Area postrema mediates gastric motor response induced by apomorphine in rats

Koga, Tomoshige; Kobashi, Motoi; Mizutani, Masatoshi; Tsukamoto, Goichi; Matsuo, Ryuji

doi:10.1016/s0006-8993(02)03801-5

Cited by 29 publications

(17 citation statements)

References 27 publications

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“…Our results are inconsistent with those reported by Koga et al (38) who found that apomorphine causes an increase in salivary secretion in rats within 5 min after dosing with 3 -10 mg/kg, i.v. The reason for this might be due to the differences in the sampling time or administration route.…”

Section: Discussioncontrasting

confidence: 99%

Various Emetogens Increase the Secretion of Salivary Amylase in Rats: a Potential Model in Emesis Research

et al. 2010

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Abstract. We investigated the effects of various emetic agents: cisplatin, apomorphine, lithium chloride (LiCl), rolipram, sibutramine, and the β 3 -adrenoceptor (AR) agonist CL316243 on salivary amylase secretion in rats. We also determined the inhibitory effect of granisetron, a 5-HT 3 -receptor antagonist, on cisplatin-induced increased salivary amylase activity and the inhibitory effect of bilateral abdominal vagotomy on increases in salivary amylase activity induced by cisplatin and LiCl. Granisetron was administered 15 min before and 1 h after cisplatin administration. Cisplatin (10 -15 mg/kg, i.v.) increased salivary amylase activity dose-dependently and induced an acute increase from 1.5 h post-treatment with 15 mg/kg. Apomorphine (1 -3 mg/kg, s.c.), LiCl (120 mg/kg, i.p.), rolipram (3 -10 mg/kg, p.o.), and sibutramine (10 mg/kg, p.o.) induced significant increases in salivary amylase secretion. On the other hand, CL316243 did not stimulate salivary amylase secretion. The increased amylase activity induced by cisplatin (15 mg/kg, i.v.) was inhibited significantly by granisetron (1 or 3 mg/kg × 2, i.v.) or tended to be inhibited by bilateral abdominal vagotomy, whereas an increase in amylase activity produced by LiCl was not inhibited by abdominal visceral nerve section. These results suggest that salivary amylase activity is useful as a marker for emesis in rats, a species that does not exhibit vomiting.

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Section: Discussioncontrasting

confidence: 99%

Various Emetogens Increase the Secretion of Salivary Amylase in Rats: a Potential Model in Emesis Research

et al. 2010

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“…Our previous study (26) in the proximal stomach revealed that administration into the fourth ventricle of orexin-A, an appetite-enhancing peptide produced in the hypothalamus like NPY, induced gastric relaxation. On the contrary, anorexic agents, such as apomorphine, increased the IGP of the proximal stomach (30). We infer that IGP in the proximal stomach, which works as a reservoir, might be an appropriate index to ascertain the appetite of an animal.…”

Section: Discussionmentioning

confidence: 80%

“…Appetite-enhancing peptides facilitate phasic contractions and gastric emptying (2,13,26,31). On the contrary, anorexic agents depress phasic contractions (11,30). These phenomena are to be expected, because enhanced appetite facilitates digestion and anorexia induces dyspepsia.…”

Section: Discussionmentioning

confidence: 99%

Central neuropeptide Y induces proximal stomach relaxation via Y1 receptors in the dorsal vagal complex of the rat

Kobashi¹,

Shimatani²,

Shirota³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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feeding; vagus; fundus; gastric; medulla NEUROPEPTIDE Y (NPY) is a peptide of 36 amino acids isolated from porcine brain (46). Potent appetite-stimulating effects of NPY are well known (8, 9). NPYergic transmissions are considered to be an essential component of the common final pathway in the hypothalamic integration of energy homeostasis. Kalra et al. (24), citing a large number of studies, described NPY as the only messenger molecule for a physiological appetite transducer in the brain. Several studies revealed that the Y1 receptor subtype (Y1R) is the most prominent factor in mediating feeding induced by NPY (22,23,47). Feeding responses induced by melanin-concentrating hormone was attenuated by the antagonistic effects of Y1R (5). Neurons containing other appetite-stimulating peptides, such as orexin or ghrelin, send information to NPY-containing neurons (12), and NPY is a key peptide in the regulation of body energy homeostasis.Besides the role of NPY in feeding behavior, NPY is involved in several abdominal functions. Centrally administered NPY regulated gastric acid secretion (14,17,34,38) and stimulated bile secretion via the Y1R (48). Microinjection of NPY into the dorsal vagal complex (DVC) enhanced basal motility of the antrum via Y1Rs (7). Centrally administered NPY delayed gastric emptying via Y2 receptors (Y2R) (18) and inhibited gastric distension-induced pyloric relaxation via Y1Rs (19). Thus NPY contributes to the control of digestion via upper abdominal functions. Gastric contractile activities that occur in the distal stomach are particularly important for digestion. In addition, accommodation of food is important for a smooth digestion. Tack et al. (45) described impaired accommodation related to functional dyspepsia symptoms. Gastric relaxation in the proximal stomach to accommodate ingested food is achieved by the intramural nervous system and extrinsic nervous system. Receptive relaxation is a well-known response achieved by the extrinsic nervous system (4), which arises from neurons in the dorsal motor nucleus of the vagus (DMV) (42). Thus the hindbrain is involved in the control of gastric motor activities. However, the relationship between NPY and gastric relaxation of the proximal stomach, which serves as a reservoir, has never been clarified. Recently, we suggested that administration of orexin-A, which is one of the appetite-stimulating peptides produced in the hypothalamus, into the fourth ventricle induced relaxation of the proximal stomach as well as an enhancement of distal stomach contractility (26). Because NPY affects DVC neurons that receive afferent information from the stomach (44) and send efferent information through axons to the gastrointestinal tract (3), it is possible that NPY induces gastric relaxation to accommodate ingested food.The present study was undertaken to demonstrate the role of NPY in gastric relaxation of the proximal stomach to accommodate food intake. The contribution of Y1Rs in the dorsal medulla to the relaxation of the proximal stomach induced by N...

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“…For instance, intravenous administration of apomorphine, that is a nonspecific dopaminergic agonist and induces emesis, evokes two distinct gastric motor responses in rat. One is the inhibition of phasic contractions that appear just after administration (Abrahamsson et al, 1973;Blancquaert et al, 1985), and the other is an increase in the frequency of small phasic contractions accompanied by increased gastric tone appearing with a relatively longer delay (Koga et al, 2003). Nicotine is also known to induce excitatory and inhibitory effects on the gastrointestinal tract, some of which may be caused by interaction of nicotine with nAChR in the medullla oblongata (Nagata and Osumi, 1991;Ferreira et al, 2000Ferreira et al, , 2001.…”

Section: Discussionmentioning

confidence: 99%

Effects of Z-338, a novel gastroprokinetic agent, on the actions of excitatory and inhibitory neurotransmitters on neurons in area postrema

Akaike

Jang

Hori

et al. 2010

J. Smooth Muscle Res.

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We investigated the effects of the novel gastroprokinetic agent Z-338 on the actions of excitatory and inhibitory neurotransmitters on neurons in area postrema (AP). Iontophoretic applications of acetylcholine (ACh), AMPA and NMDA increased, while GABA suppressed the firing rates of AP neurons recorded by extracellular electrodes. Z-338 (10 µM) suppressed the ACh-induced acceleratory and GABA-induced inhibitory actions without affecting the excitatory actions of AMPA and NMDA. Under voltageclamp conditions, nicotine, NMDA, kainic acid (KA) and ATP evoked inward currents in dissociated single AP neurons recorded by whole-cell patch clamp technique, and GABA produced outward currents, at holding potentials (VH) of -60 or 0 mV. Z-338 (>3 µM) specifically suppressed the nicotine-and GABA-induced currents without affecting the currents induced by NMDA, KA and ATP. In addition, we found that Z-338 (30 µM) suppressed the spontaneous inhibitory postsynaptic currents (sIPSCs) recorded from AP neurons in slice preparations. Experiments with microelectrode and histochemical methods revealed the presence of direct excitatory and di-synaptic inhibitory neural connections from AP to dorsal motor nucleus of the vagus (DMV). In some AP neurons, Z-338 (10 µM) enhanced the spontaneous firing rates recorded by extracellular electrode.The excitatory or inhibitory effects of Z-338 on the firing rates or actions of nicotine and GABA on AP neurons observed in the present study may explain the postmeal relaxation induced by Z-338 in patients with functional dyspepsia.

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Area postrema mediates gastric motor response induced by apomorphine in rats

Cited by 29 publications

References 27 publications

Various Emetogens Increase the Secretion of Salivary Amylase in Rats: a Potential Model in Emesis Research

Various Emetogens Increase the Secretion of Salivary Amylase in Rats: a Potential Model in Emesis Research

Central neuropeptide Y induces proximal stomach relaxation via Y1 receptors in the dorsal vagal complex of the rat

Effects of Z-338, a novel gastroprokinetic agent, on the actions of excitatory and inhibitory neurotransmitters on neurons in area postrema

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