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  • 1
    Electronic Resource
    Electronic Resource
    Depression in Parkinson’s disease: brainstem midline alteration on transcranial sonography and magnetic resonance imaging (1999)
    Springer
    Journal of neurology 246 (1999), S. 1186-1193 
    Details
    ISSN: 1432-1459
    Keywords: Key words Parkinson’s disease ; Depression ; Brainstem midline ; changes ; Transcranial sonography ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies using transcranial sonography (TCS) have provided evidence of alterations in the mesencephalic midline structures in patients with unipolar depression and depression in Parkinson’s disease (PD), suggesting an involvement of the basal limbic system in primary and secondary mood disorders. This study tested the hypothesis of brainstem midline abnormality in depression and investigated 31 PD patients by magnetic resonance imaging (MRI) and TCS. Signal intensity of the pontine and mesencephalic brainstem midline was rated on T2-weighted images and measured by relaxometry. In addition, two blinded investigators assessed the echogenicity of the brainstem midline by TCS. The severity of motor symptoms and depression were graded independently using standard research scales. Rating of signal intensity and T2 relaxometry of the pontomesencephalic midline structures revealed significant difference between depressed and nondepressed PD patients (P 〈 0.05). This corresponded to a significant reduction in mesencephalic midline echogenicity of depressed PD patients on TCS images. No correlation was found between raphe signal intensity, T2 relaxation times, or TCS echogenicity and the severity of motor symptoms or depression. This study is the first to show changes in signal intensity and T2 relaxation time of the pontomesencephalic midline structures on MRI in depressed PD patients confirming previous TCS findings. As these midline structures comprise fiber tracts and nuclei of the basal limbic system, the findings may support the hypothesis of an alteration in the basal limbic system in mood disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004150050541
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  • 2
    Electronic Resource
    Electronic Resource
    The competitive NMDA antagonist CPP protects substantia nigra neurons from MPTP-induced degeneration in primates (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 586-592 
    Details
    ISSN: 1432-1912
    Keywords: Excitatory amino acids ; CPP ; 3-((±)-2carboxypiperazin-4-yl)-propyl-1-phosphonic acid ; NMDA receptor antagonist ; Dopamine ; MPTP ; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Common marmosets ; Substantia nigra degeneration ; Parkinsonism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Degeneration of nigrostriatal dopaminergic neurons is the primary histopathological feature of Parkinson's disease. The neurotoxin MPTP (1-methyl-4phenyl-1,2,3,6-tetrahydropyridine) induces a neurological syndrome in man and non-human primates very similar to idiopathic Parkinson's disease by selectively destroying dopaminergic nigrostriatal neurons. This gives rise to the hypothesis that Parkinson's disease may be caused by endogenous or environmental toxins. Endogenous excitatory amino acids (EAAs) such as l-glutamate could be involved in neurodegenerative disorders including Parkinson's disease. We report in this study that the competitive NMDA antagonist CPP (3-((±)-2-carboxypiperazin-4yl)-propyl-1-phosphonic acid) protects nigral tyrosine hydroxylase (TH) positive neurons from degeneration induced by systemic treatment with MPTP in common marmosets. This indicates that EAAs are involved in the pathophysiological cascade of MPTP-induced neuronal cell death and that EAA antagonists may offer a neuroprotective therapy for Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00167234
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  • 3
    Electronic Resource
    Electronic Resource
    Motor activity following the administration of selective D-1 and D-2 dopaminergic drugs to normal common marmosets (1991)
    Springer
    Psychopharmacology 105 (1991), S. 303-309 
    Details
    ISSN: 1432-2072
    Keywords: D-1 receptor ; D-2 receptors ; Functional interaction ; Locomotor activity ; Common marmosets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In normal common marmosets administration of the D-1/D-2 agonist apomorphine or the selective D-2 agonist quinpirole caused a dose-dependent increase in motor activity and induced stereotyped behaviour. Both the selective D-2 antagonist raclopride and the selective D-1 antagonist SCH 23390 inhibited normal locomotor activity and induced catalepsy. Quinpirole- and apomorphine-induced motor activity were potently inhibited by pretreatment with raclopride. The effects of quinpirole, but not apomorphine, were weakly inhibited by SCH 23390. The selective D-1 partial agonist SKF 38393 decreased motor activity and did not induce grooming, oral movements or other behaviours. SKF 38393 inhibited motor activity induced by the administration of quinpirole but did not alter apomorphine-induced motor behaviour. Locomotor activity in normal common marmosets appears to be mediated mainly via D-2 systems. In contrast to rodents, administration of SKF 38393 does not induce behavioural activation and there does not appear to be a facilitating effect of D-1 systems on D-2 function in the normal common marmoset. However, the ability of both SKF 38393 and SCH 23390 to inhibit quinpirole locomotor activity suggests some interaction between D-1 and D-2 systems to occur in this species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02244422
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  • 4
    Electronic Resource
    Electronic Resource
    Motor activity following the administration of selective D-1 and D-2 dopaminergic drugs to MPTP-treated common marmosets (1992)
    Springer
    Psychopharmacology 109 (1992), S. 49-56 
    Details
    ISSN: 1432-2072
    Keywords: Raclopride ; Quinpirole ; SCH 23390 ; Apomorphine ; Marmosets ; Dopamine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ability of selective D-1 agonist and antagonist drugs to alter motor deficits and locomotor activity was studied in MPTP-treated common marmosets. Both the D-2 agonist quinpirole and the mixed D-1/D-2 agonist apomorphine reversed the motor impairments and induced locomotor activity. The D-1 antagonist SCH 23390 and the D-2 antagonist raclopride given alone further reduced motor function in MPTP-treated animals. The actions of quinpirole were potently and completely inhibited by raclopride but only partially and inconsistently by SCH 23390. In contrast, the effects of apomorphine were markedly but incompletely inhibited by both raclopride and SCH 23390. The D-1 agonist SKF 38393 alone caused a dose related reduction in motor activity. SKF 38393 weakly and partially inhibited the improvements in motor function produced by quinpirole but had a more pronounced effect on apomorphine induced motor activity. The induction of motor activity in MPTP treated common marmosets may separately involve both D-1 and D-2 receptors. Comparison with our previous data on the effect of the same drugs in normal common marmosets provides some evidence for a breakdown of linkage between D-1 and D-2 systems following MPTP treatment. The actions of SKF 38393 in MPTP-treated common marmosets contrasts with its ability to induce behavioural activation and a facilitation of D-2 mediated behaviour in rodents. SKF 38393 may not be the compound with which to delineate the role of D-1 receptors in primates.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02245479
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    Paper (German National Licenses)
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