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  • 1975-1979  (4)
  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —The distribution of choline acetyltransferase (ChAc, EC 2.3.1.6) and l-glutamate 1-carboxylyase (glutamate decarboxylase, GAD, EC 4.1.1.15) was studied in serial frontal slices of the substantia nigra (SN) (pars compacta, PC; pars reticulata, PR; an intermediate region, IR) as well as in other brain areas from post mortem tissue of control and Parkinsonian patients.Within the SN from control brain ChAc and GAD activities showed a distinctive distribution: ChAc activity in PC was higher than in PR and IR by 427% and 253% respectively and within PC the enzyme activity in the rostral part exceeded that in the control part by 353%. The GAD activity in PC was higher by 41% than that in PR and within PC seemed to be higher in the caudal than in the rostral part. For both enzyme activities there were no significant differences between PR and IR or within these regions.In Parkinsonian brain both ChAc and GAD activities were reduced to 15-25% of controls in all 3 regions of the SN. The distinctive distribution of ChAc and GAD activity found in the SN of control brain was abolished: no difference was observed between the 3 regions. However, within PC the ChAc activity was lower in the medial than in the rostral part.Since nigral ChAc is possibly located in interneurons, the decrease in enzyme activity may be connected with the cell loss observed in the SN of Parkinsonian brain.By contrast, nigral GAD is probably contained in terminals of strio-nigral neurons and the decrease in enzyme activity in Parkinson's disease in the absence of striatal cell loss, may reflect a change in the functional state of these GABA neurons.Among various areas of control brains ChAc activity was highest in caudate nucleus and putamen while GAD was highest in SN. caudate nucleus, putamen and cerebral cortex. In Parkinsonian brain the most severe reduction in ChAc and GAD activities was found in the SN.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 31 (1975), S. 560-562 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Zusammenfassung Hirnregionen der gallamin-immobilisierten Katze wurde mittels «push-pull»-Kanülen perfundiert. Die im Perfusat freigesetzten endogenen Katecholamine wurden radioenzymatisch gemessen. Chlorpromazin,d-Amphetamin oder Oxotremorin (i. v.) erhöhten den «output» von Dopamin aus dem Nucleus caudatus und Chlorpromazin zusätzlich denjenigen von hypothalamischem Noradrenalin durch verschiedene Mechanismen.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 288 (1975), S. 1-6 
    ISSN: 1432-1912
    Keywords: Chlorpromazine ; Septal Stimulation ; Limbic Neurotransmitters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of chlorpromazine (10 mg/kg i.v.) on the spontaneous release of endogenous dopamine (DA), noradrenaline (NA) and acetylcholine (ACh) within limbic areas perfused by means of the push-pull cannula was investigated in the gallamine-immobilized cat. Chlorpromazine increased the liberation of DA and NA in the nucleus accumbens septi, indicating blockade of the amine receptors. However, the drug did not change the output of ACh from this nucleus nor from ventral and dorsal hippocampal formation which receive a cholinergic input from the septum as indicated by several published findings and by the increased liberation of ACh after electrical stimulation of the homolateral nucleus medialis septi. These results seem to exclude that cholinergic neurons of some limbic areas mediate the effect of the blockade of DA (and of NA) receptors which is possibly involved in the antipsychotic action of neuroleptic drugs.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-7381
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Degeneration of adrenergic axons after 6-hydroxydopamine (6-OH-DA), 2 × 68 mg kg−1 i.v. within 6 h, and the subsequent regeneration process over the following 205 days were studied in rat mesenteric vessels, right atria and irides, using the histochemical fluorescence method of Falck and Hillarp. The objective of the study was to determine why noradrenaline is less depleted and recovers much more rapidly in the mesentery than in other tissues after 6-OH-DA (Finchet al., 1973). The mesentery was further studied by electron microscopy and noradrenaline content analyses, until day 29 after 6-OH-DA treatment. Virtually all adrenergic terminal axons in these tissues were destroyed one day after 6-OH-DA. The large nonterminal axon bundles which occur along the mesenteric vessels and rarely in the heart survived and revealed an intensified catecholamine fluorescence; correspondingly, the mesenteric noradrenaline content was only reduced to 29% of control values. In contrast, such large nonterminal axon bundles were not observed in control iris preparations, and no adrenergic fibres survived in the irides, as suggested by fluorescence microscopy. Regenerating axons were observed in all organs after 3–8 days. The number of nerve terminals along the circumference of the external elastic lamina, as observed in ultrathin cross sections of mesenteric vessels, appeared virtually normal 4 weeks after treatment. Meanwhile, the noradrenaline content of the mesentery returned to approximately 85% of control values. As suggested by fluorescence microscopy, complete adrenergic regeneration occurred in mesenteric vessels between days 46 and 105, while regeneration in atrium and iris was incomplete even at day 205. The density of adrenergic axons in the iris, morphometrically determined, was only 76% and 88% of controls on days 160 and 205, respectively. The survival of the many large nonterminal axon bundles in the mesentery with increased NA content explains the relatively small NA depletion of the mesentery. The rapid recovery of the mesenteric NA content is due to faster regeneration of adrenergic terminal axons in the mesentery as compared with iris and atrium. This is tentatively explained in terms of sprouting from the large axon bundles surviving close to the destroyed terminal axons of the mesenteric vessels, whereas in the other tissues no (iris) or only a few (atrium) large nonterminal axon bundles occur and persist to act as a source of quickly regenerated terminal axons.
    Type of Medium: Electronic Resource
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