Midbrain dopaminergic neurons in the mouse that contain calbindin-D(28k) exhibit reduced vulnerability to MPTP-induced neurodegeneration

Chang Lin Liang, Christopher M. Sinton, Patricia K. Sonsalla, Dwight C. German

Research output: Contribution to journalArticle

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Abstract

The calcium-binding protein calbindin-D(28k) (CB) is located in midbrain dopaminergic (DA) neurons that are less vulnerable to degeneration in Parkinson's disease and in an animal model of the disorder, the MPTP-treated monkey. The present study sought to determine whether CB-containing DA neurons are also less vulnerable to degeneration in the MPTP-treated mouse. Double-labelling immunocytochemical staining and computer imaging techniques were employed to map and quantify the tyrosine hydroxylase-, CB- and CB-containing tyrosine hydroxylase neurons in portions of nucleus A9 and nucleus A10 (ventral tegmental area and central linear nucleus) following MPTP treatment in the C57BL/6 mouse. A cumulative dose of 140 mg/kg MPTP produced a significantly greater loss of DA neurons that lack CB in both nucleus A9 (71 ± 4%) and the ventral tegmental area (70 ± 4%), compared to the loss of DA neurons that contain CB (44 ± 6% and 25 ± 14%, respectively). In the central linear nucleus there was no loss of CB-containing DA neurons. These data demonstrate that the presence of CB in midbrain DA neurons identifies a population of cells in the mouse that are less vulnerable to MPTP-induced degeneration. The mouse, therefore, can serve as a useful model in which to investigate the putative neuroprotective effects of CB in an animal model of Parkinson's disease.

Original languageEnglish (US)
Pages (from-to)313-318
Number of pages6
JournalNeurodegeneration
Volume5
Issue number4
DOIs
StatePublished - Dec 1996

Fingerprint

Calbindins
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Dopaminergic Neurons
Mesencephalon
Ventral Tegmental Area
Tyrosine 3-Monooxygenase
Parkinson Disease
Animal Models
Calcium-Binding Proteins
antineoplaston A10
Neuroprotective Agents
Inbred C57BL Mouse
Haplorhini
Staining and Labeling
Neurons
Population

Keywords

  • Calbindin-D(28k) double-labelling immunocytochemistry
  • Midbrain dopaminegic neurons
  • Mouse
  • MPTP

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Pathology and Forensic Medicine
  • Clinical Neurology

Cite this

Midbrain dopaminergic neurons in the mouse that contain calbindin-D(28k) exhibit reduced vulnerability to MPTP-induced neurodegeneration. / Liang, Chang Lin; Sinton, Christopher M.; Sonsalla, Patricia K.; German, Dwight C.

In: Neurodegeneration, Vol. 5, No. 4, 12.1996, p. 313-318.

Research output: Contribution to journalArticle

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abstract = "The calcium-binding protein calbindin-D(28k) (CB) is located in midbrain dopaminergic (DA) neurons that are less vulnerable to degeneration in Parkinson's disease and in an animal model of the disorder, the MPTP-treated monkey. The present study sought to determine whether CB-containing DA neurons are also less vulnerable to degeneration in the MPTP-treated mouse. Double-labelling immunocytochemical staining and computer imaging techniques were employed to map and quantify the tyrosine hydroxylase-, CB- and CB-containing tyrosine hydroxylase neurons in portions of nucleus A9 and nucleus A10 (ventral tegmental area and central linear nucleus) following MPTP treatment in the C57BL/6 mouse. A cumulative dose of 140 mg/kg MPTP produced a significantly greater loss of DA neurons that lack CB in both nucleus A9 (71 ± 4{\%}) and the ventral tegmental area (70 ± 4{\%}), compared to the loss of DA neurons that contain CB (44 ± 6{\%} and 25 ± 14{\%}, respectively). In the central linear nucleus there was no loss of CB-containing DA neurons. These data demonstrate that the presence of CB in midbrain DA neurons identifies a population of cells in the mouse that are less vulnerable to MPTP-induced degeneration. The mouse, therefore, can serve as a useful model in which to investigate the putative neuroprotective effects of CB in an animal model of Parkinson's disease.",
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