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  • DL-threo-dihydroxyphenylserine  (2)
  • Dorsal respiratory group  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Effect of increased pancreatic islet norepinephrine, dopamine and serotonin concentration on insulin secretion in the Golden hamster (1980)
    Springer
    Diabetologia 18 (1980), S. 341-346 
    Details
    ISSN: 1432-0428
    Keywords: Insulin secretion ; golden hamsters ; pancreatic islets ; norepinephrine ; dopamine ; serotonin ; monoamine oxidase ; DL-threo-dihydroxyphenylserine ; L-3,4-dihydroxyphenylalanine ; 5-hydroxytryptophan ; tranylcypromine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of this study was to determine if increased concentrations of pancreatic islet norepinephrine, dopamine, or serotonin alter insulin secretion. Golden hamsters received intraperitoneal injections of the norepinephrine precursor DL-threo-dihydroxyphenylserine, the dopamine precursor L-3,4-dihydroxyphenylalanine, or the serotonin precursor 5-hydroxytryptophan with and without pretreatment of the hamsters with the monoamine oxidase inhibitor tranylcypromine. Administration of the monoamine precursors to animals pretreated with tranylcypromine resulted in a mean increase in plasma glucose of 192% and a mean decrease in plasma insulin of 58%. Using a collagenase isolation technique, islets from control and treated animals were evaluated for monoamine content and insulin secretory capacity. The monoamine concentrations in control islets, in μmol/kg wet weight, were: norepinephrine 42±8; dopamine 8±2; and serotonin 26±9. Administration of the appropriate precursor to control hamsters resulted in a 1.9-fold (norepinephrine), 6-fold (dopamine), and 22-fold (serotonin) increase in monoamines. There was no alteration in the glucose (16.3 mmol/l)-stimulated in vitro insulin secretion from islets obtained from these hamsters. Administration of the precursors to hamsters pretreated with tranylcypromine resulted in a 3.5-fold (norepinephrine), 22-fold (dopamine), and 59-fold (serotonin) increase in monoamines. Glucose-stimulated in vitro insulin secretion from islets obtained from these hamsters was completely blocked. This study suggests that high concentrations of norepinephrine, dopamine, and serotonin in the pancreatic islets can decrease glucose-stimulated insulin secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00251017
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of pharmacological agents and fasting on pancreatic islet norepinephrine in the golden hamster (1979)
    Springer
    Diabetologia 17 (1979), S. 169-174 
    Details
    ISSN: 1432-0428
    Keywords: Monoamine oxidase ; catechol-o-methyl-transferase ; DL-threo-dihydroxyphenylserine ; nor-epinephrine ; pancreatic islets ; reserpine ; cate-cholamines ; insulin secretion ; fasting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Using a specific and sensitive radioenzymatic assay that utilizes the partially purified enzyme phenylethanolamine-N-methyltransferase, studies were done to determine if pharmacological agents and/or fasting alter the norepinephrine concentration of collagenase-isolated golden hamster pancreatic islets. The norepinephrine concentration (42.1±8.07 μmol/kg net weight, mean±SEM) and the monoamine oxidase activity (5,407±530 pmol product /mg tissue/min) of hamster pancreatic islets was at least five times higher than acinar pancreas, kidney, heart, median eminence or cerebral cortex. The catechol-o-methyltransferase activity of hamster islets (7±2.3 pmol product/mg tissue/min) was one half or less than the other tissues. Islet norepinephrine was not increased by two days administration of the monoamine oxidase inhibitor tranylcypromine. Islet norepinephrine concentration was increased 2-fold by administration of the norepinephrine precursor DL-threo-dihydroxyphenylserine. This increase was enhanced by prior administration of tranylcypromine (3.5-fold) and prevented by prior administration of the decarboxylase inhibitor N1-(DL-seryl)-N2-(2,3,4-trihydroxybenzyl) hydrazine (RO-4-4602). There was a good correlation between the islet norepinephrine concentration and the plasma glucose concentration after pharmacological agents. Reserpine administration markedly depleted the islet norepinephrine concentra tion. Fasting of 24, 48 and 72 h did not alter the norepinephrine concentration in islets and heart. It is concluded that the pancreatic islets of the hamster have an active noradrenergic system, but that islet norepinephrine does not appear to play an important role in the impaired insulin secretion of fasting hamsters.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01219745
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Role of the ventrolateral region of the nucleus of the tractus solitarius in processing respiratory afferent input from vagus and superior laryngeal nerves (1987)
    Springer
    Experimental brain research 67 (1987), S. 449-459 
    Details
    ISSN: 1432-1106
    Keywords: Dorsal respiratory group ; Nucleus tractus solitarius ; Superior laryngeal nerve ; Respiratory control ; Pulmonary stretch receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of respiratory neurons located within and adjacent to the region of the ventrolateral nucleus of the tractus solitarius (vlNTS) in processing respiratory related afferent input from the vagus and superior laryngeal nerves was examined. Responses in phrenic neural discharge to electrical stimulation of the cervical vagus or superior laryngeal nerve afferents were determined before and after lesioning the vlNTS region. Studies were conducted on anesthetized, vagotomized, paralyzed and artificially ventilated cats. Arrays of 2 to 4 tungsten microelectrodes were used to record neuronal activity and for lesioning. Constant current lesions were made in the vlNTS region where respiratory neuronal discharges were recorded. The region of the vlNTS was probed with the microelectrodes and lesions made until no further respiratory related neuronal discharge could be recorded. The size and placement of lesions was determined in subsequent microscopic examination of 50 μm thick sections. Prior to making lesions, electrical stimulation of the superior laryngeal nerve (4–100 μA, 10 Hz, 0.1 ms pulse duration) elicited a short latency increase in discharge of phrenic motoneurons, primarily contralateral to the stimulated nerve. This was followed by a bilateral decrease in phrenic nerve discharge and, at higher currents, a longer latency increase in discharge. Stimulation of the vagus nerve at intensities chosen to selectively activate pulmonary stretch receptor afferent fibers produced a stimulus (current) dependent shortening of inspiratory duration. Responses were compared between measurements made immediately before and immediately after each lesion so that changes in response efficacy due to lesions per se could be distinguished from other factors, such as slight changes in the level of anesthesia over the several hours necessary in some cases to complete the lesions. Neither uni- nor bi-lateral lesions altered the efficacy with which stimulation of the vagus nerve shortened inspiratory duration. The short latency excitation of the phrenic motoneurons due to stimulation of the superior laryngeal nerve was severely attenuated by unilateral lesions of the vlNTS region ipsilateral to the stimulated nerve. Neither the bilateral inhibition nor the longer latency excitation due to superior laryngeal nerve stimulation was reduced by uni- or bi-lateral lesions of the vlNTS region. These results demonstrate that extensive destruction of the region of the vlNTS: a) does not markedly affect the inspiratory terminating reflex associated with electrical stimulation of the vagus nerve in a current range selective for activation of pulmonary stretch receptor afferents, and b) abolishes the short-latency increase, but not the bilateral decrease or longer latency increase in phrenic motoneuronal discharge which follows stimulation of the superior laryngeal nerve. We conclude that respiratory neurons in the region of the vlNTS do not play an obligatory role in the respiratory phase transitions in this experimental preparation. Neurons in the vlNTS region may participate in other reflexes, such as the generation of augmented phrenic motoneuronal discharge in response to activation of certain superior laryngeal or vagus nerve afferents.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00247278
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    Paper (German National Licenses)
    Fulltext
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