Abstract
Changes in the structure of the olfactory bulbs after long-term intranasal administration of pesticide rotenone, a classical inductor of parkinsonism, to rats were studied by the methods of immunomorphology. In rats intranasally receiving rotenone in a dose of 2.5 mg/kg every other day over 2 weeks, a decrease in the density of dopaminergic neurons and the area of astrocyte processes in the olfactory bulbs, activation of microglia in the glomerular layer, and enhanced α-synuclein phosphorylation and its accumulation in the bodies of mitral layer neurons were observed. The observed changes agree with the hypothesis on pathological α-synuclein transport via the olfactory route in Parkinson's disease and confirm relevance of the rotenone model of Parkinson's disease for studies of the pathological accumulation of α-synuclein.
Keywords:
dopaminergic neurons; olfactory bulbs; parkinsonism; rotenone; α-synuclein.
MeSH terms
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Administration, Intranasal
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Animals
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Dopaminergic Neurons / drug effects
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Dopaminergic Neurons / metabolism*
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Dopaminergic Neurons / pathology
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Gene Expression Regulation
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Glial Fibrillary Acidic Protein / genetics
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Glial Fibrillary Acidic Protein / metabolism
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Immunohistochemistry
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Male
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Microglia / drug effects
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Microglia / metabolism*
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Microglia / pathology
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Olfactory Bulb / drug effects
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Olfactory Bulb / metabolism*
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Olfactory Bulb / pathology
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Parkinson Disease, Secondary / chemically induced
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Parkinson Disease, Secondary / genetics*
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Parkinson Disease, Secondary / metabolism
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Parkinson Disease, Secondary / pathology
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Rats
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Rats, Wistar
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Rotenone / administration & dosage*
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Tyrosine 3-Monooxygenase / genetics
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Tyrosine 3-Monooxygenase / metabolism
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alpha-Synuclein / genetics*
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alpha-Synuclein / metabolism
Substances
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GFAP protein, rat
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Glial Fibrillary Acidic Protein
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alpha-Synuclein
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Rotenone
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Tyrosine 3-Monooxygenase