Axonal Degeneration | ScienceGate

Objective: The aim of this study was to investigate the effects of systemic administration of decorin (DC) on facial nerve (FN) regeneration. Methods: A total of 32 female albino Wistar rats were divided into 4 groups: control (C) group: no bilateral FN neurorrhaphy (B-FNN), no DC application, sham-operated group: B-FNN without DC application, DC group: DC application without B-FNN, and B-FNN + DC group: B-FNN and DC application. Nerve conduction studies were performed before and after skin incisions at 1st, 3rd, 5th, and 7th weeks in all groups. The amplitude and latency of compound muscle action potentials were recorded. FN samples were obtained and were investigated under light microscopy and immunohistochemical staining. The nerve and axon diameter, number of axons, H score, Schwann cell proliferation, and myelin and axonal degeneration were recorded quantitatively. Results: In the sham group, the 3rd and 5th postoperative week, amplitude values were significantly lower than those of the B-FNN + DC group (p < 0.05). Nerve diameters were found to be significantly larger in the sham, DC, and B-FNN + DC groups than in the C group (p < 0.05). The number of axons, the axon diameter, and the H scores were found to be significantly higher in the B-FNN + DC group than in the sham group (p < 0.05). The Schwann cell proliferation, myelin degeneration, and axonal degeneration scores were significantly lower in the B-FNN + DC group than in the sham group (p < 0.05). Conclusion: Electrophysiological and histopathological evaluation revealed the potential benefits provided by DC. This agent may increase FN regeneration.

Download Full-text

Hereditary polyneuropathy in the Alaskan Malamute

Tierärztliche Praxis Ausgabe K Kleintiere / Heimtiere ◽

10.1055/s-0038-1623617 ◽

2012 ◽

Vol 40 (01) ◽

pp. 26-34 ◽

Cited By ~ 3

Author(s):

T. Bilzer ◽

S. Petri ◽

G. Schanen ◽

M. Fehr ◽

O. Distl ◽

...

Keyword(s):

Segregation Analysis ◽

Nerve Conduction Velocity ◽

Axonal Degeneration ◽

Phenotypic Expression ◽

Disease Status ◽

Nerve Biopsy ◽

Hereditary Disease ◽

Genetic Transmission ◽

Clinically Normal ◽

Background Material

Summary Objective: To prove the hypothesis that a polyneuropathy in Alaskan Malamutes has a genetic background. Material and methods: Pedigrees of 131 related Alaskan Malamutes were included in the current study. Neurological examination, electrodiagnosis as well as muscle and nerve biopsies could be performed in 10 dogs. Information about the disease status of the other 121 Alaskan Malamutes were supplied by referring veterinarians, breeders and owners. Segregation analysis using four different models (monogenic, polygenic, mixed monogenicpolygenic and the phenotypic model) was performed on 71 dogs to test the different mechanisms of genetic transmission. Results: In seven clinically affected dogs abnormal electromyographic findings and reduced nerve conduction velocity were detected. Suspected diagnosis of polyneuropathy was confirmed by nerve biopsy results, characterized by axonal degeneration and hypomyelination. Muscle specimens revealed signs of neurogenic myopathy. Three related clinically normal Alaskan Malamutes also displayed moderate neuromuscular changes in histopathology. In the segregation analysis the polygenic model proved as best suitable to explain the observed segregation pattern among all other models tested. Conclusion: The current study could demonstrate that polyneuropathy in Alaskan Malamutes is a hereditary disease with variable phenotypic expression ranging from severely affected to subclinical forms, which has to be considered in future gene analysis studies.

Download Full-text