Kainate treatment alters TGF-β3 gene expression in the rat hippocampus

Hyoung Chun Kim, Guoying Bing, Seong Jin Kim, Wang Kee Jhoo, Eun Joo Shin, Myung Bok Wie, Kwang Ho Ko, Won Ki Kim, Kathleen C. Flanders, Shin Geon Choi, Jau Shyong Hong

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


In order to evaluate the role of transforming growth factor (TGF)-β3 in the neurodegenerative process, we examined the levels of mRNA and immunocytochemical distribution for TGF-β3 in the rat hippocampus after systemic kainic acid (KA) administration. Hippocampal TGF-β3 mRNA level was reduced 3 h after KA injection. However, the levels of TGF-β3 mRNA were elevated 1 day post-KA and lasted for at least 30 days. A mild TGF-β3 immunoreactivity (TGF-β3-IR) in the Ammon's horn and a moderate TGF-β3-IR in the dentate granule cells were observed in the normal hippocampus. The CA1 and CA3 neurons lost their TGF-β3-IR, while TGF-β3-positive glia-like cells proliferated mainly throughout the CA1 sector and had an intense immunoreactivity at 7, 15 and 30 days after KA. This immunocytochemical distribution of TGF-β3-positive non-neuronal populations was similar to that of glial fibrillary acidic protein (GFAP)-positive cells. Double labeling immunocytochemical analysis demonstrated colocalization of TGF-β3- and GFAP-immunoreactivity in the same cells. These findings suggest a compensatory mechanism of astrocytes for the synthesis of TGF-β3 protein in response to KA-induced neurodegeneration. In addition, exogenous TGF-β3 (5 or 10 ng/i.c.v.) significantly attenuated KA-induced seizures and neuronal damages in a dose-related manner. Therefore, our results suggest that TGF-β3 plays an important role in protective mechanisms against KA-induced neurodegeneration.

Original languageEnglish
Pages (from-to)60-70
Number of pages11
JournalMolecular Brain Research
Issue number1-2
StatePublished - Dec 16 2002

Bibliographical note

Funding Information:
This work was supported by the Brain Korea 21 Project, and by a grant (1998-019-F00050) from Korea Research Foundation, Republic of Korea. Equipment at the Institute of Pharmaceutical Science (Kangwon National University) was used in this study.


  • Astrocyte
  • Exogenous TGF-β3
  • Hippocampus
  • Kainic acid
  • Neurodegeneration
  • Transforming growth factor-β3

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience


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