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  • 1
    Electronic Resource
    Electronic Resource
    Electrophysiological and neurochemical correlates of the neurotoxic effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on central catecholamine neurons in the mouse (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 331 (1985), S. 1-6 
    Details
    ISSN: 1432-1912
    Keywords: MPTP ; Striatum ; Parkinson's disease ; Catecholamines ; Electrophysiology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is an agent which produces a parkinsonian syndrome in man. To explore the use of MPTP in a rodent model of parkinsonism, male albino mice (NMRI) were given MPTP (50 mg/kg, s.c.) twice with a 6–8 h interval. Up to 10 weeks after injection, mice were killed and high-pressure liquid chromatography was used to assay dopamine (DA) and noradrenaline (NA) concentrations in various regions of the CNS. At 4 and 10 weeks after injection, DA levels were significantly reduced in occipital cortex (-40%), hippocampus (-30%), and striatum (-60%). NA levels were reduced by 60–80% in frontal and occipital cortex, hippocampus, and cerebellum. Neither DA nor NA concentration was reduced in spinal cord. Dopaminergic denervation was also suggested by electrophysiological data which showed that treatment with MPTP increased the spontaneous discharge rate of caudate neurons and decreased the potency of locally administered phencyclidine, an indirect DA agonist. However, denervation was evidently not complete enough to produce postsynaptic receptor supersensitivity, as MPTP treatment did not increase the potency of locally applied DA, and it did not increase 3H-spiperone binding in striatal membrane preparations. These results suggest that MPTP causes regionally selective and long-term reductions of catecholamine transmission in the CNS of the mouse.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498844
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  • 2
    Electronic Resource
    Electronic Resource
    Ibotenic acid-induced neuronal degeneration: A morphological and neurochemical study (1979)
    Springer
    Experimental brain research 37 (1979), S. 199-216 
    Details
    ISSN: 1432-1106
    Keywords: Ibotenic acid ; Kainic acid ; Neurotoxins ; Neuronal degeneration ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Possible neurotoxic actions of intracerebral injections of ibotenic acid, a conformationally restricted analogue of glutamic acid, have been evaluated in rat brain and compared with those of kainic acid. Light microscopical analysis revealed that ibotenic acid produced a marked disappearance of nerve cells in all areas studied, namely striatum, the hippocampal formation, substantia nigra and piriform cortex. Lesions in areas distant to the injection site were not seen. Axons of passage and nerve terminals of extrinsic origin did not seem to be damaged, since, e.g., no apparent degeneration of the dopaminergic terminals in the neostriatum was observed except for a small area surrounding the cannula. In the neostriatum, enkephalin immunoreactive neuronal cell bodies as well as nerve terminals disappeared after injection of ibotenic acid into this nucleus. After injection into the substantia nigra tyrosine hydroxylase immunoreactive cell bodies in the zona compacta disappeared, whereas no certain effect could be seen on the enkephalin immunoreactive nerve fibers. In vitro experiments, conducted with striatal synaptosomal and membrane preparations, showed that ibotenic acid differed from kainic acid by being devoid of a significant inhibitory effect on high affinity glutamate uptake and by having a low affinity for 3H-kainic acid binding sites. Furthermore, ibotenic acid did not interfere with the binding of a number of radioligands for other transmitter receptors. As compared to kainic acid, ibotenic acid has the advantage of being less toxic to the animals and of producing more discrete lesions, possibly due to faster metabolism and/or other fundamental biochemical differences. Because of these special features, ibotenic acid seems to represent a valuable new tool in the morphological and functional analysis of central neuronal systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00237708
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  • 3
    Electronic Resource
    Electronic Resource
    Saccadic reaction times, eye-arm coordination and spontaneous eye movements in normal and MPTP- treated monkeys (1989)
    Springer
    Experimental brain research 78 (1989), S. 253-267 
    Details
    ISSN: 1432-1106
    Keywords: MPTP ; Dopamine ; Eye movements ; Eye-arm coordination ; Reaction times ; Parkinsonism ; Monkey
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The oculomotor performance of monkeys was investigated before and after destruction of nigrostriatal dopamine neurons by MPTP (1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine). Stimulus-triggered saccades and their relationships to arm movements were measured in a reaction time task. Spontaneous eye movements were recorded while monkeys sat in a primate chair and looked around the laboratory without performing any task. In the reaction time task, saccades and arm movements were commonly triggered by the rapid, visible and audible opening of a small food-containing box which was located at a constant position in front of the animal at eye level. Median saccadic latencies ranged from 68 to 118 ms in intact animals. Saccades were followed by onset of electromyographic (EMG) activity in the extensor digitorum communis and the biceps brachii, the prime mover muscles for the following arm reaching movement. Latencies of stimulus-triggered saccades showed an absence of linear relationship to EMG or arm movement reaction time in intact animals (correlation coefficients of 0.15–0.56). This suggests that eye and arm movements were initiated independently from each other in this experimental situation. Treatment with MPTP resulted in 98–99.5% loss of striatal dopamine in both monkeys. This induced a 29–93% increase in saccadic latency in the reaction time task. The sequential occurrence of saccade, EMG activity and arm movement in each trial was preserved, although intervals between onset of saccades and onsets of EMGs and arm movements were prolonged by 53–173% and 33–679% respectively. Onsets of individual saccades remained uncorrelated with onsets of EMG activity or arm movement. Spontaneous eye movements were strongly reduced in frequency and amplitude after MPTP. Administration of the dopamine precursor L-Dopa increased spontaneous eye movements for less than two hours. The severe deficits in stimulus-triggered and spontaneous saccadic eye movements are oculomotor components of hypokinesia arising after MPTP-induced lesions of the nigrostriatal dopamine system in primates. The data are further evidence for a role of midbrain dopamine neurons in behavioral responsiveness and spontaneous activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00228897
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  • 4
    Electronic Resource
    Electronic Resource
    The catecholamine uptake blocker nomifensine protects against MPTP-induced parkinsonism in monkeys (1986)
    Springer
    Experimental brain research 63 (1986), S. 216-220 
    Details
    ISSN: 1432-1106
    Keywords: MPTP ; Parkinsonism ; Dopamine ; Nomifensine ; Degeneration prevention
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Administration of MPTP (1-methyl-1,2,3,6-tetrahydropyridine) to Macaca fascicularis monkeys produced severe parkinsonism (hypokinesia, tremor, rigidity, aphagia, adipsia) and more than 90% loss of nigral dopamine neurons, striatal dopamine content and striatal 3H-mazindol binding. Treatment with the catecholamine uptake blocker nomifensine counteracted the behavioral, histological and neurochemical effects induced by MPTP. For obtaining best protection, nomifensine had to be administered for weeks after MPTP. The results suggest that the selective target-directed neurotoxic action of MPTP on dopamine neurons in monkeys is mediated via the dopamine uptake mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00235666
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    Paper (German National Licenses)
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