Abstract
In 1995, we developed an animal model of transient homolateral facial nerve paralysis by inoculating Herpes simplex virus type 1 (HSV-1) into the auricle of mice. This study examined the mechanism of facial nerve paralysis in this model histopathologically. Using the immunofluorescence technique with anti-HSV-1 antibody, the time course of viral spread and the site of viral replication were investigated over the entire course of the facial nerve. Furthermore, viral replication and nerve degeneration at the site of viral replication were observed by electron microscopy. On the 7th day after inoculation, facial paralysis was observed in more than 60% of mice. Immunofluorescence study revealed HSV-1 in the geniculate ganglion, the descending root, and the facial nucleus at this stage. On the 9th day, the descending root in the sections stained with osmium looked pale, because prominent demyelination had occurred in this region; electron micrographs showed many degenerated oligodendrocytes and large naked axons. In contrast, the facial nucleus neurons showed no remarkable degeneration, despite HSV-1 particles in their cytoplasm. From these findings, we concluded that facial nerve paralysis in this model is caused mainly by facial nerve demyelination in the descending root.
| Original language | English |
|---|---|
| Pages (from-to) | 68-79 |
| Number of pages | 12 |
| Journal | Experimental Neurology |
| Volume | 178 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2002 |
| Externally published | Yes |
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Keywords
- Bell's palsy
- Demyelination
- Facial nerve
- Herpes simplex virus type 1
- Motor nerve dysfunction
ASJC Scopus subject areas
- Neurology
- Neuroscience(all)
Cite this
Demyelination associated with HSV-1-induced facial paralysis. / Wakisaka, Hiroyuki; Hato, Naohito; Honda, Nobumitsu; Takahashi, Hirotaka; Kisaki, Hisanobu; Murakami, Shingo; Gyo, Kiyofumi; Mominoki, Katsumi; Kobayashi, Naoto; Matsuda, Seiji.
In: Experimental Neurology, Vol. 178, No. 1, 2002, p. 68-79.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Demyelination associated with HSV-1-induced facial paralysis
AU - Wakisaka, Hiroyuki
AU - Hato, Naohito
AU - Honda, Nobumitsu
AU - Takahashi, Hirotaka
AU - Kisaki, Hisanobu
AU - Murakami, Shingo
AU - Gyo, Kiyofumi
AU - Mominoki, Katsumi
AU - Kobayashi, Naoto
AU - Matsuda, Seiji
PY - 2002
Y1 - 2002
N2 - In 1995, we developed an animal model of transient homolateral facial nerve paralysis by inoculating Herpes simplex virus type 1 (HSV-1) into the auricle of mice. This study examined the mechanism of facial nerve paralysis in this model histopathologically. Using the immunofluorescence technique with anti-HSV-1 antibody, the time course of viral spread and the site of viral replication were investigated over the entire course of the facial nerve. Furthermore, viral replication and nerve degeneration at the site of viral replication were observed by electron microscopy. On the 7th day after inoculation, facial paralysis was observed in more than 60% of mice. Immunofluorescence study revealed HSV-1 in the geniculate ganglion, the descending root, and the facial nucleus at this stage. On the 9th day, the descending root in the sections stained with osmium looked pale, because prominent demyelination had occurred in this region; electron micrographs showed many degenerated oligodendrocytes and large naked axons. In contrast, the facial nucleus neurons showed no remarkable degeneration, despite HSV-1 particles in their cytoplasm. From these findings, we concluded that facial nerve paralysis in this model is caused mainly by facial nerve demyelination in the descending root.
AB - In 1995, we developed an animal model of transient homolateral facial nerve paralysis by inoculating Herpes simplex virus type 1 (HSV-1) into the auricle of mice. This study examined the mechanism of facial nerve paralysis in this model histopathologically. Using the immunofluorescence technique with anti-HSV-1 antibody, the time course of viral spread and the site of viral replication were investigated over the entire course of the facial nerve. Furthermore, viral replication and nerve degeneration at the site of viral replication were observed by electron microscopy. On the 7th day after inoculation, facial paralysis was observed in more than 60% of mice. Immunofluorescence study revealed HSV-1 in the geniculate ganglion, the descending root, and the facial nucleus at this stage. On the 9th day, the descending root in the sections stained with osmium looked pale, because prominent demyelination had occurred in this region; electron micrographs showed many degenerated oligodendrocytes and large naked axons. In contrast, the facial nucleus neurons showed no remarkable degeneration, despite HSV-1 particles in their cytoplasm. From these findings, we concluded that facial nerve paralysis in this model is caused mainly by facial nerve demyelination in the descending root.
KW - Bell's palsy
KW - Demyelination
KW - Facial nerve
KW - Herpes simplex virus type 1
KW - Motor nerve dysfunction
UR - http://www.scopus.com/inward/record.url?scp=0036447088&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036447088&partnerID=8YFLogxK
U2 - 10.1006/exnr.2002.8035
DO - 10.1006/exnr.2002.8035
M3 - Article
VL - 178
SP - 68
EP - 79
JO - Experimental Neurology
JF - Experimental Neurology
SN - 0014-4886
IS - 1
ER -