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Considerable attention has been focused on the role of corticotropin releasing factor (CRF) as well as CRF-binding protein (CRF-BP) in neuropsychiatric disorders and neurodegenerative diseases including epilepsy. Therefore, in the present study, we investigated the temporal and spatial alteration of CRF and CRF-BP in the gerbil hippocampal complex in order to characterize the possible changes and associations with different sequelae of spontaneous seizure in these animals. CRF immunoreactivity was shown in the interneurons of the hippocampal complex at 30 min following seizure. Additionally, alteration of CRF-BP immunoreactivity was restricted to the entorhinal cortex after seizure. These results indicate some factors for consideration. First, in the gerbil hippocampal complex, the delayed increase of CRF immunoreactivity, in spite of its excitatory function, may attenuate seizure activity, but may not do so in epileptogenesis. Second, in contrast to the hippocampl complex, the increase in CRF-BP immunoreactivity in the entorhinal cortex following seizure may participate in feedback inhibitory modulation. (C) 2003 Elsevier Science Ltd. All rights reserved

Activity. --- Animal. --- Animals. --- Association. --- Attention. --- Behavioral-responses. --- Brain. --- Convulsive seizures. --- Cortex. --- Corticotropin-releasing-factor. --- Crf. --- Dentate gyrus. --- Disease. --- Diseases. --- Disorder. --- Entorhinal cortex. --- Epilepsies. --- Epilepsy. --- Expression. --- Feedback. --- Function. --- Gerbil. --- Hippocampal complex. --- Hippocampal. --- Hippocampus. --- Immunoreactive neurons. --- Immunoreactivity. --- Increase. --- Kainate-elicited seizures. --- Modulation. --- Mongolian gerbil. --- Protein. --- Rat. --- Seizure. --- Somatostatin. --- Spatial. --- Spontaneous seizure. --- Subiculum. --- Synaptic connections. --- Time.