Consequences of a single short lasting cerebral oligemia and the influence of iron injected into the substantia nigra or in the ventrolateral striatum of the rat. Trigger of Parkinson's disease pathogenesis?

Christine Marcelle Heim, T. A. Sontag, W. Kolasiewicz, F. Ulrich, I. Pardowitz, H. J. Horn, M. Gerlach, P. Riederer, K. H. Sontag

Research output: Contribution to journalArticle

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Abstract

One BCCA-phase (bilateral clamping of carotid arteria) leads to an extensive release of striatal dopamine with a subsequent formation of free radicals (Heim et al., 200b). Early investigations did not show histological damage to cerebral structures after 24 and 60 min duration of a BCCA phase (Melzacka et al., 1994). The study here turned out that oligemic damage and an increase in iron (FeCl3) concentration in the ventral striatum was responsible for most of the defective performance of the animals investigated. Striatal damaged animals were unable to correct their deficient performance to the same extent as was possible for animals which had been damaged through BCCA and FeCl3 in the substantia nigra. Furthermore it turn out that with the use of a comprehensive behaviour profile which was able to gather 22 parameters simultaneously, 15 of these parameters did not correspond in the performance of the controls already after BCCA alone. Since during the ageing process, pathological effects may occur in vulnerable structures not only from disturbances to cerebral blood-perfusion but also from enrichment of iron in vulnerable structures (Connor, 1992) the question arose whether this situation did not reveal pathological mechanisms that might triggered the early symptoms of Parkinson's disease.

Original languageEnglish (US)
Pages (from-to)641-666
Number of pages26
JournalJournal of Neural Transmission
Volume111
Issue number6
DOIs
StatePublished - Jun 1 2004

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Substantia Nigra
Parkinson Disease
Corpus Striatum
Iron
Pathologic Processes
Constriction
Free Radicals
Dopamine
Perfusion

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

Cite this

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title = "Consequences of a single short lasting cerebral oligemia and the influence of iron injected into the substantia nigra or in the ventrolateral striatum of the rat. Trigger of Parkinson's disease pathogenesis?",
abstract = "One BCCA-phase (bilateral clamping of carotid arteria) leads to an extensive release of striatal dopamine with a subsequent formation of free radicals (Heim et al., 200b). Early investigations did not show histological damage to cerebral structures after 24 and 60 min duration of a BCCA phase (Melzacka et al., 1994). The study here turned out that oligemic damage and an increase in iron (FeCl3) concentration in the ventral striatum was responsible for most of the defective performance of the animals investigated. Striatal damaged animals were unable to correct their deficient performance to the same extent as was possible for animals which had been damaged through BCCA and FeCl3 in the substantia nigra. Furthermore it turn out that with the use of a comprehensive behaviour profile which was able to gather 22 parameters simultaneously, 15 of these parameters did not correspond in the performance of the controls already after BCCA alone. Since during the ageing process, pathological effects may occur in vulnerable structures not only from disturbances to cerebral blood-perfusion but also from enrichment of iron in vulnerable structures (Connor, 1992) the question arose whether this situation did not reveal pathological mechanisms that might triggered the early symptoms of Parkinson's disease.",
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Consequences of a single short lasting cerebral oligemia and the influence of iron injected into the substantia nigra or in the ventrolateral striatum of the rat. Trigger of Parkinson's disease pathogenesis? / Heim, Christine Marcelle; Sontag, T. A.; Kolasiewicz, W.; Ulrich, F.; Pardowitz, I.; Horn, H. J.; Gerlach, M.; Riederer, P.; Sontag, K. H.

In: Journal of Neural Transmission, Vol. 111, No. 6, 01.06.2004, p. 641-666.

Research output: Contribution to journalArticle

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AU - Sontag, T. A.

AU - Kolasiewicz, W.

AU - Ulrich, F.

AU - Pardowitz, I.

AU - Horn, H. J.

AU - Gerlach, M.

AU - Riederer, P.

AU - Sontag, K. H.

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