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  • 1
    Electronic Resource
    Electronic Resource
    Mechanism of pressor effect of 5,6-dihydroxytryptamine in pithed rats (1972)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 274 (1972), S. 375-384 
    Details
    ISSN: 1432-1912
    Keywords: 5,6-Dihydroxytryptamine ; Chemical Degeneration ; Blood Pressure ; Pithed Rats ; 5-Hydroxytryptamine Receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 5,6-dihydroxytryptamine (5,6-DHT) — a neurotoxic drug causing a chemical degeneration of 5-hydroxytryptamine (5-HT) neurones in brain and to a lesser extend of peripheral adrenergic neurones—provokes a dose-dependent increase in the blood pressure of pithed rats after its intravenous injection. Although the noradrenaline content of the heart, spleen, rectum, and vas deferens is reduced by 50–68% 3 h after the i.p. injection, an indirect sympathomimetic effect does not contribute to the pressor effectof 5,6-DHT. Furthermore, 5,6-DHT does not directly interact with adrenoceptors of the cardiovascular system. The pressor effect of 5,6-DHT thus rests solely on a direct stimulation of 5-HT receptors. The following findings support these statements: 1. Neither pretreatment with reserpine nor application of cocaine attenuates the pressor effect of 5,6-DHT. 2. 2 [β-(4-Hydroxyphenyl)-ethyl-aminomethyl]-tetralone, a selective blocker for α-adrenoceptors, does not alter the effect of 5,6-DHT. 3. The non-competitive 5-HT antagonist phentolamine inhibits the 5,6-DHT effect in a non-competitive manner. 4. The selective, competitive 5-HT antagonist methysergide inhibits the pressor effect of 5,6-DHT in a competitive fashion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501274
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  • 2
    Electronic Resource
    Electronic Resource
    Evidence for a degeneration of indoleamine containing nerve terminals in rat brain, induced by 5,6-dihydroxytryptamine (1972)
    Springer
    Cell & tissue research 125 (1972), S. 553-569 
    Details
    ISSN: 1432-0878
    Keywords: Indoleamine containing nerve terminals ; Chemically induced degeneration ; 5,6-dihydroxytryptamine ; Rat brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary 5,6-dihydroxytryptamine (5,6-DHT) has been found to induce a substantial degree of “chemical degeneration” of indoleamine containing nerve terminals in the rat brain following a single intraventricular injection of 75 μg 5,6-DHT per animal. The disintegration of varicose terminal portions of serotonin containing neurons is reflected 1. by a loss of yellow fluorescent varicosities in certain defined parts of the rat CNS, despite a mild inhibition of the serotonin catabolizing enzyme monoamine oxidase with nialamide in the pretreated animals, 2. by a significant drop of the chemically measurable 5-hydroxytryptamine content in nearly all parts of the rat brain and spinal cord, 3. by the appearance of highly, orange or brownish fluorescent axons provided with numerous unusually large, distorted and intensely fluorescent swellings (“droplets”), resembling proximal stumps of mechanically severed indoleamine containing axons, 4. a temporary increase in the amount of indoleamine fluorophores stored in some neuronal pericarya, and 5. the electron microscopical demonstration of degenerating synaptic swellings of unmyelinated axons at all sites investigated. The selectivity of the effect of 5,6-DHT on indoleamine neurons is indicated by the absence of similar signs of injury in catecholamine containing neurons of the rat CNS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00306659
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  • 3
    Electronic Resource
    Electronic Resource
    The disposition of intraventricularly injected 14C-5,6-DHT-Melanin in, and possible routes of elimination from the rat CNS (1980)
    Springer
    Cell & tissue research 212 (1980), S. 279-294 
    Details
    ISSN: 1432-0878
    Keywords: 14C-5,6-DHT-Melanin ; Phagocytotic stimulant ; Intrathecal and subependymal phagocytes ; Microglia ; Peripheral disposition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary 14C-5,6-DHT-Melanin was injected into the left lateral ventricle of adult rats and its fate followed by light and EM autoradiography and by TEM of structures identified as labeled in preceding light micrographs. Shortly after injection, melanin particles were seen ingested by supraependymal and epiplexus cells, by cells residing in the pia-arachnoid, i.e. free subarachnoidal cells and perivascular cells, and by subependymally located microglia-like cells with intraventricular processes. Up to day four, an increase in the number of labelled phagocytes in the CSF was noted which transformed into typical reactive macrophages. After this time, many intraventricular melanin-laden phagocytes formed rounded clusters; cells of such clusters were subsequently found to invade the brain parenchyma by penetrating the ependymal lining and to accumulate in the perivascular space of brain vessels. 14C-Melanin-storing macrophages were found in the marginal sinus of the deep jugular lymph nodes suggesting emigration of CNS-derived phagocytes via lymphatics or prelymphatics that contact the subarachnoidal space compartment. This does not exclude the possibility that some of the macrophages leave the brain via the systemic circulation by penetrating the vascular endothelium; these may be disposed of in peripheral organs other than the lymph nodes. The ability of supraependymal, epiplexus, free subarachnoidal and perivascular cells in the pia and of subependymal microglia cells to accumulate synthetic melanin by phagocytosis suggests that these cells are local variants of the same type of resting potential phagocytes of the mammalian brain. The present study shows that 14C-5,6-DHT-melanin is an ideal phagocytic stimulant and marker for phagocytosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233961
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    Paper (German National Licenses)
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