Effects of enzyme inhibitors of catecholamine metabolism and of haloperidol on the pancreatic secretion induced by L-DOPA and by dopamine in dogs.
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1. Effects of inhibitors of DOPA decarboxylase, dopamine beta-hydroxylase and monoamine oxidase, and haloperiodol on the secretion of pancreatic juice induced by L-DOPA and dopamine were studied in preparations of the isolated blood-perfused canine pancreas.2. The increased secretion induced by the infusion of L-DOPA (100 mug/min) was completely antagonized by Ro 4-4602 (300 mug), a DOPA decarboxylase inhibitor.3. The secretogogue effect of dopamine (1-10 mug) intra-arterially was not affected by Ro 4-4602, but was enhanced by the infusion of fusaric acid (100 mug/min), a dopamine beta-hydroxylase inhibitor.4. The increase in the secretion induced by dopamine (1-10 mug) was enhanced by treatment with nialamide (100 mg/kg), a monoamine oxidase inhibitor, given intravenously.5. Haloperidol (1 mg) intra-arterially attenuated the dopamine-induced pancreatic secretion.6. It is concluded that L-DOPA is converted to dopamine in the acinar cells which causes an increase in the secretion of pancreatic juice, thus the intracellular level of dopamine may be controlled by enzymatic equilibrium. (+info)
Histochemical localization of adrenergic nerves in the guinea-pig trachea.
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1. Specific catecholamine fluorescence was demonstrated in guinea-pig trachea in fine, varicose, nerve fibres running parallel to the tracheal smooth muscle fibres.2. The density of nerves in tracheal smooth muscle was greater at the laryngeal end than at the bronchial end of the trachea.3. The findings confirm pharmacological evidence for an adrenergic innervation of the guinea-pig isolated tracheal chain preparation. (+info)
A histochemical study of extraneuronal accumulation of noradrenaline in the guinea-pig trachea.
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1. Accumulation of noradrenaline in extraneuronal tissue of the guinea-pig trachea has been studied by the use of the fluorescence histochemical technique of Falck and Hillarp.2. After incubation in solutions of noradrenaline, fluorescence developed in cellular structures (tracheal smooth muscle, vascular smooth muscle and endothelium, fibroblasts and chondroblasts), in the intercellular matrix of the cartilage and throughout the loose connective tissue of the adventitia and submucosa.3. The effect of various experimental procedures on the development of this fluorescence has been examined i.e. incubation with noradrenaline at reduced temperature (0 degrees C), removal of fluorescence by washing with Krebs solution at 37 degrees C or 0 degrees C, incubation with phenoxybenzamine (10(-4)M) or metanephrine (10(-4)M).4. From these observations it has been concluded that noradrenaline accumulates in the trachea:(a) in cellular structures where it is firmly bound, i.e. not easily removed by washing at 0 degrees C, and where the accumulation is prevented by phenoxybenzamine, metanephrine or cold.(b) in the intercellular matrix of the cartilage where it is also firmly bound, but where the accumulation is not prevented by phenoxybenzamine, metanephrine or cold. This probably represents binding to sulphated mucopolysaccharides.(c) in the adventitia and submucosa where it is loosely bound and easily removed by washing.5. Some implications of these findings in pharmacological experiments with guinea-pig trachea are discussed. (+info)
Release of 5-hydroxytryptamine from caudate nucleus and septum.
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1. The anterior horn of one lateral ventricle was perfused in anaesthetized cats treated with inhibitors of monoamine oxidase, and the effluent was tested for 5-hydroxytryptamine (5-HT).2. The basal release of 5-HT varied from 0.25 to 4 ng in 25 min, and was usually about 1 ng.3. The basal release rose and fell with body temperature.4. Electrical stimulation for 15 min of the nucleus linearis intermedius or of the nucleus linearis rostralis caused a release of 5-HT which rarely outlasted the collection period of 25 min.5. Low frequencies (0.5/sec) were, per stimulus, more effective than high frequencies in releasing 5-HT. Over a 15 min period of stimulation, however, the highest total yield was at 20/sec; it fell abruptly at still greater frequencies.6. No release was obtained if the stimulating electrode was positioned in a variety of brain structures outside the two linear nuclei.7. The experiments indicate that 5-HT acts as a transmitter of impulses in neurones originating in the linear nuclei and terminating in caudate nucleus and septum. (+info)
Release of transmitters on stimulation of the nucleus linearis raphe in the cat.
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The nucleus linearis intermedius raphe and the nucleus linearis rostralis were stimulated during the perfusion of the anterior horn of the right lateral ventricle of anaesthetized cats. Whereas release of 5-hydroxytryptamine (5-HT) was consistently obtained, there was no release of acetylcholine (ACh). The independence of the release of 5-HT from that of ACh was seen both during low basal release of ACh (rising base line), and during the period when a plateau of resting release had been reached. It was also demonstrated in experiments in which the same perfusate was examined for both compounds. (+info)
Passage into the rat brain of dopa and dopamine injected into the lateral ventricle.
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1. The green fluorescence of catechols of the brain was studied in rats after intraventricular injection of L-dopa or dopamine in untreated rats as well as in rats in which dopa decarboxylase (DC) was inhibited by Ro 4602, or the monoamine oxidase by nialamide.2. From the patterns of fluorescence obtained in these conditions, it is concluded that in the areas close to the liquor space dopa is rapidly taken up by the endothelium of the brain capillaries and then converted into dopamine; when the DC is inhibited the dopa passes freely from the endothelium into the brain tissue.3. On the other hand, dopamine passes from the liquor space via the ependyma directly into the brain tissue and from there into the capillary endothelium which is thus permeable to the amine in the direction from the brain tissue, in contrast to the impermeability in the direction from the capillary lumen. (+info)
Physiological and drug-induced changes in the glycogen content of mouse brain.
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1. The effect of the method of killing on the concentration of glycogen in mouse brain was determined. The cerebral glycogen content of mice killed by immersion in liquid nitrogen did not differe significantly from that of animals decapitated and the heads immediately frozen. A delay before freezing led to the rapid loss of brain glycogen, with a 17% fall at 10 s and an 82% loss after 5 min.2. Hyperglycaemia, induced by the administration of D-glucose, resulted in an 8.3% loss of brain glycogen after 120 min. Insulin hypoglycaemia produced a 10.7% fall in glycogen at 60 min followed by an 11.2% increase at 120 min.3. Exposure to either high (32 degrees C) or low (10 degrees C) ambient temperatures caused a depletion of brain glycogen.4. A circadian rhythm of brain glycogen concentration was found, with a nadir which was coincident with the peak of locomotor activity and body temperature.5. Drugs from several pharmacological classes were studied for their in vivo effect on the concentration of glycogen in mouse brain.6. Brain glycogen was increased by all the depressant drugs tested, and by some drugs which had little effect on behaviour (diphenhydramine, phenytoin and propranolol), or which caused excitation (caffeine and nialamide).7. Glycogen was depleted only by amphetamine-like compounds or by bemegride-induced convulsions.8. The results are discussed with particular reference to the possible relation between catecholamines and glycogen metabolism in the brain. (+info)
A method for investigating the effects of drugs on the exploratory behaviour of mice.
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1. Exploratory behaviour in mice was observed when they were put on a wooden board to which twelve tunnels were fixed. The number of different tunnels entered (indicating exploration) and the total entries into tunnels were recorded over 5 min on 2 successive days.2. Untreated mice entered more different tunnels in the first minute on the second day on the tunnel board, and this difference in behaviour was taken as an indication that exploration had occurred on the first day. When the behaviour of the treated mice on the second day was similar to that of inexperienced mice on the first day it was inferred that drug treatment had adversely affected exploration.3. Haloperidol 4 mg/kg, chlorpromazine 8 mg/kg and thioridazine 16 mg/kg adversely affected exploration at doses which almost immobilized the mice.4. Amphetamine at 8 mg/kg disrupted exploratory behaviour in the mice, although the mice were observed to move round the board very quickly.5. With tranylcypromine 2 mg and nialamide 100 mg, increased exploratory behaviour by comparison with controls was recorded in the mice when they were tested 24 h after drug treatment.6. Imipramine at 20 mg/kg reduced the total number of tunnels entered by the mice on the first day, but on the second day the mice behaved in a similar way to mice treated with monoamine oxidase inhibitors. (+info)