title: Lithium pilocarpine-induced status epilepticus in postnatal day 20 rats results in greater neuronal injury in ventral versus dorsal hippocampus.
abstract: Many quantitative animal studies examining the possible relationship between hippocampal neuronal loss and the development of epilepsy have examined only the dorsal hippocampus. The ventral hippocampus, however, represents the more homologous structure to the anterior hippocampus in humans, which is the area associated with the maximal damage in patients with temporal lobe epilepsy. This study tested the hypothesis that the ventral hippocampus has greater neuronal injury than the dorsal hippocampus in an animal model of chemoconvulsant-status epilepticus at postnatal day 20. Status epilepticus was induced in postnatal day 20 Sprague-Dawley rat pups with the chemoconvulsant lithium-pilocarpine and brain tissue was examined with Fluoro-Jade B. Horizontal sections (n=7) favoring a visualization of the ventral hippocampus showed marked Fluoro-Jade B staining in CA1, CA3, and hilar region. Coronal sections favoring a visualization of the dorsal hippocampus did not consistently show as robust a staining pattern in these regions. In coronal sections where both the dorsal and ventral hippocampus could be viewed, greater staining was always seen in ventral versus dorsal hippocampus. Quantitative analysis of cell counts demonstrated a significant difference between ventral and dorsal hippocampus in CA1 and CA3, but not hilus. These results demonstrate that in ventral hippocampus, lithium pilocarpine-induced status epilepticus consistently results in hippocampal neuronal injury in postnatal day 20 rats. This study shows the importance of including the ventral hippocampus in any analysis of seizure-induced hippocampal neuronal injury, and raises concerns about the accuracy of studies quantifying hippocampal neuronal loss when only the dorsal hippocampus is examined.
authors.affiliation: Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, UT 84108, USA. jeffrey.ekstrand@hsc.utah.edu
authors.forename: J J
authors.initials: JJ
authors.lastname: Ekstrand
authors.forename: W
authors.initials: W
authors.lastname: Pouliot
authors.forename: P
authors.initials: P
authors.lastname: Scheerlinck
authors.forename: F E
authors.initials: FE
authors.lastname: Dudek
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006624:Hippocampus / Q000473:pathology*; D018721:Muscarinic Agonists / Q000633:toxicity; D009474:Neurons / Q000473:pathology*; D010862:Pilocarpine / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology*
chemical_list: D018721:Muscarinic Agonists; D010862:Pilocarpine