title: Stereologic estimation of hippocampal GluR2/3- and calretinin-immunoreactive hilar neurons (presumptive mossy cells) in two mouse models of temporal lobe epilepsy.
abstract: OBJECTIVE
  Hippocampal mossy cells receive dense innervation from dentate granule cells and, in turn, mossy cells innervate both granule cells and interneurons. Mossy cell loss is thought to trigger granule cell mossy fiber sprouting, which may affect granule cell excitability. The aim of this study was to quantify mossy cell loss in two animal models of temporal lobe epilepsy, and determine whether there exists a relationship between mossy cell loss, mossy fiber sprouting, and granule cell dispersion.
  
  
  METHODS
  Representative hippocampal sections from p35 knockout mice and mice with unilateral intrahippocampal kainate injection were immunolabeled for GluR2/3, two subunits of the amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor and calretinin to identify mossy cells. Mossy fibers were immunostained against synaptoporin.
  
  
  RESULTS
  p35 Knockout mice showed no hilar cell death, but moderate mossy fiber sprouting and granule cell dispersion. In the kainate-injected hippocampus, there was an 80% and 85% reduction of GluR2/3- and GluR2/3/calretinin-positive hilar neurons, respectively, and dense mossy fiber sprouting and significant granule cell dispersion. In the contralateral hippocampus there was a 52% loss of GluR2/3-, but only a 20% loss of GluR2/3-calretinin-immunoreactive presumptive mossy cells, and granule cell dispersion; no mossy fiber sprouting was observed.
  
  
  CONCLUSIONS
  These results indicate a probable lack of causality between mossy cell death and mossy fiber sprouting.
authors.affiliation: Department of Neurosurgery, University Medical Center, Albert-Ludwigs-University, Freiburg, Germany.
authors.forename: Florian
authors.initials: F
authors.lastname: Volz
authors.forename: Hans H
authors.initials: HH
authors.lastname: Bock
authors.forename: Mortimer
authors.initials: M
authors.lastname: Gierthmuehlen
authors.forename: Josef
authors.initials: J
authors.lastname: Zentner
authors.forename: Carola A
authors.initials: CA
authors.lastname: Haas
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Freiman
mesh_terms: D000818:Animals; D064032:Calbindin 2; D002452:Cell Count / Q000379:methods; D004195:Disease Models, Animal; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000235:genetics / Q000473:pathology*; D007839:Functional Laterality; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics; D006624:Hippocampus / Q000473:pathology*; D007211:Indoles; D007608:Kainic Acid; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009474:Neurons / Q000378:metabolism*; D010770:Phosphotransferases; D018091:Receptors, AMPA / Q000378:metabolism*; D064030:S100 Calcium Binding Protein G / Q000378:metabolism*; D013238:Stereotaxic Techniques; D016708:Synaptophysin / Q000378:metabolism
chemical_list: C576511:Calb2 protein, mouse; D064032:Calbindin 2; C492236:Cdk5r1 protein, mouse; D007211:Indoles; D018091:Receptors, AMPA; D064030:S100 Calcium Binding Protein G; D016708:Synaptophysin; C504261:Synpr protein, mouse; C104723:glutamate receptor ionotropic, AMPA 3; C007293:DAPI; D010770:Phosphotransferases; C104722:glutamate receptor ionotropic, AMPA 2; D007608:Kainic Acid