Calretinin/PSA-NCAM immunoreactive granule cells after hippocampal damage produced by kainic acid and DEDTC treatment in mouse.
There is a dramatic increase in the number of lightly immunoreactive calretinin cells in the granular layer of the dentate gyrus of the mouse hippocampus 1 day after excitotoxic injury using kainic acid combined with the zinc chelator diethyldithiocarbamate. At 7 days after treatment, these cells are strongly immunoreactive for calretinin and for the polysialated form of the glycoprotein neural cell adhesion molecule (PSA-NCAM). The reexpression of calretinin and PSA-NCAM after treatment corresponds well with the loss of input from the damaged hilar mossy cells. These cells could be considered immature granule cells since they are immunoreactive to markers for immature cells such as PSA-NCAM, and are not immunoreactive to calbindin D28k and neuronal nuclear specific protein NeuN (present in mature granule cells), or GABA (present in interneurons). Ultrastructural analysis of these cells indicates that they are immature. Labelling of cell proliferation with 5-bromo-2'-deoxyuridine (BrdU) shows that by day 1 no calretinin immunoreactive cell of the dentate gyrus corresponds to newly generated cells. By day 7 only 6% of the calretinin immunoreactive cells in the dentate gyrus are marked for BrdU. Our data indicate that the CR/PSA-NCAM immunoreactive cells of the dentate gyrus, in spite of their immature characteristics, are not the products of reactive neurogenesis. These cells could represent a reservoir of pre-existing not completely differentiated granule cells that react to damage.
Domínguez
María Isabel
MI
Departamento de Biología Celular, Facultad de Ciencias Biológicas, Universidad de Valencia, Str. Dr Moliner 50, E-46.100, Burjasot, Spain.
Blasco-Ibáñez
José Miguel
JM
Crespo
Carlos
C
Marqués-Marí
Ana Isabel
AI
Martínez-Guijarro
Francisco José
FJ
D000818:Animals; D064032:Calbindin 2; D002614:Chelating Agents / Q000633:toxicity*; D004050:Ditiocarb / Q000031:analogs & derivatives* / Q000633:toxicity*; D004357:Drug Synergism; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity*; D006624:Hippocampus / Q000187:drug effects* / Q000293:injuries / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D007150:Immunohistochemistry / Q000379:methods; D007608:Kainic Acid / Q000633:toxicity*; D051379:Mice; D008854:Microscopy, Electron / Q000379:methods; D039842:Neural Cell Adhesion Molecule L1 / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000378:metabolism*; D012794:Sialic Acids / Q000378:metabolism*; D013997:Time Factors
C576511:Calb2 protein, mouse; D064032:Calbindin 2; D002614:Chelating Agents; D018690:Excitatory Amino Acid Agonists; D039842:Neural Cell Adhesion Molecule L1; D064030:S100 Calcium Binding Protein G; D012794:Sialic Acids; C103469:polysialyl neural cell adhesion molecule; D004050:Ditiocarb; D010751:Phosphopyruvate Hydratase; C039353:dihydroxyethyldithiocarbamate; D007608:Kainic Acid