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Distribution of trkA in cerebral cortex and diencephalon of the mongolian gerbil after birth
Journal of Veterinary Science ; : 303-307, 2004.
Article in English | WPRIM | ID: wpr-79784
ABSTRACT
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.
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Full text: Available Index: WPRIM (Western Pacific) Main subject: Immunohistochemistry / Cerebral Cortex / Gerbillinae / Receptor, trkA / Nerve Growth Factor / Diencephalon / Animals, Newborn Type of study: Prognostic study Limits: Animals Language: English Journal: Journal of Veterinary Science Year: 2004 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Immunohistochemistry / Cerebral Cortex / Gerbillinae / Receptor, trkA / Nerve Growth Factor / Diencephalon / Animals, Newborn Type of study: Prognostic study Limits: Animals Language: English Journal: Journal of Veterinary Science Year: 2004 Type: Article