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Absence of Gliosis in the Brains of Epileptic Fowl

Published online by Cambridge University Press:  18 September 2015

D.G. Munoz ,
B. McNab ,
D.H. George  and
D. Johnson
D.G. Munoz*
Affiliation:
Departments of Pathology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 0W0
B. McNab
Affiliation:
Departments of Pathology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 0W0
D.H. George
Affiliation:
Departments of Pathology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 0W0
D. Johnson
Affiliation:
Departments of Pathology and Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N 0W0
*
Department of Pathology, Health Sciences Building, Saskatoon, Saskatchewan, Canada S7N 0W0
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Abstract:

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Chickens homozygous for the epi gene (epileptics) suffer from spontaneous seizures throughout their life, whereas heterozygous (carriers) are phenotypically normal. Seizures can also be evoked in epileptics by photic stimulation. In addition, epileptic chickens' brains are 25% heavier than those of carriers. We have investigated whether hyperplasia or hypertrophy of astrocytes or increased numbers of astrocytic processes are involved in the development of seizures and the megalencephaly in this model by quantitative comparison of sections immunocytochemically stained for glial fibrillary acidic protein (GFAP). No statistically significant differences between epileptics and controls were found in any of seven areas selected for comparison. In this model gliosis is not involved in the development of epilepsy, nor does it result from repeated seizures.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 15 , Issue 4 , November 1988 , pp. 409 - 412
Copyright
Copyright © Canadian Neurological Sciences Federation 1988

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