fibers use glutamate as their main transmitter onto NTS neurons (Andresen and Yang, 1990;Smith et al, 1998;Jean, 2001;Baptista et al, 2005b;Travagli et al, 2006) and intraperitoneal administration of satiety agents (e.g., CCK, glucagon-like peptide-1, or cocaine-and amphetamine-regulated transcript) increases c-Fos expression in NTS (Rinaman et al, 1993;Zittel et al, 1999;Sayegh and Ritter, 2000;Zheng et al, 2002b;Cano et al, 2003;Gulley et al, 2005;Arora and Anubhuti, 2006;Berthoud et al, 2006), including the POMC neurons of the caudal NTS (Appleyard et al, 2005). This c-Fos expression is likely caused by increased glutamate release, because administration of glutamatergic antagonists decreases satiety (Covasa et al, 2004a,b;Zheng et al, 1999Zheng et al, , 2002a.…”

Section: Implications For the Control Of Food Intakementioning

confidence: 99%

Presynaptic Melanocortin-4 Receptors on Vagal Afferent Fibers Modulate the Excitability of Rat Nucleus Tractus Solitarius Neurons

Wan¹,

Browning²,

Coleman³

et al. 2008

J. Neurosci.

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Vagus nerve participates in CCK-induced Fos expression in hindbrain but not myenteric plexus

Cited by 50 publications

References 28 publications

Effects of cholecystokinin-8s in the nucleus tractus solitarius of vagally deafferented rats

Effects of cholecystokinin-8s in the nucleus tractus solitarius of vagally deafferented rats

Apolipoprotein A-IV: a protein intimately involved in metabolism

Presynaptic Melanocortin-4 Receptors on Vagal Afferent Fibers Modulate the Excitability of Rat Nucleus Tractus Solitarius Neurons

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