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PubMed1966

The uptake and release of radioactive noradrenaline by the splenic nerves of cats.

1. DL-[(3)H]noradrenaline was infused close-arterially into the spleens of chloralosed cats at rates of 0.625 or 1.25 mug/min for 10 or 20 min and the recovery of noradrenaline and its metabolites in the venous blood measured during the infusion and after nerve stimulation at various times after the infusion.2. During the infusion 41% of the noradrenaline was recovered in the blood as such and 11% as metabolites. The remaining 48% was retained within the spleen.3. The noradrenaline retained in the spleen was slowly released to appear as metabolites in the blood stream. In normal animals the rate of loss from the spleen was 0.22% per minute. In animals given phenoxybenzamine after the end of the infusion this rate was several times greater.4. Splenic nerve stimulation in normal animals or in animals treated with phenoxybenzamine resulted in an increase in the radioactivity of the blood leaving the spleen. Paper chromatography showed this to be radioactive noradrenaline.5. In normal animals the specific activity of the transmitter liberated by nerve stimulation was less than that of the stores of noradrenaline within the spleen. In animals treated with phenoxybenzamine these two values were similar.6. It is suggested that the infused noradrenaline retained in the spleen is largely taken up into nerve fibres and is available for subsequent release by nervous activity.

Animals↗
PubMed1967

Inhibition of gastrointestinal movement by sympathetic nerve stimulation: the site of action.

1. The mechanism of sympathetic nervous inhibition of gastrointestinal movement was investigated in order to determine whether the primary action of sympathetic nerve stimulation was on ganglia or on the smooth muscle itself.2. The effect of sympathetic nerve stimulation did not resemble the effect of ganglionic blockade or that of removing all nervous tone with tetrodotoxin.3. The same frequency of sympathetic nerve stimulation to the rabbit jejunum which inhibited the myogenic spontaneous activity blocked excitatory responses to transmural post-ganglionic cholinergic nerve stimulation and antagonized contractions in response to drugs acting directly on the smooth muscle.4. Acetylcholine output was measured as an indicator of post-ganglionic nervous activity. In contrast to hexamethonium, stimulation of sympathetic nerves at frequencies of stimulation sufficient to relax the muscle did not reduce the output of acetylcholine.5. Vagus nerves and sympathetic nerves to the guinea-pig stomach were stimulated individually and simultaneously in the presence of hyoscine. The relaxant responses to stimulation of the two nerves summated when they were stimulated simultaneously, indicating that the transganglionic vagal pathway was not blocked.6. It is concluded that the effect of sympathetic nerve stimulation is due to the direct action of the released noradrenaline on the smooth muscle.

Acetylcholine↗
PubMed1989

Neurotensin facilitates release of substance P in the guinea-pig inferior mesenteric ganglion.

1. Intracellular, electrophysiological techniques were combined with radio-immunological, chromatographic and pharmacological techniques to determine if nerve terminals containing substance P mediated transient depolarizing responses of principal ganglion cells induced by neurotensin. Experiments were performed in vitro on guinea-pig inferior mesenteric ganglia. 2. In 61% of principal ganglion cells tested in normal ganglia, neurotensin caused a transient membrane depolarization. In ganglia which were removed from animals which had been pre-treated with capsaicin, transient responses to neurotensin were virtually abolished. 3. In normal ganglia, neurotensin increased the amplitude and duration of noncholinergic slow EPSPs evoked by electrical stimulation of the lumbar colonic nerve. Such increases were absent in ganglia obtained from animals pre-treated with capsaicin. 4. In guinea-pigs pre-treated with capsaicin, the content of substance P-like material was significantly reduced in inferior mesenteric and coeliac ganglia, dorsal root ganglia and lumbar spinal cord, compared to control animals. The content of substance P-like material in segments of distal colon was slightly reduced. The content of vasoactive intestinal polypeptide-, cholecystokinin- and bombesin-like material in the same tissues from animals pre-treated with capsaicin was not significantly different from control animals. 5. Chromatographic analysis using HPLC (high-performance liquid chromatography) techniques revealed that the material depleted from inferior mesenteric and coeliac ganglia, dorsal root ganglia and lumbar spinal cord by capsaicin pre-treatment co-eluted with synthetic substance P. 6. Electrical stimulation of the lumbar colonic nerve released substance P-like material from isolated inferior mesenteric ganglia as determined by radioimmunoassay of samples of superfusate. Exogenous administration of neurotensin caused a significant increase in the amount of substance P-like material released during nerve stimulation. 7. Transient depolarizing responses evoked by neurotensin were markedly attenuated when ganglion cells were postsynaptically desensitized to exogenously administered substance P. 8. Taken together, these findings suggest that transient depolarizations mediated by an indirect action of neurotensin and facilitation of electrically evoked non-cholinergic slow EPSPs by neurotensin involved presynaptic release of substance P from collateral nerve terminals of primary afferent nerve fibres in the inferior mesenteric ganglion. 9. It was suggested that under normal in vivo conditions, neurotensin or a C-terminal-related peptide contained in central preganglionic nerve endings might function as an excitatory neuromodulator to enhance the release of substance P from primary afferent nerve terminals thereby facilitating non-cholinergic peripheral afferent synaptic input to prevertebral ganglion cells.

Action Potentials↗
PubMed1995

Electrophysiological properties of P2X-purinoceptors in rat superior cervical, nodose and guinea-pig coeliac neurones.

1. Whole-cell recordings were made from guinea-pig coeliac, rat nodose and rat superior cervical (SCG) neurones in culture, and currents in response to fast-flow (concentration clamp) application of ATP and other ATP analogues were measured. 2. At a holding potential of -70 mV, ATP evoked inward currents in all neurons. ATP-induced currents reversed at approximately 0 mV and showed strong inward rectification. Halving the external sodium concentration shifted the reversal potential by -15 to -17 mV, while increasing external potassium from 2 to 20 mM produced a 6-10 mV shift in reversal potential. Latency to onset of ATP current was < 1 ms; rise time was concentration dependent with maximum time to peak of 5-20 ms in nodose and coeliac neurones but 80 ms in superior cervical neurones. 3. Threshold concentrations of ATP were 0.1 microM for nodose and coeliac neurones but 10 microM for superior cervical neurones; EC50 values were approximately 3 microM for both nodose and coeliac neurones and 43 microM for superior cervical ganglia. Hill slopes for ATP concentration-response curves were not significantly different from unity in nodose and coeliac neurones whereas the Hill slope in superior cervical neurones was two. 4. 2-MethylthioATP (2-MeSATP) acted as a full agonist in all three neuronal preparations; EC50 values were 0.4, 2.8 and 46 microM for nodose, coeliac and superior cervical neurones, respectively. alpha,beta-Methylene ATP (alpha,beta-MeATP) was a full agonist in nodose and coeliac neurones with EC50 values of 9 and 13 microM, respectively. 5. In superior cervical neurones alpha,beta-MeATP had little or no agonist action but produced a concentration-dependent attenuation of the ATP current. Thus, alpha, beta-MeATP appears to behave as a partial agonist at P2X-purinoceptors in superior cervical neurones. 6. The non-selective purinoceptor antagonists suramin (1-100 microM) and pyridoxal-5'-phosphate (30 microM), as well as the putative P2Y-selective antagonist, Cibacron Blue (30 microM), inhibited all agonist-evoked responses to a similar degree in all three neuronal populations. 7. This study demonstrates that an agonist potency profile of 2-MeSATP > or = ATP > or = alpha,beta-MeATP is characteristic of ligand-gated P2X-purinoceptors in isolated peripheral neurones. We also suggest that the P2X-receptor in superior cervical neurones may represent a distinct subtype of P2X-purinoceptor from that present in nodose and coeliac neurones.

Adenosine Triphosphate↗
PubMed1999

Effect of caffeine on neonatal splanchnic blood flow.

Doppler ultrasound was used to study the effect of the first intravenous dose of caffeine on splanchnic haemodynamics in preterm neonates. Peak systolic velocity in the superior measenteric artery and coeliac axis was significantly reduced for 6 hours after caffeine infusion. The effect of this reduction in blood flow to the neonatal gut is not known.

Blood Flow Velocity↗
PubMed1975

Effect of extragastric and truncal vagotomy on pancreatic secretion in the dog.

In four dogs with chronic pancreatic and gastric fistulas, dose-response studies of pancreatic bicarbonate and protein secretion were done with intravenous infusions of secretin, octapeptide of cholecystokinin (OP-CCK), and 2-deoxyglucose (2-DG). The pancreatic response to a meal and to duodenal perfusion of graded concentrations of HCl, sodium oleate, and tryptophan were also studied. These observations were repeated after division of both the hepatic and celiac vagal branches to produce extragastric vagotomy, and subsequently after transthoracic truncal vagotomy. The responses to secretin, OP-CCK, and to duodenal perfusion of HCl were either unaltered or only slightly decreased by either extragastric or truncal vagotomy. Basal pancreatic secretion and the responses to duodenal perfusion of oleate and tryptophan were markedly depressed by extragastric vagotomy. These findings indicate that tonic vagal activity contributes to basal pancreatic secretion but has little effect on the response of the pancreas to secretin or CCK or on the release of secretin from the intestine. The decreased pancreatic response to intestinally perfused oleate and tryptophan seen after extragastric vagotomy could be caused either by interruption of reflex paths between gut and pancreas or by interference with CCK release. Extragastric vagotomy reduced pancreatic responses to a meal and to 2-DG and subsequent truncal vagotomy caused still further reduction, possibly, at least in part, by depressing release of antral gastrin.

Animals↗
PubMed1991

Gene expression of tyrosine hydroxylase and neuropeptide Y in prevertebral ganglia of renal hypertensive rats.

The gene expression of tyrosine hydroxylase (TH) and neuropeptide Y (NPY) was studied in prevertebral ganglia and adrenal glands of adult male rats during the development of renal hypertension (removal of 1 kidney/constriction of other kidney). Only tissues from rats with arterial pressures significantly elevated by day 3 were compared with those from controls. At 4 or 5 days after renal surgery, superior cervical ganglia, celiac-mesenteric plexus, adrenal glands, and stellate ganglia were surgically removed from nonfixed rats for Northern blot analysis or from perfusion-fixed rats for in situ hybridization. In all tissues, levels of TH mRNA were decreased in hypertensive rats; cells with decreased levels were scattered throughout each tissue. In contrast, levels of NPY mRNA were unchanged in hypertensive rats compared with controls. Changes in TH mRNA levels suggest that the developing phase of renal hypertension is associated with a decrease in sympathetic outflow to the periphery. In contrast, the failure of NPY mRNA levels to change suggests a different regulatory mechanism for NPY expression or a different role for NPY in sympathetic neurotransmission.

Adrenal Glands↗
PubMed1995

Suppression of meal size by intestinal nutrients is eliminated by celiac vagal deafferentation.

The arrival of nutrients in the gastrointestinal tract suppresses intake. To specify the neural pathways and receptor locations of this feedback, we examined the effects of intraduodenal infusions of 10 nutrients plus saline on short-term food intake of rats with selective deafferentations of vagal celiac branches. Three response profiles were observed: 1) isotonic saline, 5.6% glycerol, and 3% fructose did not inhibit intake of controls or selectively deafferented animals; 2) 3% glucose, 3% maltose, 3% L-phenylalanine, 12% Isocal, and 1.4% oleic acid suppressed intake of controls, but this inhibition was eliminated by vagal celiac deafferentation; and 3) 3% casein hydrolysate and 24% Isocal suppressed intake of controls and rats with selective vagotomies, although the latter exhibited significantly less suppression. In addition, elimination of celiac afferents chronically reduced meal size (i.e., first 30-min intake) without reducing daily food intake or body weight. Furthermore, D-phenylalanine infusions produced a delayed suppression of food intake in controls (possibly from intraluminal irritation); however, this reduction was eliminated with celiac deafferentation. Overall, this experiment indicates that vagal celiac afferents are critical for preabsorptive detection of some energy-yielding molecules or properties of nutrient solutions (as well as, perhaps, intraluminal inflammation), but not others, which are still detected, although only partially.

Afferent Pathways↗
PubMed2000

Responses of celiac and cervical vagal afferents to infusions of lipids in the jejunum or ileum of the rat.

Multiunit celiac and single-unit cervical recordings of vagal afferents were performed before and during infusions of fatty acids, triglycerides, or saline into either the ileum or jejunum of the rat. In multiunit recordings, lipids increased activity of vagal afferents to a greater extent than saline. The greatest increases in vagal afferent activity resulted from infusions of linoleic acid, conjugated linoleic acid, or oleic acid. The triglycerides, corn oil or Intralipid, were less effective than the fatty acids in affecting vagal afferent activity. Ileal pretreatment with the hydrophobic surfactant Pluronic L-81 significantly attenuated the response of celiac vagal afferents to ileal infusion of linoleic acid. Single-unit recordings of cervical vagal afferents supported the multiunit data in showing lipid-induced increased vagal afferent activity in approximately 50% of ileal units sampled and 100% of a limited number of jejunal units sampled. These data demonstrate that free fatty acids can activate ileal and jejunal vagal afferents in the rat, and this effect can be attenuated by pretreatment with a chylomicron inhibitor. These data are consistent with the view that lipid-induced activation of vagal afferents could be a potential substrate for the inhibitory effects of intestinal lipids on gastrointestinal function, food intake, and body weight gain.

Animals↗
PubMed1993

Potassium currents and their modulation by muscarine and substance P in neuronal cultures from adult guinea pig celiac ganglia.

1. Intracellular microelectrode and whole-cell patch-clamp recordings were obtained from adult guinea pig celiac ganglion neurons grown in tissue culture for 7-14 days. Over 90% of neurons showed phasic-type action-potential discharge with the use of either type of recording electrode; they stained immunohistochemically for catecholamines, tyrosine hydroxylase, and neuropeptide Y. Input resistance (140 M omega) and action-potential amplitude (103 mV) were significantly greater with whole-cell than with microelectrode recordings, but other passive electrical properties were similar. 2. Five potassium currents were characterized: an apamin-sensitive after hyperpolarizing current (IAHP), an apamin and tetraethylammonium-insensitive slow IAHP, an M-like current, a transient outward IA current, and a delayed rectifier IK current. A hyperpolarization-activated cationic Ih current was also present. The first three currents were not observed with whole-cell recordings. 3. Cadmium (200 microM), cobalt (1 mM), lanthanum (30 microM), or a low calcium/high magnesium solution blocked both IAHPS and the M-like current; barium (1 mM) also blocked these currents. 4. Kinetics of the M-like current were best described by a double exponential fit to deactivating tail currents with time constants of 50 and 390 ms at -50 mV. The apamin-sensitive and slow IAHP decayed exponentially with time constants of 145 ms and 3.5 s, respectively. There was no correlation between occurrence of M-like current (95% of neurons) and slow IAHP (40% of neurons), nor any correlation between magnitude of M-like current and IAHP in those cells exhibiting both currents. 5. Muscarine and substance P (SP) caused depolarizations or inward currents (under voltage clamp) at the resting potential (-55 mV) associated with a decreased membrane conductance. The slow IAHP and the M-like current, but not the apamin-sensitive IAHP nor the IA, were blocked by muscarine and SP (IC50 3 microM and 100 nM, respectively). Muscarine and SP also decreased a "leak" potassium current. 6. We conclude that celiac neurons express two calcium-dependent IAHP currents and a calcium-dependent M-current; these are seen by fine-tipped intracellular microelectrodes but not by whole-cell patch electrodes. These currents are not required for spike frequency accommodation. Muscarine and SP reduce these currents, as well as voltage-independent leakage potassium current.

Animals↗
PubMed2000

Benign pancreatic duct strictures: medical and endoscopic therapy.

Pancreatic duct strictures usually reflect underlying pancreatic disease and are likely caused by one or more of the following: acute or chronic pancreatitis, benign or malignant pancreatic neoplasm, pseudocyst and trauma. The characteristics of pancreatic strictures are identified, and medical and endoscopic therapy options are reviewed.

Analgesics↗
PubMed2000

Modulation of early immune responses and suppression of Trypanosoma brucei brucei infections by surgical denervation of the spleen.

OBJECTIVE: To examine critical interactions between the nervous system and the immune system during experimental African trypanosomiasis. METHODS AND RESULTS: Inoculation of Trypanosoma brucei brucei resulted in early interferon (IFN)-gamma production, elevated corticosterone and prostaglandin E(2) (PGE(2)) levels and increased splenocyte proliferation, as measured by enzyme-linked immunospot assay, radioimmunoassay and thymidine incorporation assay, respectively. Splenic denervation suppressed IFN-gamma, corticosterone and PGE(2) production, enhanced splenocyte proliferation, and significantly reduced parasitemia and prolonged rat survival. CONCLUSIONS: Our data show substantial effects of the nervous system on early immune responses that may influence the outcome of this disease. These effects were not dependent on cytokine inhibitory mediators such as prostaglandins or stress hormones. More investigations are required to understand the evident neural control over the immune system during infectious challenges, which may assist in novel therapeutic approaches.

Animals↗