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PubMed1982

Morphine-like effects of clonidine on the EEG, slow wave sleep and behavior in the dog.

EEG, behavioral and autonomic effects of morphine and clonidine were compared in the unrestrained beagle dog placed in a dimly-lit, sound-attenuated chamber equipped with video monitors. Intravenous (i.v.) morphine (0.5, 1 and 2 mg/kg) and clonidine (11, 33 and 100 microgram/kg) caused parallel dose-related increases in NREM sleep with clonidine being 43 times more potent than morphine. Other similar effects were: an initial transient EEG-behavioral dissociation; increases in spectral power (8-16 Hz); decreases in temperature and heart and respiratory rates; emesis, miosis and salivation. Intraventricular (i.v.t.) morphine (33, 100 and 300 microgram) and clonidine (10 and 30 microgram) caused qualitatively similar EEG, sleep and behavioral effects. Naloxone (30 microgram/kg i.v.) prevented EEG synchrony and behavioral effects of i.v. morphine (1 mg/kg) but not those of i.v. clonidine (100 microgram/kg). Yohimbine pretreatment (0.1 mg/kg i.v.) was more effective in antagonizing clonidine than morphine. These results suggest that morphine and clonidine induce similar EEG, behavioral and autonomic effects through actions upon different receptors on the same or parallel neural pathways. The results further emphasize the importance of an alpha 2-adrenergic-opioid interaction to regulate sleep in the dog.

Animals↗
PubMed1988

Morphine antagonizes TRH-induced intestinal transit and hyperserotonemia in rabbits.

Thyrotropin releasing hormone (TRH), administered intracerebroventricularly (i.c.v.) in microgram quantities to anesthetized rabbits, produces marked stimulation of colonic motility, transit, and fluid accumulation, and is accompanied by a portal hyperserotonemia. In this study we found that pretreatment of rabbits with morphine (10 mg/kg i.v.) completely blocked the TRH-induced colonic transit and increase in luminal fluid, as well as the hyperserotonemia. A small dose of morphine (200 micrograms) given i.c.v., but not i.v., also inhibited the intestinal transit and portal hyperserotonemia. These results suggest that morphine inhibits TRH-induced intestinal transit and fluid accumulation, at least in part, by inhibition of a neural pathway mediating intestinal serotonin release.

Animals↗
PubMed1989

Contractions of the guinea-pig ileum evoked by stimulation of the submucous plexus.

Neural pathways from the submucous plexus to the longitudinal muscle of an adjacent segment of isolated guinea-pig ileum were studied. It was found that electrical field stimulation of a strip of submucosa-submucous plexus produced frequency-dependent longitudinal contractions of an intact segment of intestine lying oral to the point of stimulation. The responses were reduced to less than 10% of control by tetrodotoxin, atropine, morphine and chymotrypsin and by desensitization to substance P (SP). The responses were only inhibited by one-third by hexamethonium and were not affected by desensitization to 5-hydroxytryptamine. The effect of desensitization to SP was reversible, but the effect of chymotrypsin was irreversible. SP-induced desensitization and chymotrypsin did not inhibit the twitch response produced by field stimulation of the whole ileal segment. The same results were observed with preparations made from ileal segments that had been extrinsically denervated. The results suggest that intrinsic neurons with processes in the submucous plexus can excite cholinergic and SP-containing neurons in the myenteric plexus, thereby causing the longitudinal muscle to contract.

Animals↗
PubMed1989

Median raphe, but not dorsal raphe, application of the 5-HT1A agonist 8-OH-DPAT stimulates rat motor activity.

Local application of the selective 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) in the median raphe of rats caused locomotor stimulation. In contrast, dorsal raphe application of the compound induced flat body posture, which was discontinuous and not dose-dependent, and therefore distinct from that characteristic for postsynaptic 5-HT receptor-mediated behaviour. Injection of 8-OH-DPAT into the dorsal raphe or median raphe caused neither forepaw treading nor head-weaving; stiff tail and sniffing occurred inconsistently. By activating somatodendritic 5-HT1A autoreceptors in the median raphe, 8-OH-DPAT may disinhibit locomotor-enforcing neural pathways that receive 5-HT afferents from this nucleus. The data suggest that median raphe and dorsal raphe 5-HT neurons have different roles in motor control.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

Mesolimbic sites mediate the discriminative stimulus effects of morphine.

The neuroanatomical basis of opiate addiction has been studied using a variety of behavioural techniques. Mesolimbic structures such as the ventral tegmental area and nucleus accumbens appear to be critical in mediating the expression of rewarding effects of opiates. However, the role of these brain structures in mediating the discriminative stimulus effects have not been fully examined. The aim of the present study was to investigate the role of the ventral tegmental area and the nucleus accumbens in a two-lever operant drug discrimination paradigm. Male Wistar rats were trained to discriminate morphine (3.0 mg/kg s.c.) from saline with a fixed ratio schedule of food reinforcement (FR10). Once rats had acquired the discrimination, a randomised sequence of morphine microinjections (1-10 micrograms) were evaluated. Subsequently, tests with morphine (1.0-10.0 mg/kg s.c.) administered systemically were performed to confirm the integrity of the discrimination. Small doses of morphine (1-3 micrograms) administered into the ventral tegmental area proved sufficient to produce generalisation to the systemic cue, whereas similar injections into the nucleus accumbens produced only partial generalisation. Furthermore, these intra-nucleus accumbens injections (3-10 micrograms) produced significant increases in the latency to complete the first ratio. Similar doses of morphine administered into the striatum failed to show generalisation. These results demonstrate that activation of opioid receptors located within mesolimbic structures mediate, in part, the discriminative stimulus effects of morphine. Furthermore, the finding that the discriminative stimulus effects and rewarding effects share common neural pathways suggest a possible linkage between the two stimulus properties.

Animals↗
PubMed1995

Mechanisms involved in the relaxant response of bradykinin in epithelium intact strips of the guinea-pig trachea.

Kinins caused graded relaxations in guinea-pig trachea with epithelium under spontaneous or carbachol-induced tone. The order of potency was: [Tyr8]bradykinin > lysyl-bradykinin > bradykinin > methionyl-lysyl- bradykinin. The bradykinin B1 receptor agonist des-Arg9-bradykinin (1 microM) was inactive. Relaxation in response to bradykinin (100 nM) was unaffected by tetrodotoxin (0.3 microM), nicardipine (1 microM), Ca(2+)-free solution without or plus ryanodine (10 microM), propranolol (1 microM), glibenclamide (1 microM), staurosporine (0.3 microM), nickel chloride (100 microM) or [D-p-Cl-Phe6,Leu17]VIP (a vasoactive intestinal peptide receptor antagonist, 0.03 microM), but was partially inhibited by apamin (0.3-1 microM). Both HOE 140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin) and NPC 17761 (D-Arg0[Hyp3,D-HypeE(trans-thiophenyl)7,Oic8]bra dykinin) (0.1-1000 nM) caused graded, reversible and selective inhibition of the bradykinin (100 nM) relaxation, with IC50 values of 1.4 and 19.1 nM, respectively. HOE 140 and NPC 17761 (0.1-10 nM) produced a graded shift to the right of the bradykinin concentration-response curves associated with a reduction of the maximum relaxation. The kinin B1 receptor antagonist, des-Arg9-[Leu8]bradykinin (1 microM), was inactive. Thus, bradykinin-induced relaxation in guinea-pig trachea results from activation of bradykinin B2 receptors and can be antagonized with high affinity in a selective and reversible manner, through noncompetitive mechanism, by both HOE 140 and NPC 17761. In addition, the bradykinin response does not involve neural pathways, extracellular Ca2+ influx or mobilization of intracellular Ca2+ stores sensitive to ryanodine, but is modulated by small conductance Ca(2+)-activated K+ channels.

Animals↗
PubMed1988

Expression of c-src and c-abl in embryonal carcinoma cells and adult mouse tissues.

We have studied the expression of c-src and c-abl proto-oncogenes in early mouse development using embryonal carcinoma (EC) cells as a model system, and compared this to the expression pattern in adult tissues. In all three EC lines tested (F9, PC13, and P19), c-src and c-abl mRNA can be detected. When F9 and PC13 are induced to differentiate they form endodermal cells characteristic of the early embryo, and we found no change in c-src or c-abl expression. In contrast, P19 cells showed increased levels of both mRNAs both mRNAs when induced to differentiate along the neural pathway by retinoic acid, whereas differentiation along the muscle pathway by dimethyl sulfoxide resulted in decreased levels of c-abl expression. These results are consistent with the idea that c-src and c-abl have important functions in the differentiation of the cell types of the later embryo, but not in those of the early embryo.

Animals↗
PubMed1983

Effects of phenytoin, carbamazepine, and clonazepam on cortex- and amygdala-evoked potentials.

Multiple doses of phenytoin, carbamazepine, and clonazepam were tested against single- and double-pulse evoked potentials. Evoked responses were triggered from either the amygdala or the cortex and were recorded in both monosynaptic sites and the mesencephalic reticular formation (MRF). In accordance with previous studies of spinal potentials, it was expected that all three drugs would display a depressant action. Contrary to expectation, only clonazepam had any significant effect, and this drug was effective only against potentials triggered in the amygdala and recorded in the MRF. These data appear inconsistent with the traditional belief that anticonvulsants block seizure spread by antagonizing transmission in neural pathways.

Amygdala↗
PubMed1984

Changes in thalamic nociception resulting from morphine- and meperidine-dependence in rats.

Rats were injected with progressively increasing doses of morphine or meperidine during a period of 3 to 40 days. From this colony of animals individual rats were used at 3- to 4-day intervals for electrophysiologic experiments to analyze the activity of nociceptive neurons in the somesthetic thalamus. After an i.p. injection of chloralose-urethane and the appropriate preparation for a stereotaxic microelectrode penetration of the thalamus, a nociceptive neuron was identified in the nucleus ventralis posterolateralis by its unique spacing of spike potentials emitted in response to pricking the foot with a pin. In addition to the short-latency response that formed a high activity peak on poststimulus time histograms, spikes following the stimulus up to 500 ms also formed activity peaks. Single-pulse stimulation of the sciatic nerve evoked the same response as pinpricks, but innocuous stimuli (pin shielded with a piece of cork) evoked a response without the late activity peaks. Only neurons that exhibited this differential response were regarded as nociceptive. Their response and spontaneous activity were accumulated separately on a digital computer. Following this, naloxone was infused i.v. and the computer accumulations were repeated. It was found that during naloxone-precipitated narcotic withdrawal, innocuous stimuli evoked responses indicative of pain; the nociceptive system was sensitized. Furthermore, a small dose or morphine or meperidine heightened the sensitization. This action of the narcotic agents was reversed by 5-hydroxytryptophan, which assisted the narcotics in suppressing pain in morphine- or meperidine-dependent rats but had no demonstrable effect in control animals. The spontaneous tonic activity of the nociceptive neurons of the somesthetic thalamus was high in rats exhibiting narcotic dependence. Naloxone decreased the count, but not to the value of the control animals. The sensitization of nociception can be explained by a decreased action of a neural pathway that descends from the periaqueductal gray matter via the nucleus raphe magnus to the spinal cord and there blocks the excitation of the spinothalamic tract cells by A-delta and C fibers. The mechanisms that increase the spontaneous activity of the thalamic nociceptive neurons remain unclear.

Animals↗
PubMed1987

Hypothalamic afferent connections mediating adrenocortical responses that follow hippocampal stimulation.

This study identified some neural pathways which mediate the adrenocortical responses that follow hippocampal stimulation. The increase in plasma corticosterone following dorsal hippocampus stimulation, in rats with electrodes chronically implanted under pentobarbital anesthesia, was blocked by dorsal fornix and lateral septal lesions and by small posterior hypothalamic deafferentation. Fimbria transection, lateral septal lesions, and posterior hypothalamic deafferentation, but not midbrain reticular formation lesions, also blocked the adrenocortical responses to ventral hippocampus stimulation. Our present and previous studies indicate that the dorsal and ventral hippocampal effects on the hypothalamus, which increase plasma corticosterone concentrations, are mediated by the dorsal fornix and fimbria, respectively, as well as by the lateral septum. A posterior hypothalamic input, which does not involve the medial forebrain bundle or the midbrain reticular formation is also essential for the activation of this response.

Adrenal Cortex↗
PubMed1987

Spontaneous and neurogenic constriction of microvasculature in the rat hippocampal slice.

The hippocampal slice is characterized by laminar organization and defined synaptic circuitry and provides an in vitro model system for the study of neuronal membrane properties, the action of putative neurotransmitters, and synaptic plasticity. Because the hippocampus is densely vascularized and hippocampal microvessels respond to a variety of stimuli that also affect the activity of neurons in the slice, the preparation is also especially well suited to investigating the physiologic relationship between neurons and intraparenchymal blood vessels. Here we address the issue of potential neurogenic control of cerebral microvasculature using electrical stimuli and specific neurotoxins. A small proportion of slice microvessels displayed spontaneous rhythmic activity that was independent of any exogenous stimulus. The majority of slices examined contained microvessels that responded to a train of electrical impulses delivered to discrete neural pathways. Under particular stimulus conditions, the vascular response could be completely blocked by 1 microM tetrodotoxin. The results are taken to support the existence of a neurogenic influence on penetrating arterioles.

Animals↗
PubMed1986

Evidence of local mechanism involvement in vasoactive intestinal polypeptide release from canine small intestine.

We studied the effect of intraileal administration of a 100-ml test meal, 100 ml of 5% glucose, amino acids, 10% Intralipos, or bile on canine plasma immunoreactive vasoactive intestinal polypeptide (VIP) levels in the mesenteric and femoral veins of dogs. The effects of intravenous administration of caerulein on plasma immunoreactive VIP levels were examined, with or without intraduodenal ballooning, to rule out the effect of bile and pancreatic and gastric juice. In addition, hexamethonium bromide or atropine sulfate was given intravenously before the administration of bile or intravenous caerulein to study the role of the neural pathway on the release of VIP. Basal plasma VIP levels in the mesenteric vein were significantly higher than those in the femoral vein. Intraileal administration of the test meal, 5% glucose, amino acids, or 10% Intralipos induced no variation of mesenteric VIP. Intraileal administration of bile or intravenous caerulein, with or without intraduodenal ballooning, produced a significant increase of plasma VIP in the mesenteric vein. Pretreatment with atropine completely blocked the bile-stimulated VIP release and significantly inhibited the caerulein-stimulated release of VIP. On the other hand, pretreatment with hexamethonium did not significantly decrease the VIP response by bile or caerulein. Thus, the muscarinic receptor probably plays an important role in bile- or caerulein-stimulated release of VIP.

Amino Acids↗
PubMed1987

Effects of bombesin on the release of glycine-extended progastrin (gastrin G) in rat antral tissue culture.

Recently, glycine-extended processing intermediates of progastrin were identified in porcine stomach using a radioimmunoassay with conventional polyclonal antisera developed against a synthetic peptide analogue for progastrin processing intermediates, gastrin 6-G(Tyr-Gly-Trp-Met-Asp-Phe-Gly). We developed monoclonal antibodies specific for glycine-extended processing intermediates of progastrin (gastrin G). Monoclonal antibody 109-21 appeared to require the carboxyl-terminal pentapeptide structure of gastrin 6-G for maximal binding. Cross-reactivities of 109-21 against gastrin 17 I, gastrin 17 II, cholecystokinin-octapeptide, des(SO3) cholecystokinin-octapeptide, and gastrin 6-G-R-R were respectively 1%, less than 0.1%, less than 0.1%, 0.1%, and 0.5%. With this monoclonal antibody and a polyclonal gastrin antibody we examined the concentrations of gastrin and gastrin G in tissue and the effects of bombesin on the release of gastrin and gastrin G from rat antral mucosa in tissue culture. The gastrin G to gastrin ratio was 2.2 in rat antral mucosa and 0.66 in rat duodenal mucosa. In tissue culture, bombesin significantly stimulated gastrin and gastrin-G secretion at doses of 10(-8) and 3 X 10(-8) M. Atropine (10(-6) M) abolished the actions of carbachol to stimulate gastrin and gastrin-G secretion but had no effect on bombesin-stimulated gastrin and gastrin-G secretion. These results suggest that gastrin G is cosecreted with gastrin in response to carbachol and bombesin, and the stimulation of gastrin and gastrin-G secretion by bombesin does not involve cholinergic neural pathways and may reflect a direct action on gastrin cells.

Animals↗
PubMed1987

Central administration of benzodiazepines alters water absorption by the rat ileum in vivo.

Two types of benzodiazepine receptors have been identified in the central nervous system. The aim of these experiments was to determine if ligands for these receptors alter basal water absorption by rat ileum in vivo after central administration. Specifically, the effects on net water flux of the systemic and central administration of diazepam and the central administration of RO 5-4864, a "peripheral" receptor agonist, and of the "central" receptor agonists clonazepam and lorazepam were determined. Diazepam increased absorption at 4.3 mg/250 g body wt i.p. but not at 430 micrograms/250 g body wt. Intracerebroventricular diazepam (28 micrograms) increased water absorption. Larger doses had a greater effect. Intracerebroventricular RO 5-4864 (100 micrograms) increased net water absorption; intracerebroventricular lorazepam (50 or 100 micrograms) or clonazepam (100 micrograms) reduced basal water absorption. Systemic atropine (2 mg/kg i.v.) abolished the effect of lorazepam (100 micrograms i.c.v.). To evaluate the possibility that diazepam and RO 5-4864 have effects similar to those of calcium channel antagonists, nifedipine, nitrendipine, and diltiazem were administered intracerebroventricularly. The dihydropyridine calcium channel antagonists nifedipine and nitrendipine increased basal water absorption. Diltiazem, a benzothiazepine compound, did not alter basal water absorption. We conclude that the binding of benzodiazepine agonists to receptors located in the central nervous system alters net water absorption by the rat ileum. Agonists of the central benzodiazepine receptor reduce basal water absorption via a cholinergic neural pathway. Peripheral agonists increase net water absorption. In this model, diazepam behaves as a peripheral receptor agonist. This study provides further evidence of a role for the central nervous system in the regulation of intestinal absorption of water and ions.

Animals↗
PubMed1990

Central nervous system action of peptides to influence gastrointestinal motor function.

The central action of peptides to influence GI motility in experimental animals is summarized in Table 1. TRH stimulates gastric, intestinal, and colonic contractility in rats and in several experimental species. A number of peptides including calcitonin, CGRP, neurotensin, NPY, and mu opioid peptides act centrally to induce a fasted MMC pattern of intestinal motility in fed animals while GRF and substance P shorten its duration. The dorsal vagal complex is site of action for TRH-, bombesin-, and somatostatin-induced stimulation of gastric contractility, and for CCK-, oxytocin- and substance P-induced decrease in gastric contractions or intraluminal pressure. The mechanisms through which TRH, bombesin, calcitonin, neurotensin, CCK, and oxytocin alter GI motility are vagally mediated. An involvement of central peptidergic neurons in the regulation of gut motility has recently been demonstrated in Aplysia, indicating that such regulatory mechanisms are important in the phylogenesis. Alterations of the pattern of GI motor activity are associated with functional changes in transit. TRH is so far the only centrally acting peptide stimulating simultaneously gastric, intestinal, and colonic transit in various animals species. Opioid peptides acting on mu receptor subtypes in the brain exert the opposite effect and inhibit concomitantly gastric, intestinal, and colonic transit. Bombesin and CRF were found to act centrally to inhibit gastric and intestinal transit and to stimulate colonic transit in the rat. The antitransit effect of calcitonin and CGRP is limited to the stomach and small intestine. The delay in GI transit is associated with reduced GI contractility for most of the peptides except central bombesin that increases GI motility. Nothing is known about brain sites through which these peptides act to alter gastric emptying and colonic transit. Regarding brain sites influencing intestinal transit, TRH-induced stimulation of intestinal transit in the rat is localized in the lateral and medial hypothalamus and medial septum. The periaqueductal gray matter is a responsive site for mu receptor agonist- and neurotensin-induced inhibition of intestinal transit. The neural pathways from the brain to the gut whereby these peptides express their stimulatory or inhibitory effects on GI transit is vagal dependent with the exception of calcitonin. It is not known whether the vagally mediated inhibition of GI transit by these peptides results from a decrease activity of vagal preganglionic fibers synapsing with excitatory myenteric neurons or an activation of vagal preganglionic neurons synapsing with inhibitory myenteric neurons. The lack of specific antagonists for these peptides has hampered the assessment of their physiological role.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Arginine vasopressin inhibits phasic contractions and stimulates giant contractions in monkey colon.

Abdominal cramps and urgent defecation are common side effects of clinical doses of arginine vasopressin, indicating that the drug may have stimulating effects on colonic motor activity. Four strain-gauge transducers were implanted on the colon in six monkeys. A blood flow probe was fixed on the inferior mesenteric artery. After a 1-hour control recording, vasopressin, 0.13, 1.3, or 13.0 ng.kg-1.min-1, was infused intravenously for 90 minutes. The frequency of basal colonic contractions was reduced with increasing doses of vasopressin, but their mean amplitude and duration were not altered. Giant migrating contractions associated with defecation were initiated by the highest dose of vasopressin. Atropine had no effect on these giant migrating contractions but completely inhibited normal phasic contractions. Hexamethonium completely inhibited both giant migrating contractions and phasic contractions. Parasympathetic denervation of the colon did not inhibit giant migrating contractions initiated by vasopressin. Our findings suggest that the physiological concentrations of serum vasopressin present perioperatively may transiently inhibit spontaneous colon contractions but are unlikely to be the major cause of postoperative ileus. The giant migrating contractions initiated by vasopressin may account for the defecation associated with pharmacological doses of vasopressin. The initiation of giant migrating contractions by vasopressin may be mediated through a neural pathway.

Animals↗
PubMed1993

Mechanism of gastroprokinetic effect of EM523, an erythromycin derivative, in dogs.

BACKGROUND: The pharmacological properties of EM523, a nonpeptide motilin agonist, have not been well characterized. METHODS: The prokinetic effect of EM523 on motor-stimulating activity in the stomach, duodenum, and jejunum in seventeen conscious dogs was studied using force transducers implanted long term. EM523 (0.3-10.0 micrograms/kg) and receptor antagonists were injected intravenously during the interdigestive state. RESULTS: EM523 induced phase III-like contractions in a dose-dependent manner, and the contractions were inhibited dose dependently by pretreatment with cholinergic and 5-HT3 receptor antagonists and dopamine but not by adrenoceptor and opiate antagonists or methysergide. The plasma immunoreactive motilin level was increased after EM523 to 60% of the mean maximum value during the spontaneous phase III contractions. Pretreatment with anti-canine motilin serum inhibited EM523-induced contractions by 19.2% in the motor index, but the contractile pattern was not affected. CONCLUSIONS: EM-523-induced phase III-like contractions are brought about through the cholinergic neural pathway and 5-HT3 receptors, and endogenous motilin release is partially involved.

Animals↗