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Immunocytochemical mapping of Fos protein following seizures in gerbils indicates the activation of hippocampal neurons
Author(s) -
Mirzaeian Lovik,
Ribak Charles E.
Publication year - 2000
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/(sici)1098-1063(2000)10:1<31::aid-hipo3>3.0.co;2-l
Subject(s) - hippocampal formation , dentate gyrus , neuroscience , granule cell , piriform cortex , subiculum , premovement neuronal activity , hippocampus , pyramidal cell , immunocytochemistry , gerbil , biology , endocrinology , medicine , ischemia
The expression of the proto‐oncogene, c‐fos, and its protein, Fos, has been shown to be a useful marker for elevated levels of neuronal activity generated in the brain following different stimuli, including seizures. Since previous studies indicated hippocampal involvement in seizure activity in gerbils, Fos immunocytochemistry was used to determine whether hippocampal neurons become activated following environmentally induced seizures in this animal. Gerbils with maximal seizures showed many Fos‐immunolabeled neurons in the granule cell layer and hilus of the dentate gyrus, as well as in CA3 and CA1 of the hippocampus. These gerbils had significantly greater numbers of Fos‐immunolabeled dentate granule cells than gerbils with less severe seizures or no seizures. The number of dentate granule cells and CA3 pyramidal cells with Fos immunolabeling increased in an exponential manner with increased seizure severity. Many Fos‐immunolabeled neurons were found in several regions of the neo‐ and paleocortex and in other limbic structures including the piriform cortex, cortical amygdaloid nucleus, and arcuate nucleus of the hypothalamus. These results indicate that hippocampal neurons are activated following seizures in a genetic model, and provide further proof that the hippocampal formation is involved in the circuitry for seizures in gerbils. Hippocampus 2000;10:31–36. © 2000 Wiley‐Liss, Inc.