title: Reorganization of CA3 area of the mouse hippocampus after pilocarpine induced temporal lobe epilepsy with special reference to the CA3-septum pathway.
abstract: We showed that when CA3 pyramidal neurons in the caudal 80% of the dorsal hippocampus had almost disappeared completely, the efferent pathway of CA3 was rarely detectable. We used the mouse pilocarpine model of temporal lobe epilepsy (TLE), and injected iontophoretically the anterograde tracer phaseolus vulgaris leucoagglutinin (PHA-L) into gliotic CA3, medial septum and the nucleus of diagonal band of Broca, median raphe, and lateral supramammillary nuclei, or the retrograde tracer cholera toxin B subunit (CTB) into gliotic CA3 area of hippocampus. In the afferent pathway, the number of neurons projecting to CA3 from medial septum and the nucleus of diagonal band of Broca, median raphe, and lateral supramammillary nuclei increased significantly. In the hippocampus, where CA3 pyramidal neurons were partially lost, calbindin, calretinin, parvalbumin immunopositive back-projection neurons from CA1-CA3 area were observed. Sprouting of Schaffer collaterals with increased number of large boutons in both sides of CA1 area, particularly in the stratum pyramidale, was found. When CA3 pyramidal neurons in caudal 80% of the dorsal hippocampus have almost disappeared completely, surviving CA3 neurons in the rostral 20% of the dorsal hippocampus may play an important role in transmitting hyperactivity of granule cells to surviving CA1 neurons or to dorsal part of the lateral septum. We concluded that reorganization of CA3 area with its downstream or upstream nuclei may be involved in the occurrence of epilepsy.
authors.affiliation: Epilepsy Research Lab, National Neuroscience Institute, Singapore.
authors.forename: Dong Liang
authors.initials: DL
authors.lastname: Ma
authors.forename: Yong Cheng
authors.initials: YC
authors.lastname: Tang
authors.forename: Peng Min
authors.initials: PM
authors.lastname: Chen
authors.forename: Shwn Chin
authors.initials: SC
authors.lastname: Chia
authors.forename: Feng Li
authors.initials: FL
authors.lastname: Jiang
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Burgunder
authors.forename: Wei Ling
authors.initials: WL
authors.lastname: Lee
authors.forename: Feng Ru
authors.initials: FR
authors.lastname: Tang
mesh_terms: D000818:Animals; D064032:Calbindin 2; D064026:Calbindins; D002452:Cell Count / Q000379:methods; D002772:Cholera Toxin; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004195:Disease Models, Animal; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced* / Q000473:pathology; D006624:Hippocampus / Q000473:pathology*; D007150:Immunohistochemistry / Q000379:methods; D007478:Iontophoresis / Q000379:methods; D008297:Male; D051379:Mice; D009434:Neural Pathways / Q000473:pathology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000145:classification / Q000378:metabolism / Q000473:pathology*; D010320:Parvalbumins / Q000378:metabolism; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D010835:Phytohemagglutinins; D010862:Pilocarpine / Q000633:toxicity*; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D020665:Septum of Brain / Q000473:pathology*
chemical_list: C576511:Calb2 protein, mouse; D064032:Calbindin 2; D064026:Calbindins; D010320:Parvalbumins; D010835:Phytohemagglutinins; D064030:S100 Calcium Binding Protein G; C100156:leukoagglutinins, plants; D010862:Pilocarpine; D002772:Cholera Toxin; D002795:Choline O-Acetyltransferase; D010751:Phosphopyruvate Hydratase