Central inhibitory action of peptide YY on gastric motility in rats

Chen, Chi-Hsiang; Rogers, R. Curtis

doi:10.1152/ajpregu.1995.269.4.r787

Cited by 32 publications

(50 citation statements)

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“…Findings include 1) peripherally administered PYY (1-36) binds in a saturable manner to specific areas in the DVC (23) and induces c-Fos immunoreactivity in these areas (6); 2) PYY(1-36) and NPY(3-36) (a Y 2 agonist) dose dependently inhibit excitatory postsynaptic currents in cholinergic neurons of the dorsal motor nucleus of the vagus (10); 3) injection of PYY or Y 2 agonists [NPY or PYY ] into the DVC inhibits neurons of the dorsal motor nucleus of the vagus, as well as TRH-induced gastric motility (11,12,14); 4) intracisternal injections of PYY(1-36) inhibit gastric emptying, and this inhibition is attenuated by vagotomy (13); and 5) intracerebroventricular injection of NPY(3-36) (Y 2 agonist) dose dependently delays gastric emptying of solids, as well as impairs antral contractions and antropyloric coordination in the emptying period (25). In contrast to these Y 2 receptor-dependent effects, Y 1 receptor-mediated effects on gastric emptying appear to be stimulatory.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the inhibitory effects of PYY(3-36) and PYY(1-36) on gastric emptying in rats

Chelikani

Haver²,

Reidelberger³

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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We compared the effects of the two molecular forms of the brain-gut peptide YY (PYY), PYY(1-36) and PYY(3-36), on gastric emptying. Unanesthetized rats received 20-min intravenous infusions of rat PYY(1-36) (0, 1.7, 5, 17, 50, 100, 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) and rat PYY(3-36) (0, 0.5, 1.7, 5, 17, 50, 100, 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 ), either alone or combined, and gastric emptying of saline was measured during the last 10 min of infusion. For comparison, human PYY(3-36) was administered at 0, 17, and 50 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 . Gastric emptying was decreased by 11, 24, 26 and 38% in response to 17, 50, 100, and 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 of rat PYY(1-36); by 10, 26, 41, 53, and 57% in response to 5, 17, 50, 100, and 170 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 of rat PYY(3-36); and by 35 and 53% in response to 17 and 50 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 of human PYY(3-36), respectively. Estimated ED50s were 470 and 37 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 for rat PYY(1-36) and PYY(3-36), respectively. In general, within an experiment, coadministration of PYY(1-36) and PYY(3-36) inhibited gastric emptying by an amount that was comparable to that produced when either peptide was given alone. We conclude that 1) intravenous infusion of PYY(1-36) and PYY(3-36) each produces a dose-dependent inhibition of gastric emptying in rats, 2) PYY(3-36) is an order of magnitude more potent than PYY(1-36) in inhibiting gastric emptying, 3) human PYY(3-36) and rat PYY(3-36) inhibit gastric emptying similarly, and 4) PYY(1-36) and PYY(3-36) do not appear to interact in an additive or synergistic manner to inhibit gastric emptying. intravenous infusion; dose response; interaction PEPTIDE YY (PYY), neuropeptide Y (NPY), and pancreatic polypeptide (PP) comprise the "PP-fold" family of structurally related brain-gut peptides. PYY is synthesized in the gastrointestinal tract, as well as in the central and peripheral nervous systems. Endocrine cells of the ileum, colon, and rectum provide a major source of PYY (2, 47). PYY has also been detected in gastric mucosa, pancreatic islets, myenteric and serosal ganglia, sympathetic neurons, adrenal gland, spinal cord, and brain, including the hypothalamus, pituitary, pons, medulla oblongata, and the brain stem (7-9, 15, 16, 22, 30, 32, 37).Food intake releases PYY into the circulation (2, 47). Systemic administration of PYY inhibits food intake, gastric emptying, intestinal fluid and electrolyte secretion, gallbladder contraction, and exocrine pancreatic secretion (5, 36). Whether PYY acts physiologically by endocrine, neurocrine, and/or paracrine mechanisms to produce these effects remains to be determined. If PYY acts as a blood-borne hormonal signal to produce an effect, then it is important to determine whether the effect is produced by intravenous doses of PYY that reproduce meal-induced increases in plasma PYY.The two major molecular forms of PYY found in the gut and circulation are PYY(1-36) and PYY(3-36) (19 -21). In humans, plasma concentrations of PYY were reported to be 11 pM in the fasted state with PYY(3-36) contributing 37% ...

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Section: Discussionmentioning

confidence: 99%

Comparison of the inhibitory effects of PYY(3-36) and PYY(1-36) on gastric emptying in rats

Chelikani

Haver²,

Reidelberger³

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The majority of local synaptic inputs onto DMV neurons arises from the adjacent NTS, which contains the A2 catecholaminergic group (14). With the noticeable exception of the esophageal-mediated gastric relaxation (21,28), the vast majority of vagovagal reflexes induce a powerful inhibition of the DMV firing rate via activation of inhibitory NTS neurons, which then inhibit DMV vagal output (4,7,8,10,13,16,22,28,29). An inhibitory effect on gastric tone and motility, however, can also be attained by stimulation of DMV neurons forming inhibitory nonadrenergic, noncholinergic pathways (12,28).…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine effects on identified neurons of the rat dorsal motor nucleus of the vagus

Valenzuela

Rogers

Hermann

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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The dorsal motor nucleus of the vagus (DMV) receives more noradrenergic terminals than any other medullary nucleus; few studies, however, have examined the effects of norepinephrine (NE) on DMV neurons. Using whole cell recordings in thin slices, we determined the effects of NE on identified gastric-projecting DMV neurons. Twenty-five percent of DMV neurons were unresponsive to NE, whereas the remaining 75% responded to NE with either an excitation (49%), an inhibition (26%), or an inhibition followed by an excitation (4%). Antrum/pylorus-and corpus-projecting neurons responded to NE with a similar percentage of excitatory (49 and 59%, respectively) and inhibitory (20% for both groups) responses. A lower percentage of excitatory (37%) and a higher percentage of inhibitory (36%) responses were, however, observed in fundus-projecting neurons. In all groups, pretreatment with prazosin or phenylephrine antagonized or mimicked the NE-induced excitation, respectively. Pretreatment with yohimbine or UK-14304 antagonized or mimicked the NE-induced inhibition, respectively. These data suggest that NE depolarization is mediated by ␣1-adrenoceptors, whereas NE hyperpolarization is mediated by ␣2-adrenoceptors. In 16 neurons depolarized by NE, amplitude of the action potential afterhyperpolarization (AHP) and its kinetics of decay () were significantly reduced vs. control. No differences were found on the amplitude and of AHP in neurons hyperpolarized by NE. Using immunohistochemical techniques, we found that the distribution of tyrosine hydroxylase fibers within the DMV was significantly different within the mediolateral extent of DMV; however, distribution of cells responding to NE did not show a specific pattern of localization. brain stem; electrophysiology; gastrointestinal-receptive relaxation SENSORY INFORMATION FROM THE gastrointestinal (GI) tract is received and integrated by neurons in the nucleus of the solitary tract (NTS), in which it is modulated and transferred to neurons in the dorsal motor nucleus of the vagus (DMV) (1, 2, 21). DMV neurons then provide efferent outflow to the GI tract (28, 29). Catecholamine-containing neurons originating in the locus coeruleus as well as A 2 noradrenergic neurons within the NTS project to nuclei within the brain stem (9,14,25). Within the brain stem, the DMV receives more projections from noradrenergic fiber terminals than any of the other medullary nuclei (20). Sumal et al. (24) showed that the A 2 noradrenergic area receives direct excitatory synaptic inputs from sensory vagal afferents, whereas Fukuda et al. (9) demonstrated that electrical stimulation of the A 2 area induces profound catecholaminergic effects on unidentified DMV neurons. Finally, Miyamoto et al. (17) showed that local brain stem application of norepinephrine (NE) increases cervical vagal efferent discharge via an effect on ␣-adrenoceptors, and more recently, we (5) have demonstrated that endogenous catecholamines modulate the glutamatergic pathway from the subnucleus commissuralis of the NTS to the DM...

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“…33 The left DVC represents a specific site of action for [Leu 31 , Pro 34 ]NPY to elicit central stimulation of bile secretion, because the peptide was ineffective when delivered to sites close to, but outside of, the left DVC and also delivered to the right DVC. In addition, the complete suppression of the bile response to [Leu 31 , Pro 34 ]NPY microinjected to the left DVC by hepatic branch vagotomy suggests that the peptide may primarily or secondarily activate preganglionic neurons contributing to vagal innervation of the liver. This finding is further supported by previous studies that indicate that microinjection of NPY or PYY into the DVC induces physiological modulations through the vagus nerve.…”

Section: Discussionmentioning

confidence: 99%

“…This finding is further supported by previous studies that indicate that microinjection of NPY or PYY into the DVC induces physiological modulations through the vagus nerve. 13,30,34 Retrograde tracing techniques have revealed that most of the hepatic vagal preganglionic efferent neurons originate from the left DMN, and orthograde tracing has revealed a predominant pattern of hepatic vagal afferent terminations within the left NST, and some hepatic vagal nerve fibers also have projections from the nucleus ambiguus. [35][36][37] Furthermore, interconnections between the NST and the DMN allow cross-talk between the afferent and efferent loops of the vagal nerve.…”

Section: Discussionmentioning

confidence: 99%

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Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats

et al. 1998

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Neuropeptide Y (NPY), a 36-amino acid peptide, was first isolated from porcine brain and is the member of a family of structurally related peptides that includes peptide YY (PYY) and pancreatic polypeptide. 1,2 NPY is localized in the central nervous system, as well as the peripheral nervous system. 3 In the brain, NPY immunoreactive nerve fibers and terminals and NPY receptors are localized in the paraventricular nucleus of the hypothalamus and the dorsal vagal complex (DVC), including the dorsal motor nucleus of the vagus (DMN) and the nucleus of the solitary tract (NST), 4-6 which are important sites for the autonomic nervous regulation of gastrointestinal function. 7 Central administration of NPY affects several physiological functions. 8 With respect to the gastrointestinal system, central injection of NPY modifies gastric and pancreatic secretion in animal models. 9,10 Recently, Farouk et al. observed that intracerebroventricular injection of NPY stimulates bile acid-independent bile secretion through vagal pathways in rats and dogs, 11 and we have confirmed this effect by intracisternal injection of NPY in rats. 12 Moreover, we have found very recently that the left vagal complex is the specific brain site of action for NPY to induce bile stimulation. 13 It is now generally accepted on the basis of functional and ligand binding studies that NPY binds to and activates six different receptor subtypes, designated Y1, 2, 3, 4 (PP receptor), 5, and 6. 14-18 Y1 receptors exhibit similar affinity for NPY, PYY and [Leu 31 , Pro 34 ]NPY analog, and poor affinity for the C-terminal fragments of NPY/PYY, while Y2 receptors display affinity for NPY/PYY and C-terminal fragments of the peptides but not to the Y1 and 3 selective agonist, [Leu 31 , Pro 34 ]NPY. 14,19-23 PYY has been suggested to have high affinity for Y1 and 2 receptors, and less affinity for Y3 receptors. 14,20,24 Although Y1 receptors were suggested as postsynaptic and Y2 receptors as presynaptic, 25 later studies demonstrated that Y2 receptors are also localized presynaptically. 26 Both Y1 and Y2 receptors are localized in the DVC, 27 which has been identified as the specific brain site for NPY to stimulate bile secretion. 13 Peripherally released PYY binds to the DVC, 28 and microinjection of PYY into the DVC modified gastrointestinal functions. 29,30 The identity of the receptor subtype for NPY in the medulla that mediates the stimulation of bile acid-independent and bicarbonate-dependent bile secretion remains to be established. The present studies were performed to address this question by examining the effect of microinjection of NPY and NPY analogs into the DVC on bile secretion in rats. MATERIALS AND METHODS Animals.Male Wistar rats weighing 270 to 330 g (Charles River Japan Inc., Yokohama, Japan) were housed in group cages under conditions of controlled temperature (22-24°C) and illumination (12-hour light cycle starting at 8 AM) for at least 7 days before the experiments. Animals were maintained on laboratory chow and tap water. Experiments w...

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Central inhibitory action of peptide YY on gastric motility in rats

Cited by 32 publications

References 0 publications

Comparison of the inhibitory effects of PYY(3-36) and PYY(1-36) on gastric emptying in rats

Comparison of the inhibitory effects of PYY(3-36) and PYY(1-36) on gastric emptying in rats

Norepinephrine effects on identified neurons of the rat dorsal motor nucleus of the vagus

Neuropeptide Y stimulates bile secretion via Y1 receptor in the left dorsal vagal complex in rats

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