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PubMed2006

The "human visceral homunculus" to pain evoked in the oesophagus, stomach, duodenum and sigmoid colon.

The oesophagus, stomach, duodenum and sigmoid colon were electrically stimulated in 12 healthy volunteers with a thin nasal endoscope. The painful cortical evoked potentials (EPs) were recorded from 64 surface electrodes. The early EPs with latencies < 200 ms were studied and the corresponding dipole sources were calculated. The electrical current intensities needed to evoke pain were highest in the stomach and duodenum, compared to the other segments (F = 7.8; P < 0.001; post hoc analysis P < 0.05). The EP latencies after stimulation of the stomach and sigmoid colon were shorter compared with those to stimulation of the oesophagus and duodenum (all P values < 0.001). The EP amplitudes were higher to oesophagus stimulation (all P values < 0.001 except for the early positivity). The potential fields obtained after stimulation of the most distal segments (duodenum and sigmoid colon) were in general distributed more posteriorly compared to those recorded in the more proximal regions. The EP topographies to stimulation of all gut tracts were explained by a bilateral source in the second somatosensory (SII) area, by a dipole in the anterior cingulate cortex (ACC), and by a bilateral generator in the insular cortex. However, the position of the sources significantly changed depending on the stimulated gut tract. Moreover, while the SII and ACC sources were initially activated to oesophagus and stomach stimulation, the ACC and insular activities were the earliest ones after stimulation of the lower gut segments. The findings reflect differences in pathways and brain processing of visceral nociceptive inputs coming from either upper or lower gut and may improve our understanding of the brain-gut axis in health and disease.

Adult↗
PubMed2000

Apoptosis in murine duodenum during embryonic development.

Duodenum is thought to go through a solid-core stage followed by recanalization during its development. This study investigates the role of apoptosis in normal duodenal development, especially during widening of the lumen, and hence, the possible role of apoptosis in duodenal atresia (DA). Twenty-four time-mated Sprague-Dawley rats were killed from day 13 to day 20 of gestation. Duodenums of 3 fetuses were chosen randomly from each rat and processed. Apoptosis was determined by the terminal deoxytransferase-mediated biotin dUTP nick-end labeling (TUNEL) technique (ApopTag). Apoptosis count and cross-sectional areas were measured with an image analyzer (MetaMorph). The number of apoptotic cells per unit area duodenum peaked on day 15 for the mucosal/submucosal layer and on day 14 for the muscular/mesenchymal layer. The maximal number of apoptotic cells per cross-section of duodenum was between 7 and 8. The cross-sectional areas of the duodenal wall and lumen increased exponentially between day 17 and day 19 while duodenal-wall thickness remained relatively constant throughout duodenal development. The localization, timing, and intensity of apoptosis do not suggest that apoptosis is responsible for the widening of the duodenal lumen; enlargement of the lumen is related to the increase in duodenal circumference. Apoptosis thus may not be involved in the pathogenesis of DA.

Animals↗
PubMed2000

Direct neuronal interactions between the duodenum and the sphincter of Oddi.

The sphincter of Oddi (SO) is a complex structure that must function in coordination with the motor activities of the gallbladder and the duodenum. It is now clear that a neural circuit exists between the duodenum and the SO, and it is likely that this network is largely responsible for the regulation of SO motility. Recent studies have demonstrated that this circuit provides excitatory cholinergic input to SO ganglia that can be activated by electrical stimulation of the duodenal mucosa, distention of the duodenum, and increased motor activity of the duodenum.

Autonomic Nervous System↗
PubMed1985

Effects of verapamil and dexamethasone on the 1,25-dihydroxyvitamin D3-mediated calcium absorptive mechanism in the organ-cultured embryonic chick duodenum.

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) is known to induce the biosynthesis of a specific, calcium-binding protein (CaBP) and to stimulate calcium transport in the organ-cultured embryonic chick duodenum. The biosynthesis of CaBP has been shown previously to exhibit an absolute dependence on the ambient calcium concentration of the culture medium. Verapamil, a calcium-channel blocker, decreased calcium influx into the organ-cultured duodenum and inhibited the induction of CaBP by 1,25(OH)2D3. Raising ambient calcium concentrations to as high as 10 mM did not prevent or reverse the inhibitory actions of verapamil. Dexamethasone, known to augment CaBP biosynthesis and calcium uptake in the organ-cultured duodenum in response to 1,25(OH)2D3, largely prevented inhibition of CaBP by verapamil. The actions of verapamil and dexamethasone were correlated with altered steady-state calcium concentrations of the organ-culture duodenum, strongly supporting a regulatory role of calcium in the 1,25(OH)2D3-mediated, intestinal calcium absorptive mechanism.

Animals↗
PubMed1985

Adrenocorticotropin and alpha-melanotropin in the myenteric plexus of the rat duodenum: an electron microscopic study.

Adrenocorticotropin (ACTH) immunoreactivity was localized at the ultrastructural level as positive 'cores' within large dense-cored vesicles (LDVs) of axons and dendrites of the rat duodenum. The immunostained vesicle 'cores' were 35-50 nm in mean diameter, corresponding to 'cores' of LDVs with a mean diameter of 80-90 nm. alpha-melanotropin (alpha-MSH) was detected also within LDVs, expressing the same mean diameter as ACTH-stained vesicles. alpha-MSH and ACTH were localized only within structures belonging to the enteric nervous system of the rat duodenum. alpha-MSH and ACTH, as detected by immunostaining, were absent in endocrine cells of the rat duodenum. These findings suggest the possibility that these peptides may have important physiological roles in the rat duodenum.

Adrenocorticotropic Hormone↗
PubMed1994

Developmental changes in the response of rat isolated duodenum to nicotine.

Developmental changes in the response to ganglionic stimulants, nicotine and dimethylphenylpiperazinium, were investigated in rat isolated duodenum by recording isotonic mechanical activity. The duodenal response to nicotine/dimethylphenylpiperazinium (3 x 10(-7) to 10(-3) M) in neonatal rats was contraction, which was blocked by hexamethonium, tetrodotoxin and hyoscine. The response to nicotine/dimethylphenylpiperazinium (10(-6) to 10(-4) M) in the adult duodenum was relaxation, which was blocked by tetrodotoxin and hexamethonium, but by neither guanethidine nor hyoscine. The transition of the response to nicotine/dimethylphenylpiperazinium from contraction to relaxation occurred at around the 3rd postnatal week. Nicotine-induced relaxation of adult duodenum was significantly inhibited by preincubation with alpha-chymotrypsin, a proteolytic enzyme, and a combination of nucleotide pyrophosphatase and 8-phenyltheophylline, a P1 purinoceptor antagonist. Nicotine-induced relaxation was desensitized by alpha, beta-methylene ATP, a stable P2x purinoceptor agonist. These results suggest that the contractile response of isolated duodenum to nicotine is mediated through cholinergic transmission in neonatal rats and the relaxant response is mediated through non-adrenergic, non-cholinergic transmission, which involves both peptidergic and purinergic transmission, in adult rats.

Adenosine Triphosphate↗
PubMed1988

Motor activity of the gastric antrum, pylorus, and duodenum under fasted conditions and after a liquid meal.

Because the mechanisms that control the movement of food and digestive juices across the human pylorus are not completely understood, the aim of this study was to document the normal patterns of pressure activity in the antrum, pylorus, and duodenum and the associated pH changes in 9 healthy volunteers. Studies were carried out under fasting conditions and after ingestion of 300 ml of chocolate milk, using a unique 11-channel intraluminal probe that incorporated a sleeve sensor positioned across the pylorus and pH electrodes situated in the terminal antrum and proximal duodenum. The most common motor pattern recorded under fasting conditions consisted of regular coordinated contractions, most of which (a) involved the antrum and duodenum, (b) showed evidence of propagation through two or more adjacent channels, and (c) were associated with transient reductions in duodenal pH and transient elevations in antral pH. Ingestion of milk changed the motor pattern to one that was composed of pressure waves, which were confined to the pylorus with few or no pressure waves in the terminal antrum or proximal duodenum. Isolated pyloric pressure waves were gradually replaced by propagated antroduodenal contractions, which eventually occurred at a regular frequency that was higher than that observed under fasting conditions. After ingestion of milk, only the coordinated contractions were associated with transient reductions in duodenal pH. Isolated pyloric pressure waves were also observed under fasting conditions just before or just after phase III of the migrating motor complex, and 17% of these were accompanied by episodes of duodenal acidification.

Adult↗
PubMed1991

Role of capsaicin-sensitive afferent neurons in alkaline secretory response to luminal acid in the rat duodenum.

The role of capsaicin-sensitive afferent neurons in acid-induced HCO3- secretion was investigated in the duodenum of anesthetized rats. The proximal duodenum was perfused with saline (pH 4.5), the pH of perfusate and the transmucosal potential differences were continuously monitored, and HCO3- output was determined by pH change. Under these conditions, duodenal pH, potential difference, and HCO3- output were significantly increased in response to IV injection of prostaglandin E2 (300 micrograms/kg) and luminal acidification (10 mmol/L HCl, 10 minutes). These responses induced by luminal acid were significantly attenuated by SC pretreatment with indomethacin (5 mg/kg), preexposure of the mucosa to lidocaine (4%, 15 minutes), functional ablation of capsaicin-sensitive afferent neurons, or even prior application of capsaicin (6 mg/mL, 30 minutes) to the duodenum. Although capsaicin application by itself (0.3-6 mg/mL) produced a concentration-dependent increase of HCO3- output, this effect was significantly reduced by lidocaine, indomethacin, or chemical deafferentation and exhibited a tachyphylaxis after repeated application at a high concentration (6 mg/mL). Neither of these treatments significantly affected the HCO3- response induced by prostaglandin E2. It was concluded that stimulation of capsaicin-sensitive afferent neurons increased duodenal HCO3- secretion and that these neurons may be involved in the mechanism of HCO3- response induced by luminal acid in the duodenum.

Animals↗
PubMed1994

Role of B1 and B2 receptors and of nitric oxide in bradykinin-induced relaxation and contraction of isolated rat duodenum.

Bradykinin (BK) and its analogues induce a typical biphasic response (relaxation followed by contraction) in the isolated rat duodenum. We studied the role of B1 and B2 BK receptors and nitric oxide (NO) in relaxation and contraction of the isolated rat duodenum. Both effects are concentration-dependent: BK has shown an EC50 (contraction) of 3.8 +/- 1.9 x 10(-7) M and an IC50 (relaxation) of 3.0 +/- 0.7 x 10(-9). Similar results were obtained with the selective B2 receptor agonists [Hyp3,Tyr(Me)8]-BK and [Phe8 psi (CH2-NH)Arg9]-BK, showing an EC50 of 9.6 +/- 1.9 x 10(-7) M and 5.6 +/- 2.9 x 10(-7) M and an IC50 of 3.5 +/- 0.6 x 10(-10) M and 6.8 +/- 1.7 x 10(-10) M, respectively. Furthermore, the effects induced by these three agonists were not altered when tissues were treated with 42.1 microM Mergetpa, a carboxypeptidase N inhibitor. While the relaxant and contractile effects elicited by BK were significantly inhibited in the presence of Hoe 140 (0.7 microM), a selective B2 receptor antagonist, those induced by the selective B1 receptor agonist desArg9-BK were not. Furthermore, [Leu8]-desArg9-BK (2.6 microM), which is both a pure and selective B1 receptor antagonist, acted as an agonist on the rat duodenum, inducing a biphasic relaxant and contractile effect. These relaxant and contractile effects were not altered by drugs that inhibit or stimulate NO production, such as L-NAME (200 microM), a combination of L-NAME (200 microM) and indomethacin (2.5 microM), L-arginine (1 mM), or superoxide dismutase (20 U/ml). However, the contractile effect was significantly reduced when tissues were preincubated with methylene blue (100 microM), which inhibits activation of guanylate cyclase. We conclude that 1) BK and its analogues selectively activate a B2 receptor, producing a biphasic effect (relaxation and contraction); 2) DesArg9-BK may either acts via a different receptor which might be another B1 receptor subtype or a typical B1 receptor where [Leu8]-desArg9-BK acts as a partial agonist; and 3) neither NO nor the prostaglandin pathway mediates BK-induced relaxation in the isolated rat duodenum.

Amino Acid Oxidoreductases↗
PubMed1991

Central and peripheral type benzodiazepine ligands displace [3H][3-ME-HIS2]TRH from its binding sites in the brain and the anterior pituitary and antagonize the effect of TRH in the rat duodenum.

The effects of central (clonazepam, an agonist, and FG 7142, an inverse agonist), mixed (diazepam) or peripheral type (Ro 5-4864) benzodiazepine receptor ligands on the action of TRH on the transmurally stimulated rat duodenum and binding of [3H][3-Me-His2] TRH in the rat anterior pituitary, hypothalamus, cortex and brainstem have been studied. TRH dose-dependently inhibited the contractions of transmurally stimulated rate duodenum. Clonazepam (5 x 10(-6) M), diazepam (10(-5) M), Ro 5-4864 (10(-5) M) or FG 7142 (10(-5) M) attenuated the response of TRH in the rat duodenum. The action of these compounds was antagonized neither by the central type benzodiazepine antagonist flumazenil nor by peripheral type antagonist PK 11195 but instead PK 11195 itself counteracted TRH. TRH displaced [3H][3-Me-His2]TRH with Ki-values ranging 0.08 to 0.31 microM. Ki-values for clonazepam diazepam, Ro 5-4864, PK 11195 and FG 7142 ranged 6-117 microM, 3-23 microM, 20-67 microM, 20-40 microM and 260-420 microM, respectively, demonstrating fairly weak affinity to TRH-receptors. In saturation experiments, clonazepam and PK 11195 significantly increased KD but not Bmax of the labelled ligand while Ro 5-4864 increased both KD and Bmax. This indicates that all these compounds competitively inhibit the binding of [3H][3-Me-His2]TRH in the CNS which may also be the mechanism for their antagonism of the effect of TRH in the rat duodenum.

Animals↗
PubMed1981

Role of the duodenum in motilin release.

In order to study the regulatory mechanism of motilin release, plasma motilin was measured in healthy dogs during the fasting state and after the ingestion of ordinary nutrient. Fasting plasma motilin levels were found to fluctuate intermittently, but ingestion of a meal completely abolished the intermittent motilin release and resulted in low motilin levels lasting for 6-8 h. To clarify the role of the duodenum in this motilin release, an operation was performed in five dogs by which we excluded from the alimentary tract the upper half of the small intestine not including the duodenum from a point 2 cm below the larger pancreatic duct. After this operation meal ingestion still caused a decrease in plasma motilin levels. However, after a modified version of the operation was performed in 5 other dogs by which the upper half of the small intestine together with the duodenum was transected at the pyloric ring, plasma motilin was not suppressed by meal ingestion. The results suggest that motilin secretion is regulated by nutrieht ingestion and that the passage of nutrients through the duodenum plays an important role in its regulation.

Animals↗
PubMedDate not supplied

Bradykinin receptors in isolated rat duodenum.

Pharmacological properties of the bradykinin receptors in the isolated rat duodenum were investigated by examining the relaxant and contractile responses to bradykinin and [des-Arg9]-bradykinin, an agonist of B1 receptors. A specific desensitization and de novo formation for B1 receptors were observed. Changes in medium pH caused a decrease in the responses to bradykinin and [des-Arg9]-bradykinin of rat duodenum. Urea incubation in test tube inhibited the responses to bradykinin and [des-Arg9]-bradykinin of rat duodenum, while urea in bathing medium was ineffective. These findings strongly suggested that (a) ionic bonds are important in the interaction between bradykinin and its receptors, and (b) B2 receptors in rat duodenum are different from those in guinea pig ileum.

Animals↗
PubMed1988

Pathologic response of the pancreas and duodenum to experimental intraoperative irradiation.

The pancreas and duodenum of 24 beagle dogs were given intraoperative irradiation (IORT) with 6 MeV electrons. The dose range was 17.5 Gy to 40 Gy. Billroth II gastrojejunostomy was performed on all dogs prior to irradiation. Six control dogs received only Billroth II surgery. Starting 2 weeks after surgery, dogs in the irradiation groups were given 50 Gy 6 MV X rays external beam radiation therapy (EBRT) to the pancreas and duodenum. The total dose of 50 Gy was given in 2 Gy fractions over 5 weeks. Dogs were monitored for 135 days then necropsied. Gross and histopathologic changes in the pancreas and duodenum were evaluated and quantitative analysis of pancreatic lesions done. Duodenal ulcers were found following 32.5 Gy and 40 Gy IORT. The pancreases were atrophic in irradiated dogs and exocrine pancreatic insufficiency occurred in one dog given 25 Gy. Gross pancreatic atrophy correlated with IORT dose. Histopathologic evidence of radiation damage to the pancreas was observed in acinar cells. Islet cell lesions were not apparent. There was pancreatic fibrosis and damage to blood vessels and ducts. Dose-response relationships were observed for the index of damage to the pancreas as a whole, for pancreatic fibrosis and a decrease in normal acinar cells. Although 25 Gy IORT plus 50 Gy EBRT was tolerated by the duodenum to 135 days, these doses may cause later pancreatic injury as an expression of damage to blood vessels and ducts. Exocrine pancreatic insufficiency and diabetes mellitus may thus represent potential late complications of IORT following 25 Gy or higher doses.

Animals↗
PubMed2004

Prolactin directly stimulated the solvent drag-induced calcium transport in the duodenum of female rats.

Prolactin has been reported to stimulate the calcium absorption of the duodenum where three components of the active calcium transport, namely transcellular active, voltage-dependent and solvent drag-induced calcium transport, were identified. It was known that the transcellular active, but not the voltage-dependent, duodenal calcium transport was directly stimulated by prolactin. The present study thus aimed to evaluate the direct action of prolactin on the solvent drag-induced duodenal calcium transport by using the Ussing chamber technique. The jejunum was used as a reference for the existence of solvent drag and the widening of tight junction induced by cytochalasin E. Results showed that the solvent drag-induced calcium transport existed in both intestinal segments, but the magnitude was significantly greater in the duodenum (29.27+/-2.27 vs. 17.31+/-1.65 nmol h(-1) cm(-2), P<0.001). We further demonstrated that 200, 600 and 800, but not 1000 ng/ml, prolactin significantly promoted the solvent drag-induced duodenal calcium transport in a dose-response manner, i.e. from the control value of (nmol h(-1) cm(-2)) 24.31+/-2.36 to 45.42+/-3.47 (P<0.01), 63.82+/-5.28 (P<0.001) and 53.93+/-5.41 (P<0.01), respectively. However, prolactin did not manifest any effect on the jejunum. Because the paracellular transport was suggested to be size-selective as well as charge-selective, further experiments were designed to evaluate the mechanism by which prolactin stimulated the solvent drag-induced calcium transport. The duodenum was exposed to 20 microM cytochalasin E, 600 ng/ml prolactin or the combination of both in the presence of a paracellular marker 3H-mannitol, while the jejunum was a positive reference. The results showed that, in the jejunum, cytochalasin E alone and cytochalasin E plus prolactin significantly increased the mannitol fluxes from (micromol h(-1) cm(-2)) 0.29+/-0.04 to 0.49+/-0.03 (P<0.05) and 0.48+/-0.05 (P<0.05), respectively, while having no effect on the calcium fluxes. Prolactin alone had no effect on the jejunal calcium flux. In the duodenum, neither mannitol nor calcium fluxes were enhanced by cytochalasin E, however, prolactin still increased the solvent drag-induced calcium flux from 27.74+/-2.41 to 51.03+/-4.35 nmol h(-1) cm(-2) (P<0.001). It was concluded that prolactin directly stimulated the solvent drag-induced duodenal calcium transport in a dose-response and biphasic manner without the widening of tight junction.

Animals↗
PubMed2006

Upregulation of aspartoacylase activity in the duodenum of obesity induced diabetes mouse: implications on diabetic neuropathy.

Aspartoacylase (ASPA) hydrolyzes N-acetylaspartic acid (NAA) into aspartate and acetate. Normal hydrolysis of NAA is important to maintain healthy neurons. Since enteric neuropathy is one of the events seen in diabetes, whether ASPA activity is affected in diabetic condition is not known. In order to investigate the possibility, ASPA activity was examined in the duodenum and brain of obesity induced diabetes model mouse. Aspartoacylase activity was high in the diabetic mouse duodenum compared to control duodenum. The same result was also observed by immunostaining of the mouse duodenum. The activity of ASPA was found to be elevated in the brain of diabetic mouse compared to the control brain. These data suggest that normal hydrolysis of NAA is affected by ASPA activity seen in the type 2 diabetes model mouse and this change is likely to contribute to neuropathy seen in diabetes, if documented also in patients with type 2 diabetes.

Amidohydrolases↗
PubMed2006

Experimental model to assess possible medicinal herb interaction with a radiobiocomplex: qualitative and quantitative analysis of kidney, liver and duodenum isolated from treated rats.

Ginkgo biloba extract (EGb) has been used as a medicinal herb. Several biological properties have been associated with this extract, especially, in the increase of the blood flow, in the action as platelet activating factor antagonism and in the prevention of the membrane against the damage caused by free radicals. Radiobiocomplexes have been utilized in various nuclear medicine procedures helping in the diagnosis and/or treatment of human diseases. Many substances have been reported to affect the bioavailability of different radiobiocomplexes. The aim of this work was to evaluate the possible influence of an EGb on the bioavailability of the sodium pertechnetate (99mTcO4Na) and on the morphometry of some organs isolated from rats. These animals were treated with EGb and 99mTcO4Na was injected. The animals were sacrificed, the organs isolated, counted in a well counter and the percentage of radioactivity per gram of each organ was calculated. The results showed that EGb decreased the uptake of the 99mTcO4Na in the duodenum (P<0.05). Moreover, morphometric analysis has revealed significant modifications (P<0.05) on kidney, liver and duodenum due to the cited treatment. It is speculated that the substances present in the EGb could act directly or generate metabolites capable to promote changes in organs (kidney, liver and duodenum), however, only significant alteration in the uptake of the 99mTcO4Na in the duodenum.

Animals↗
PubMed2004

A duodenum-preserving and bile duct-preserving total pancreatic head resection with associated pancreatic duct-to-duct anastomosis.

A duodenum-preserving pancreatic head resection technique was first reported in 1980, but the indications have been limited to benign pancreatic disease as it involves a subtotal pancreatic head resection. In 1988 we detailed a duodenum-preserving total pancreatic head resection (DPTPHR) technique. This procedure involved a total pancreatic head resection and as such expanded the indications for this approach to include tumorigenic masses. The original method involved closure of the proximal pancreatic duct and an anastomosis of the pancreatic duct of the distal pancreas to a newly created small hole in the duodenum (we termed this a "pancreatoduodenostomy"). Our current technique involves a duct-to-duct anastomosis of the proximal pancreatic duct and the distal pancreas to better preserve anatomic structure. DPTPHR was performed in 26 patients from 1988 to 2002, including 12 cases of DPTPHR with pancreatoduodenostomy and 14 cases of DPTPHR with pancreatic duct-to-duct anastomosis. No differences were observed between the two methods with respect to operative time or blood loss during surgery. Postoperatively, there was one case of cholecystitis and one case of pancreatitis in a patient who underwent a pancreatoduodenostomy; both of these patients were treated conservatively with curative intent. No complications were observed in the group undergoing duct-to-duct anastomosis. The advantage of duct-to-duct anastomosis is that the pancreatic head is totally resected, thus allowing removal of neoplastic disease such as an intraductal papillary mucinous tumor and also therapy for chronic pancreatitis. A key benefit of this procedure is that sphincter function of the duodenal papilla is preserved permitting drainage of pancreatic/bile juice into the duodenum, preserving a more physiologic state than is the case after a pancreatoduodenostomy.

Anastomosis, Surgical↗
PubMed2005

Cholecystokinin-8 increases Fos-like immunoreactivity in myenteric neurons of the duodenum and jejunum more after intraperitoneal than after intravenous injection.

The objective of this study was to measure the relative efficacy and potency of cholecystokinin-8 (CCK-8) given by intraperitoneal (i.p.) and intravenous (i.v.) injection to stimulate Fos-like immunoreactivity (Fos-LI) in neurons of the myenteric plexus in the duodenum and jejunum. The subjects for his experiment were 40 male Sprague-Dawley rats divided into eight treatment groups (n=5 rats per treatment). Four groups of rats were injected with 5, 10, and 40 microg/kg sulfated CCK-8 and saline (control) i.p., and the remaining groups with the same treatments i.v. We then detected Fos-LI, a marker for neuronal activation, in the myenteric plexus of the duodenum and jejunum, in response to the previous doses and routes. All of the CCK-8 doses administered by both routes increased Fos-LI in the myenteric plexus of the duodenum and jejunum significantly more than saline did. Although both routes were efficacious in increasing Fos-LI, CCK-8 i.p. was significantly more potent than CCK-8 i.v. These data provide immunohistochemical evidence that i.p. administration of CCK-8 is a more potent stimulant of Fos-LI in the neurons of the myenteric plexus of the duodenum and jejunum than i.v. injection.

Animals↗