Differential regulation of catalytic and non-catalytic trkB messenger RNAs in the rat hippocampus following seizures induced by systemic administration of kainate
| Autor: | T. Okazaki, Millicent M. Dugich-Djordjevic, Fukuichi Ohsawa, Jonathan R. Day, Franz Hefti, Klaus D. Beck, Nozomu Mori |
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| Rok vydání: | 1995 |
| Předmět: |
Male
medicine.medical_specialty Receptor expression Nerve Tissue Proteins Hippocampus RNA Complementary Rats Sprague-Dawley Neurotrophic factors Seizures Internal medicine medicine Animals Nerve Growth Factors RNA Messenger In Situ Hybridization Brain-derived neurotrophic factor Messenger RNA Kainic Acid biology General Neuroscience Dentate gyrus Brain-Derived Neurotrophic Factor Protein-Tyrosine Kinases Granule cell Molecular biology Rats medicine.anatomical_structure Endocrinology nervous system Trk receptor biology.protein Autoradiography Neurotrophin |
| Zdroj: | Neuroscience. 66(4) |
| ISSN: | 0306-4522 |
| Popis: | Ribonuclease protection analysis and quantitative in situ hybridization histochemistry were used to investigate the coordination and regional expression of catalytic and non-catalytic trk B messenger RNAs in the adult rat hippocampus following systemic kainate-induced seizures. Changes in trk B expression were compared with the messenger RNA expression of its neurotrophic ligands, brain-derived neurotrophic factor and neurotrophin-3. Trk B messenger RNA expression was increased in the dentate granule cells at 1–4 h following the onset of seizures, and returned to control levels 16–24 h thereafter. In addition, seizures also induced expression of trk B messenger RNA in putative non-neuronal cells at four to seven days in the molecular layer of the dentate gyrus and the stratum lacunosum moleculare of the CA1 region. Hybridization with probes specific for the non-catalytic trk B receptor and the catalytic trk B receptor revealed that the increases at four and seven days in the molecular layers of the hippocampus reflected an up-regulation of only the non-catalytic form of the receptor. Furthermore, the neuronal increases observed 1–4 h were due to an up-regulation of both trk B TK− and trk B TK+ messenger RNAs. It was established that systemic administration of kainate increased brain-derived neurotrophic factor messenger RNA levels in the pyramidal and granule cell regions of the hippocampus 1–4 h following the onset of behaviorally manifested seizure activity. Early changes in neuronal expression of trk B TK− and trk B TK+ messenger RNA paralleled changes in brain-derived neurotrophic factor messenger RNA in the dentate granule cell and CA1 pyramidal cell layers, but not in the CA3 subregion. These data suggest that concomitant regulation of brain-derived neurotrophic factor and its cognate receptor may play a role in the selective vulnerability of hippocampal subregions to kainate-induced neuropathology. Furthermore, these data suggest a dual function for trk B receptor expression in the hippocampus following kainate-induced seizures, possibly related to both the plastic and degenerative consequences of seizure induction by kainate. |
| Databáze: | OpenAIRE |
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