1.Distribution of trkA in cerebral cortex and diencephalon of the mongolian gerbil after birth.
Il Kwon PARK ; Xilin HOU ; Kyung Youl LEE ; O Sung PARK ; Kang Yi LEE ; Min Young KIM ; Tae Sun MIN ; Geun Jwa LEE ; Won Sik KIM ; Moo Kang KIM
Journal of Veterinary Science 2004;5(4):303-307
TrkA is essential components of the high-affinity NGF receptor necessary to mediate biological effects of the neurotrophins NGF. Here we report on the expression of trkA in the cerebral cortex and diencephalon of mongolian gerbils during postnatal development. The expression of trkA was identified by immunohistochemical method. In parietal cortex and piriform cortex, higher levels of trkA-IR (immunoreactivity) were detected at 3 days postnatal (P3) and at P9. Although trkA was not expressed till P3 in the parietal cortex, it was detectable at birth in the piriform cortex. Several regions, such as Layers I, IV & VI, did not show much expression. Layer I showed especially weak labeling. In the hippocampus, thalamus, and hypothalamus, higher levels of trkA-IR were detected at P6 and P12 than earlier days. But trkA was not expressed at birth in the hippocampus, at P3 in the reticular thalamic nucleus (Rt), or neonatally in the dorsomedial hypothalamic nucleus (DM). This data shows that expression of trkA is developmentally regulated and suggests that high affinity neurotrophin-receptors mediate a transient response to neurotrophines in the cerebral cortex and diencephalon during mongolian gerbil brain ontogeny.
Animals
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Animals, Newborn
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Cerebral Cortex/*metabolism
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Diencephalon/*metabolism
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Gerbillinae/*metabolism
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Immunohistochemistry/veterinary
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Nerve Growth Factor/metabolism
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Receptor, trkA/*metabolism
2.Glutamate and GABA concentrations in the cerebellum of novel ataxic mutant Pogo mice.
Ki Hyung KIM ; Jeoung Hee HA ; Seung Hyuk CHUNG ; Chul Tae KIM ; Sun Kyung KIM ; Byung Hwa HYUN ; Kazuhiko SAWADA ; Yoshihiro FUKUI ; Il Kwon PARK ; Geun jwa LEE ; Bum Kyeong KIM ; Nam Seob LEE ; Young Gil JEONG
Journal of Veterinary Science 2003;4(3):209-212
The Pogo mouse is an autosomal recessive ataxic mutant that arose spontaneously in the inbred KJR/MsKist strain derived originally from Korean wild mice. The ataxic phenotype is characterized by difficulty in maintaining posture and side to side stability, faulty coordination between limbs and trunk, and the consequent inability to walk straight. In the present study, the cerebellar concentrations of glutamate and GABA were analyzed, since glutamate is a most prevalent excitatory neurotransmitter whereas gammar-aminobutyric acid (GABA) is one of the most abundant inhibitory neurotransmitters, which may be the main neurotransmitters related with the ataxia and epilepsy. The concentration of glutamate of cerebellum decreased significantly in ataxic mutant Pogo mouse compared to those of control mouse. However, GABA concentration was not decrease. These results suggested that the decrease in glutamate concentration may contribute to ataxia in mutant Pogo mouse.
Animals
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Calcium-Binding Protein, Vitamin D-Dependent/metabolism
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Cerebellum/*metabolism/pathology
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Gait Ataxia/*metabolism/pathology
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Glutamic Acid/*metabolism
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Immunohistochemistry
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Mice
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Mice, Mutant Strains
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gamma-Aminobutyric Acid/*metabolism