The leptin receptor mutation of the obese Zucker rat causes sciatic nerve demyelination with a centripetal pattern defect

Young male Zucker rats with a leptin receptor mutation are obese, have a non-insulin-dependent diabetes mellitus (NIDDM), and other endocrinopathies. Tibial branches of the sciatic nerve reveal a progressive demyelination that progresses out of the Schwann cells (SCs) where electron-contrast deposit...

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Bibliographic Details
Published in:Ultrastructural pathology 2018-09, Vol.42 (5), p.377-408
Main Authors: Gilloteaux, Jacques, Subramanian, Kritika, Solomon, Nadia, Nicaise, Charles
Format: Article
Language:English
Subjects:
Animals
Demyelinating Diseases - genetics
Diabetes Mellitus, Type 2
Diabetic Neuropathies - pathology
Leptin receptor
Male
Mutation
myelin
Myelin Sheath - ultrastructure
Nerve Fibers, Myelinated - ultrastructure
NIDDM - obesity
Rats
Rats, Zucker
Receptors, Leptin - genetics
Schwann Cells - ultrastructure
Sciatic Nerve - pathology
sciatic nerve - Schwann cell
Sciatic Nerve - ultrastructure
Zucker rat
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Summary:Young male Zucker rats with a leptin receptor mutation are obese, have a non-insulin-dependent diabetes mellitus (NIDDM), and other endocrinopathies. Tibial branches of the sciatic nerve reveal a progressive demyelination that progresses out of the Schwann cells (SCs) where electron-contrast deposits are accumulated while the minor lines or intermembranous SC contacts display exaggerated spacings. Cajal bands contain diversely contrasted vesicles adjacent to the abaxonal myelin layer with blemishes; they appear dispatched centripetally out of many narrow electron densities, regularly spaced around the myelin annulus. These anomalies widen and yield into sectors across the stacked myelin layers. Throughout the worse degradations, the adaxonal membrane remains along the axonal neuroplasm. This peripheral neuropathy with irresponsive leptin cannot modulate hypothalamic-pituitary-adrenal axis and SC neurosteroids, thus exacerbates NIDDM condition. Additionally, the ultrastructure of the progressive myelin alterations may have unraveled a peculiar, centripetal mode of trafficking maintenance of the peripheral nervous system myelin, while some adhesive glycoproteins remain between myelin layers, somewhat hindering the axon mutilation. Heading title: Peripheral neuropathy and myelin
ISSN:0191-3123
1521-0758
DOI:10.1080/01913123.2018.1522405