Kainic acid induction of mossy fiber sprouting: Dependence on mouse strain

After seizures caused by kindling or kainic acid (KA), hippocampal granule‐cell axons, the mossy fibers, sprout into the supragranular layer of the rat. The mechanisms underlying this phenomenon remain elusive, but excitotoxic loss of hilar cells, which project to this supragranular layer, is suspected to be a critical determinant. Consistent with this hypothesis, we previously reported that while rats show mossy fiber sprouting after kainate, ICR mice do not. This may be associated with the observation that ICR mice, unlike rats, do not appear to show hilar cell death after KA (McNamara et al., Mol Brain Res 1996;40:177–187). Other strains of mice, however, such as 129/SvEMS, do show hilar cell death after KA (Schauwecker and Steward, Proc Natl Acad Sci USA 1997;94:4103–4108). We examined the possibility that the 129/SvEMS mouse strain would show granule‐cell sprouting, in contrast to ICR mice. After administration of KA, mossy fiber sprouting was indeed observed in strain 129/SvEMS, but only in animals displaying evident hilar cell death. In contrast, neither hilar cell death nor mossy fiber sprouting was observed in ICR mice, confirming previous results. Both mouse strains demonstrated comparable behavioral seizures. These results strengthen the view that hilar cell death, together with epileptogenesis, triggers reactive synaptogenesis and mossy fiber sprouting. Hippocampus 10:269–273, 2000 © 2000 Wiley‐Liss, Inc.

[1]  Y. Ben‐Ari,et al.  Maturation of kainic acid seizure-brain damage syndrome in the rat. II. Histopathological sequelae , 1984, Neuroscience.

[2]  P. Stanton,et al.  Resistance of the immature hippocampus to seizure-induced synaptic reorganization. , 1991, Brain research. Developmental brain research.

[3]  A Routtenberg,et al.  Rapid induction by kainic acid of both axonal growth and F1/GAP‐43 protein in the adult rat hippocampal granule cells , 1996, The Journal of comparative neurology.

[4]  A. Routtenberg,et al.  Activity-dependent regulation of axonal growth: posttranscriptional control of the GAP-43 gene by the NMDA receptor in developing hippocampus. , 1999, Journal of neurobiology.

[5]  D. Amaral,et al.  The development, ultrastructure and synaptic connections of the mossy cells of the dentate gyrus , 1985, Journal of neurocytology.

[6]  O. Steward,et al.  Genetic determinants of susceptibility to excitotoxic cell death: implications for gene targeting approaches. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[7]  R. Racine,et al.  Modification of seizure activity by electrical stimulation. II. Motor seizure. , 1972, Electroencephalography and clinical neurophysiology.

[8]  Y. Ben‐Ari,et al.  Kainic acid seizure syndrome and binding sites in developing rats. , 1984, Brain research.

[9]  A. Routtenberg,et al.  Distinctions between hippocampus of mouse and rat: protein F1/GAP-43 gene expression, promoter activity, and spatial memory. , 1996, Brain research. Molecular brain research.

[10]  J. L. Stringer,et al.  Is cell death necessary for hippocampal mossy fiber sprouting? , 1997, Epilepsy Research.

[11]  T. Tapiola,et al.  The Calretinin‐containing Mossy Cells Survive Excitotoxic Insult in the Gerbil Dentate Gyrus. Comparison of Excitotoxicity‐induced Neuropathological Changes in the Gerbil and Rat , 1996, The European journal of neuroscience.