Abstract
Niemann-Pick disease type C (NP-C) is a progressive neurological disorder of lipid metabolism. The Balb/C npc1 mutant strain is a genetically authentic murine model of NPC, which reproduce the clinical and histologic features of human NP-C. In the present study, we show that cholecystokinin (CCK)-immunoreactive fibers in the thalamic VPL nuclei, which are densely distributed in controls, degenerate in NPC mice. This degeneration is associated with the appearance of CCK-immunoreactive axonal spheroids containing characteristic intracellular inclusions of NP-C. These observations provide supportive evidence of the occurrence of dying-back axonopathy of neurons in the dorsal column nuclei in this mouse model.
MeSH terms
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Afferent Pathways / metabolism*
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Animals
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Axons / metabolism
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Axons / ultrastructure
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Cholecystokinin / metabolism*
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Disease Models, Animal
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Immunohistochemistry / methods
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Intracellular Signaling Peptides and Proteins
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Mice
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Mice, Inbred BALB C
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Mice, Mutant Strains
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Microscopy, Immunoelectron / methods
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Nerve Degeneration / metabolism*
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Nerve Degeneration / physiopathology
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Neurons / metabolism
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Neurons / pathology
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Neurons / ultrastructure
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Niemann-Pick C1 Protein
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Niemann-Pick Diseases / metabolism*
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Niemann-Pick Diseases / physiopathology*
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Proteins / genetics
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Ventral Thalamic Nuclei / metabolism*
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Ventral Thalamic Nuclei / pathology
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Ventral Thalamic Nuclei / ultrastructure
Substances
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Intracellular Signaling Peptides and Proteins
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Niemann-Pick C1 Protein
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Npc1 protein, mouse
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Proteins
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Cholecystokinin