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Change in Neurotrophins and Their Receptor mRNAs in the Rat Forebrain After Status Epilepticus Induced by Pilocarpine
Author(s) -
Mudò Giuseppa,
Jiang Xing H.,
Timmusk Tõnis,
Bindoni Mauro,
Belluardo Natale
Publication year - 1996
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1996.tb00012.x
Subject(s) - tropomyosin receptor kinase b , dentate gyrus , piriform cortex , neurotrophin , trk receptor , endocrinology , brain derived neurotrophic factor , medicine , tropomyosin receptor kinase a , tropomyosin receptor kinase c , neurotrophin 3 , low affinity nerve growth factor receptor , biology , hippocampus , neuroscience , neurotrophic factors , receptor , platelet derived growth factor receptor , growth factor
Summary: We studied the effects of status epilepticus (SE) induced by lithium chloride/pilocarpine treatment on gene expression of neurotrophins of the nerve growth factor (NGF) family and of their high‐affinity receptors of the tyrosine protein kinase ( trk ) family in the forebrain. Using in situ hybridization (ISH), we demonstrated an early (3 h after treatment) increase in brain‐derived neurotrophic factor (BDNF) and trkB mRNA expression in the dentate gyrus, amygdala, and piriform cortex, as well as widespread increases in the cerebral cortex. NGF mRNA, but not the mRNA of its receptor trkA , was increased in the dentate gyrus. In contrast, 12 h after treatment, neurotrophin‐3 (NT‐3) decreased, and its receptor trkC mRNA increased. There was no change in NT‐4 mRNA levels. All changes were blocked by pretreatment with scopolamine, a muscarinic antagonist. The noncompetitive N ‐methyl‐aspartate (NMDA) antagonist ketamine blocked NGF, BDNF, and trkB mRNA increases in the hippocampus and cerebral cortex, but not in the amygdala and piriform cortex. In contrast, ketamine did not affect NT‐3 and trkC changes. These results provide a complete description of changes in mRNA levels of neurotrophins and their receptors in the forebrain after SE and supply additional data supporting the view that neurotrophin gene expression is related to abnormal neuronal activity.