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PubMed1993

The central vagal efferent supply to the esophagus and lower esophageal sphincter of the cat.

BACKGROUND: Little is known of the central efferent neurons innervating the smooth muscle esophagus. The aim of this study was to define the location of the efferent neural pathways of the brain stem swallowing mechanism in the cat, particularly those supplying the esophageal body smooth muscle. METHODS: Fluorescent, retrogradely transported tracers were injected into the cervical striated muscle and thoracic smooth muscle segments of the esophagus and also the lower esophageal sphincter. RESULTS: Striated muscle efferents were found in the rostral nucleus ambiguus, but approximately 8% were located in the dorsal motor vagal nucleus. Smooth muscle efferents were present in the dorsal motor vagal nucleus in two groups, one rostral and one caudal to the obex. An additional group was found in nucleus retroambiguus. Approximately 8% of the total smooth muscle efferents were present in rostral nucleus ambiguus and were lateral to the striated muscle efferents. The lower esophageal sphincter efferents had a similar distribution to the smooth muscle efferents, but the rostral concentration of cells in the dorsal motor vagal nucleus was shifted caudally. CONCLUSIONS: Esophageal body smooth muscle motoneurons are arranged with a similar distribution to those innervating the lower esophageal sphincter but with some topographic variation.

Afferent Pathways↗

PubMed1993

Mechanism of motilin-induced contractions in isolated perfused canine stomach.

BACKGROUND: Motilin is known to induce gastric phase III contractions via neural pathways in vivo, but the local mechanism of action is not clearly determined. METHODS: An isolated perfused canine stomach was used to demonstrate the mechanism of motilin. Synthetic canine motilin at doses of 0.1, 0.3, 1.0, and 3.0 micrograms/h was infused intra-arterially, and effects of several receptor antagonists on motilin-induced contractions were examined. RESULTS: The immunoreactive motilin concentration of venous effluent showed that motilin at doses of 0.1 and 0.3 microgram/h was within the physiological range. Each dose of motilin induced phasic contractions in the isolated stomach, and a dose-related increase in frequency was observed, but not their mean amplitude. Atropine, hexamethonium, ICS205-930, BRL43694, phentolamine, yohimbine, and propranolol significantly inhibited motilin-induced contractions. Naloxone, methysergide, and timolol did not affect the response of motilin. Prazosin significantly increased the mean amplitude of motilin-induced contractions. CONCLUSIONS: Physiological dose of motilin can initiate phasic contractions in the stomach independently of the presence of the extrinsic nerves. The results suggest that cholinergic pathway, 5-hydroxytryptamine (HT)3 receptors, and alpha receptors are involved in the motilin-induced contractions.

Animals↗

PubMed1995

Intragastric capsaicin stimulates colonic motility via a neural reflex in conscious dogs.

BACKGROUND & AIMS: Capsaicin is known to contract smooth muscles and to have an excitatory action on thin, primary afferent neurons. The aim of this study was to test the hypothesis that intragastric capsaicin may have an excitatory effect on colonic motility. METHODS: Mongrel dogs equipped with five strain-gauge force transducers on the colon (C1-C5) were used. In 5 dogs, the effect of intragastric capsaicin (0.05, 0.1, 0.3, and 0.5 mg/kg) on colonic motility in the presence or absence of the cholinergic blockers atropine and hexamethonium was studied. In 4 dogs, the effect of capsaicin (0.5 mg/kg) administration into a vagally innervated or denervated gastric pouch on colonic motility was investigated. RESULTS: Motility at C2-C3, C1-C3, and C1-C5 was significantly increased by 0.1, 0.3, and 0.5 mg/kg of capsaicin, respectively. The excitatory effect of capsaicin on colonic motility was inhibited by atropine and hexamethonium. Colonic motility at C1-C4 was significantly increased by capsaicin administration into a vagally innervated pouch but was not affected by capsaicin administration into a vagally denervated pouch. CONCLUSIONS: These results indicate that intragastric capsaicin predominantly stimulates motility in the proximal half of the colon through neural pathways, probably through a vagovagal reflex, but sympathetic involvement cannot be excluded.

Animals↗

PubMed1987

The response of nucleus preopticus neurosecretory cells to ovarian pressure in the teleost, Clarias batrachus (Linn.).

The changes undergone by the neurosecretory cells of the nucleus preopticus (NPO) were investigated histologically and immunocytochemically following pressure stimulation of the ovaries in the teleost, Clarias batrachus. Application of intraovarian pressure of 10 mm Hg revealed marked hypertrophy of the cells, while pressures of 20 and 30 mm Hg resulted in hypertrophy and exhaustion of the cells. No changes were observed when the treatment was preceded by transection of the spinal cord. The results suggest the existence of a pressure-excitable neural pathway from the ovary capable of eliciting profound cytological changes in the NPO.

Animals↗

PubMed1989

Luminal adrenergic agents modulate intestinal transport.

Intestinal transport is controlled by luminal solutes, neural pathways, and paracrine or humoral agents. The current study investigated the effect of luminally administered adrenergic agents on the intestinal transport of water and electrolytes. Dogs with 25-cm jejunal Thiry-Vella loops were studied. The loops were luminally perfused with an isotonic solution containing [14C]PEG, and the fluxes of H2O, Na+, and Cl- were calculated. Each experiment consisted of three 1-hr periods: basal, luminal agent infusion, and recovery. Luminal adrenergic agents did not alter heart rate. Norepinephrine (alpha 1 greater than alpha 2 and beta adrenergic agonist) and phenylephrine (alpha 1 adrenergic agonist) caused significant absorption of water and sodium. Clonidine (alpha 2 adrenergic agonist) and isoproterenol (beta adrenergic agonist) caused significant secretion of water, sodium, and chloride. Luminally administered adrenergic agents can influence small intestinal water and electrolyte transport. Alpha 1 agonists have a proabsorptive effect, while alpha 2 and beta agonists have a secretory effect. Luminally administered proabsorptive adrenergic agents may prove useful in pathologic secretory states such as diabetic diarrhea, small bowel transplantation, or diarrhea-associated endocrinopathies.

Animals↗

PubMed1992

Extrinsic neural contribution to ileal peptide YY (PYY) release.

Peptide YY (PYY) release into the ileal lumen is stimulated by cholecystokinin (CCK) and glucose ingestion. Previous data have implicated vagal activity in the mediation of PYY release into both the systemic circulation and the ileal lumen. The present study was designed to evaluate extrinsic neural involvement in CCK and glucose-stimulated circulating and ileal intraluminal PYY release. Distal ileal Thiry-Vella loops (TVL) of 25 cm were created in seven mongrel dogs. On separate days fasted dogs were given continuous infusions of CCK at 500 ng/kg/hr during the first hour of the study or an oral glucose (1.5 g/kg) tolerance test (OGTT) was performed. Peripheral blood samples and ileal effusates were collected before tests and following either CCK or glucose stimulation for 120 min at 20-min intervals. Ileal PYY recoveries were measured by the instillation and collection of 20 cc of normal saline from the TVL for each 20-min period. The dogs were again tested after surgical denervation of the TVL. OGTT resulted in a significant rise of PYY recovery from the TVL (P less than 0.05), while not affecting circulating PYY. Intravenous CCK resulted in significant increases in both plasma and ileal PYY concentrations (P less than 0.05). Denervation of the TVL decreased PYY recovery from the TVL after both CCK and OGTT, whereas this procedure did not affect circulating PYY levels or basal luminal levels. These data demonstrate the inhibition of CCK- and glucose-stimulated ileal PYY recovery from denervated ileal loops. The extrinsic neural pathways are involved in the mediation of glucose- and CCK-stimulated mechanisms for ileal PYY release.

Animals↗

PubMed1980

Detection of uremic neuropathy by reflex response latency.

Dialysis time necessary for treatment of terminal renal failure is very different in different patients. Adequacy of therapy cannot be controlled by laboratory measures but only clinical means. Uremic peripheral neuropathy is regarded as the most reliable indicator of insufficient dialysis treatment. Serial measurements of peripheral nerve function therefore make individual adjustment of dialysis schedule possible. In some cases motor nerve conduction velocity is not sensitive enough for this purpose, as conduction velocity in afferent nerve fibers is disturbed at an earlier stage of uremic intoxication. Measurement of sensory nerve conduction velocity is time consuming and afferent fibers can also be examined in proprioceptive reflexes. Ths suitability of H-reflex response latency (RRL) for detection of slight uremic neuropathy was analysed. The wide range of RRL in healthy subjects can be explained by the different length of neural pathway in different subjects. A strong correlation between RRL and body height was found in healthy subjects. Relating RRL to the body height gives a highly sensitive measure of peripheral nerve function. Asymptomatic uremic neuropathy was detected very much earlier by RRL than by motor nerve conduction velocity. The method proved to be well suited for routine monitoring of uremic neuropathy in patients on dialysis.

H-Reflex↗

PubMed1983

The pupillary effects of opioids.

Morphine's miotic action on the pupil is an easily recognizable and quantifiable effect in man. The neural pathways responsible for regulating pupil size are reasonably well defined. Yet, the mechanisms behind this and related effects of opioids on the eye in humans and laboratory animals have just begun to be explored. In this review, we have attempted to organize the available information on pupillary actions of opioids, emphasizing the dynamic nature of the responses, their species specificity, possible mechanisms of action, and the recently discovered development of tolerance to these actions. Our current knowledge regarding differences among the opioids, the effects of endogenous opioid peptides and the role of the various opiate receptor subtypes in pupillary effects is also summarized.

Animals↗

PubMed1984

Tripelennamine: enhancement of brain-stimulation reward.

Thresholds for reinforcing electrical stimulation to the medial forebrain bundle were determined in rats by means of a rate-free psychophysical method. The acute administration of tripelennamine lowered the threshold for rewarding brain stimulation in a dose-dependent manner. These results suggest that the abuse liability of tripelennamine may be related to its ability to sensitize the central neural pathway that mediates reward.

Animals↗

PubMed1985

Central nervous system action of bombesin to inhibit gastric acid secretion.

Bombesin or gastrin releasing peptide injected into the lateral, third, or fourth ventricle, or into the cisterna magna, inhibited gastric acid secretion induced by a wide variety of gastric acid stimulants in several animal models. Studies of bombesin microinfusion into specific hypothalamic nuclei of intact rats, or injection into the cisterna magna of midbrain transected rats, indicated that the peptide can trigger inhibition of gastric acid secretion from both forebrain and hindbrain structures. The neural pathways mediating bombesin action required the integrity of the cervical spinal cord; the vagus did not play an important role. Spantide, a substance P and bombesin receptor antagonist, was not useful in studying the physiological role of bombesin. This was due both to its inability to reverse the central action of bombesin on gastric secretion, and to its in vivo toxicity.

Animals↗

PubMed1986

Sex dependent behavioral response to frontal cortical suction lesions in the rat.

Previous reports indicate that male rats given right (but not left) frontal cortical suction lesions develop hyperactivity accompanied by cortical norepinephrine depletions. In this study, female rats given such lesions to either hemisphere developed bilateral cortical norepinephrine depletions but no hyperactivity. Right lesion male rats developed both catecholamine depletions and hyperactivity. Thus, the lateralized hyperactivity response to these cortical lesions is sex-dependent and may involve sex differences in subcortical neural pathways.

Animals↗

PubMed1987

Electrical stimulation of the hypothalamic nucleus paraventricularis mimics the effects of light on pineal melatonin synthesis.

In an attempt to clarify further the role of the hypothalamic paraventricular nuclei (PVN) in the control of pineal function, the effects of 2 min electrical stimulation of these nuclei were investigated in acutely blinded, adult, male Sprague-Dawley rats. Pineal serotonin-N-acetyltransferase (NAT) activity, melatonin content and catecholamine levels were measured by means of radio-enzymatic, radioimmunoassay and high-performance liquid-chromatography methods, respectively. All three pineal parameters underwent significant declines following brief PVN stimulation during the night time. These observations lend credence to the view that the neural pathways transmitting light information to the sympathetic innervation controlling pineal melatonin synthesis.

Animals↗

PubMed1988

Effect of galanin on gastrin and somatostatin release from the rat stomach.

Galanin has been shown to be present in the gastrointestinal tract, pancreas and CNS. In the rat stomach, immunohistochemical studies have revealed the presence of galanin in the intrinsic nervous system suggesting a function as putative neurotransmitter or neuromodulator which could affect neighbouring exo- or endocrine cells. Therefore this study was performed to determine the effect of galanin on the secretion of gastrin and somatostatin-like immunoreactivity (SLI) from the isolated perfused rat stomach. The stomach was perfused via the celiac artery and the venous effluent was collected from the portal vein. The luminal content was kept at pH 2 or 7 Galanin at a concentration of 10(-10), 10(-9) and 10(-8) M inhibited basal gastrin release by 60-70% (60-100 pg/min; p less than 0.05) at luminal pH 7. At luminal pH 2 higher concentrations of galanin (10(-9) and 10(-8) M) decreased basal gastrin secretion by 60-70% (60-100 pg/min; p less than 0.05). This inhibitory effect was also present during infusion of neuromedin-C, a mammalian bombesin-like peptide that stimulates gastrin release. SLI secretion remained unchanged during galanin administration. The inhibitory action of galanin on gastrin secretion was also present during the infusion of tetrodotoxin suggesting that this effect is not mediated via neural pathways. The present data demonstrate that galanin is an inhibitor of basal and stimulated gastrin secretion and has to be considered as an inhibitory neurotransmitter which could participate in the regulation of gastric G-cell function.

Animals↗

PubMed1988

Corticotropin-releasing factor: central nervous system effects on baroreflex control of heart rate.

The effects of intracerebroventricular injections of corticotropin-releasing factor on baroreflex control of heart rate were examined in conscious, unrestrained rats. Baroreflex control of heart rate was tested by generating stimulus-response curves relating arterial pressure to pulse interval over a wide range of arterial pressures. Administration of corticotropin-releasing factor produced dose-related alterations of pressure-dependent curve parameters, e.g., range, gain and pressure at midrange. These results suggest that corticotropin-releasing factor alters transmission in neural pathways that process baroreceptor information.

Animals↗

PubMed1996

Effect of motilin, somatostatin and bombesin on gastroduodenal myoelectric activity in sheep.

The effects of motilin, erythromycin, somatostatin and bombesin on antroduodenal myoelectric activity were investigated in conscious sheep. Myoelectric recordings were obtained from electrodes chronically implanted on the antrum and duodenal bulb. Peptides or erythromycin were infused intravenously (i.v.) during 5 min. Antagonists were injected i.v. as a bolus. Neither motilin (2.5-80 ng/kg/min) nor erythromycin (2-16 micrograms/kg/min) modified the antroduodenal myoelectric activity, although a single bolus of these compounds (250 ng/kg and 50 micrograms/kg respectively) increased the antral activity. Somatostatin at 5 ng/kg/min induced a decrease in the myoelectric activity of antrum and duodenum. However, doses of 10 to 40 ng/kg/min evoked a duodenal phase III-like activity with a subsequent quiescence period and a concomitant inhibition of the antral activity. These effects were reproduced by bombesin (2.5 to 40 ng/kg/min). Furthermore, an initial increase in the myoelectric activity and in the frequency of slow waves were recorded in the antrum when the highest doses were used. On the other hand, atropine (0.2 mg/kg) or hexamethonium (2 mg/kg) caused a long-lasting inhibition of antroduodenal myoelectric activity. These cholinergic antagonists abolished the effects induced by somatostatin (20 ng/kg/min) but not those evoked by bombesin but not motilin are putative modulators of the migrating myoelectric complex (MMC) in sheep. Moreover, a cholinergic neural pathway is involved in the somatostatin but not in the bombesin-induced effects.

Animals↗

PubMed1992

Influence of dietary composition on energy expenditure during recovery of body weight in the rat: implications for catch-up growth and obesity relapse.

The influence of dietary composition on whole-body energetics was examined during the first 2 weeks of isocaloric refeeding after low food intake in a rat model. The high energetic efficiency and energy partitioning toward fat accretion characteristic of this refeeding period were unaltered by (1) dietary fat levels varying between 6% and 30% of energy intake; (2) protein levels between 15% and 40%; (3) carbohydrate types (glucose v fructose v sucrose v starch v unrefined carbohydrate); and (4) diets containing 30% fat but differing in fatty acid composition (long-chain triglycerides [LCT] v medium-chain triglycerides [MCT] v oleic v linoleic v alpha-linolenic metabolites eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA] omega-3 fatty acids). Changes were only observed for extreme diets, ie, those deficient in protein or very high in fat. Low-protein diet was the only condition in which the high metabolic efficiency characteristic of the refeeding period was partially suppressed, and this occurred despite a lack of concomitant reduction in body fat deposition. On the contrary, with high-fat diets (> 30% of dietary energy consumption) the elevated efficiency was further increased, an effect that was only partially accounted for by the lower energy cost of body fat gain from high-fat diets. These studies indicate that during body weight recovery, the mechanisms underlying the adaptive increase in metabolic efficiency favoring the replenishment of body fat stores override any effect of food type on thermogenesis, and suggest some convergence in the controlling neural pathway. The implications of these findings vis-a-vis nutritional rehabilitation (catch-up growth) and obesity relapse are discussed.

Animals↗

PubMed1995

The nature and consequences of childbirth pain.

For most women, childbirth is associated with very severe pain often exceeding all expectations. Some childbirth education groups and popular texts on the subject, however, seem disposed to encourage unrealistic expectations: claiming that labour is other than painful and that pharmacological analgesia is both unnecessary and harmful. All too often, those who promote such views witness women in labour only occasionally and are rarely responsible for patient care. Pain associated with uterine contractions should be distinguished from that associated with delivery: for there are important differences in the clinical characteristics, neural pathways and physiological responses. In the first stage of labour pain is largely visceral in origin, whereas during the transitional and second stages somatic pain becomes more pronounced. As described in this review, it is now well established that uterine contraction pain evokes a generalised neuroendocrinal stress response producing widespread physiological effects during the first stage of labour. They include increased oxygen consumption, hyperventilation and respiratory alkalosis; increased cardiac output, systemic peripheral resistance and blood pressure; delayed gastric emptying; impaired uterine contractility and diminished uterine perfusion; and metabolic acidaemia. While other factors (such as anxiety, starvation and physical exertion) are also partly responsible for inducing some of these effects, pain appears to be the most potent source because they are all obtunded by effective epidural analgesia.

Blood Pressure↗

PubMed1994

Inhibition by morphine of the cardiovascular and behavioral responses evoked by centrally administered substance P in conscious rats.

The effect of endogenous opioid receptor stimulation on the central cardiovascular and behavioral actions of substance P (SP) was examined in conscious rats. SP (55 pmol) injected intracerebroventricularly (i.c.v.) elicited increases in mean arterial pressure, heart rate, and stereotyped behavioral activation such as exploring and grooming, which were considered to be parts of the cardiovascular defense reaction. Intravenous (i.v.) pretreatment with morphine (2.5 and 5.0 mg/kg) attenuated the cardiovascular and behavioral responses produced by SP i.c.v. dose-dependently. The i.v. pretreatment with naloxone (10 mg/kg) had no effect on the central SP-induced response. Pressor responses elicited by i.c.v. injection of corticotropin-releasing factor or angiotensin II were also attenuated by pretreatment with i.v. morphine (5.0 mg/kg). Our results showed that endogenous opioid receptor stimulation antagonizes the central cardiovascular and behavioral actions of SP. Morphine may not influence the primary site of action of SP but does influence the central neural pathway which conveys the SP-induced sympathetic activation signal.

Analysis of Variance↗