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Cell survival patterns in the pedunculopontine tegmental nucleus of methyl-4-phenyl-1,2,3,6-tetrarahydropyridine-treated monkeys and 60HDA-lesioned rats: evidence for diffences to idiopathic Parkinson disease patients

Heise, Claire E; Teo, Zui Chih; Wallace, Bradley A; Ashkan, Keyoumars; Benabid, Alim-Louis; Mitrofanis, John

Description

We explore the patterns of cell loss in the pedunculopontine tegmental nucleus (PpT), a major locomotor and muscle tone suppression centre of the brainstem, in two animal models of Parkinson disease, namely MPTP (methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated monkeys and 6-hydroxydopamine(6OHDA)-lesioned rats. Although there have been many studies documenting the loss of dopaminergic cells from the substantia nigra in these animal models, there has been little, if any, documentation of a...[Show more]

dc.contributor.authorHeise, Claire E
dc.contributor.authorTeo, Zui Chih
dc.contributor.authorWallace, Bradley A
dc.contributor.authorAshkan, Keyoumars
dc.contributor.authorBenabid, Alim-Louis
dc.contributor.authorMitrofanis, John
dc.date.accessioned2015-12-13T22:59:03Z
dc.identifier.issn0340-2061
dc.identifier.urihttp://hdl.handle.net/1885/83584
dc.description.abstractWe explore the patterns of cell loss in the pedunculopontine tegmental nucleus (PpT), a major locomotor and muscle tone suppression centre of the brainstem, in two animal models of Parkinson disease, namely MPTP (methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated monkeys and 6-hydroxydopamine(6OHDA)-lesioned rats. Although there have been many studies documenting the loss of dopaminergic cells from the substantia nigra in these animal models, there has been little, if any, documentation of a loss of cells in the PpT. Results were obtained from macaque monkeys (Macaca fascicularis) and Sprague-Dawley rats. For the monkey series, animals were injected intramuscularly with MPTP (0.2 mg/kg) for 8 days consecutively and then allowed to survive for 21 days thereafter. Each monkey underwent behavioural assessment for parkinsonian symptoms. For the rat series, 6OHDA was injected into the midbrain using stereotactic coordinates. Rats were then allowed to survive for either 7, 14, 28, or 84 days thereafter. Monkey and rat brains were aldehyde-fixed and processed for routine tyrosine hydroxylase (TH; to label nigral dopaminergic cells) and nitric oxide synthase (NOs; to label PpT cholinergic cells) immunocytochemistry. In monkeys, the morphology, distribution and number of NOs+ cells in the controls and MPTP-treated cases were very similar. In fact, in terms of number, there was only a 1% difference in the mean cell number between the controls and MPTP-treated cases. A comparable pattern was evident in 6OHDA-lesioned rats; there was no substantial difference in morphology, distribution and number of NOs+ cells on the 6OHDA-lesioned cases when compared to the controls at each of the survival periods post-surgery. In summary, we show no loss of the large cholinergic/NOs+ cells in the PpT in two animal models of Parkinson disease. This is in contrast to the heavy loss of these cells reported by previous findings in idiopathic Parkinson disease in patients.
dc.publisherSpringer
dc.sourceAnatomy and Embryology
dc.subjectKeywords: aldehyde; methyl 4 phenyl 1,2,3,6 tetrahydropyridine; nitric oxide synthase; oxidopamine; pyridine derivative; tyrosine 3 monooxygenase; unclassified drug; animal experiment; animal model; animal tissue; article; brain stem; cell loss; cell survival; chol 6-Hydroxydopamine; Brainstem; Cholinergic; Dopaminergic; Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
dc.titleCell survival patterns in the pedunculopontine tegmental nucleus of methyl-4-phenyl-1,2,3,6-tetrarahydropyridine-treated monkeys and 60HDA-lesioned rats: evidence for diffences to idiopathic Parkinson disease patients
dc.typeJournal article
local.description.notesImported from ARIES
local.description.refereedYes
local.identifier.citationvolume210
dc.date.issued2005
local.identifier.absfor110999 - Neurosciences not elsewhere classified
local.identifier.ariespublicationMigratedxPub11873
local.type.statusPublished Version
local.contributor.affiliationHeise, Claire E, University of Sydney
local.contributor.affiliationTeo, Zui Chih, University of Sydney
local.contributor.affiliationWallace, Bradley A, Universite Joseph Fourier
local.contributor.affiliationAshkan, Keyoumars, Universite Joseph Fourier
local.contributor.affiliationBenabid, Alim-Louis, Universite Joseph Fourier
local.contributor.affiliationMitrofanis, John, College of Medicine, Biology and Environment, ANU
local.description.embargo2037-12-31
local.bibliographicCitation.startpage287
local.bibliographicCitation.lastpage302
local.identifier.doi10.1007/s00429-005-0053-1
dc.date.updated2015-12-12T07:26:11Z
local.identifier.scopusID2-s2.0-28244501289
CollectionsANU Research Publications

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