title: Patterns of hippocampal neuronal loss and axon reorganization of the dentate gyrus in the mouse pilocarpine model of temporal lobe epilepsy.
abstract: The patterns of hippocampal neuronal loss and rewiring of the dentate gyrus (DG) were studied in the mouse model of temporal lobe epilepsy at 2 months after pilocarpine-induced status epilepticus (PISE). NeuN immunocytochemistry showed two patterns of neuronal damage, i.e., type 1 with partial loss of pyramidal neurons in CA3 area and type 2 with almost compete loss of CA3 pyramidal neurons. Anterograde tracing with Phaseolus vulgaris leucoagglutinin (PHA-L) demonstrated that, at different rostrocaudal segments of the hippocampus, associational and commissural connections in the DG changed differently between mice with type 1 vs. type 2 neuronal loss. Calretinin (CR)-immunopositive mossy cells in ventral hilus and its fibers in inner molecular layer of bilateral DG remained in mice with type 1 but almost disappeared in mice with type 2 neuronal loss, which was further supported by retrograde labeling with cholera toxin subunit B (CTB) showing colocalization of CTB with CR in the ventral hilus of bilateral DG in mice with type 1 neuronal loss, which was lost in those with type 2 neuronal loss. Furthermore, the sprouted PHA-L-immunopositive en passant and terminal boutons from the DG were found in CA1 area to contact with surviving calbindin-, CR-, and parvalbumin-immunopositive neurons. The present study therefore suggests that different patterns of neuronal loss in CA3 area may be linked to different axon reorganizations in the DG.
authors.affiliation: Epilepsy Research Laboratory, National Neuroscience Institute, Singapore.
authors.forename: Si
authors.initials: S
authors.lastname: Zhang
authors.forename: Sanjay
authors.initials: S
authors.lastname: Khanna
authors.forename: Feng Ru
authors.initials: FR
authors.lastname: Tang
mesh_terms: D000818:Animals; D064032:Calbindin 2; D016923:Cell Death; D002772:Cholera Toxin; D004268:DNA-Binding Proteins; D004195:Disease Models, Animal; D004569:Electroencephalography; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D006624:Hippocampus / Q000473:pathology* / Q000503:physiopathology / Q000648:ultrastructure; D007150:Immunohistochemistry; D051379:Mice; D008854:Microscopy, Electron; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000473:pathology* / Q000502:physiology / Q000648:ultrastructure; D009687:Nuclear Proteins / Q000378:metabolism; D010835:Phytohemagglutinins; D010862:Pilocarpine; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D012640:Seizures
chemical_list: C576511:Calb2 protein, mouse; D064032:Calbindin 2; D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C492380:NeuN protein, mouse; D009687:Nuclear Proteins; D010835:Phytohemagglutinins; D064030:S100 Calcium Binding Protein G; C100156:leukoagglutinins, plants; D010862:Pilocarpine; D002772:Cholera Toxin