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Unilateral hippocampal CA3-predominant damage and short latency epileptogenesis after intra-amygdala microinjection of kainic acid in mice

Mouri, Genshin, Jimenez-Mateos, Eva, Engel, Tobias, Dunleavy, Mark, Hatazaki, Seiji, Paucard, Alexia, Matsushima, Satoshi, Taki, Waro, Henshall, David C.·2008·Brain Research
DOI 10.1016/j.brainres.2008.03.061
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Abstract

Mesial temporal lobe epilepsy is the most common, intractable seizure disorder in adults. It is associated with an asymmetric pattern of hippocampal neuron loss within the endfolium (hilus and CA3) and CA1, with limited pathology in extra-hippocampal regions. We previously developed a model of focally-evoked seizure-induced neuronal death using intra-amygdala kainic acid (KA) microinjection and characterized the acute hippocampal pathology. Here, we sought to characterize the full extent of hippocampal and potential extra-hippocampal damage in this model, and the temporal onset of epileptic seizures. Seizure damage assessed at four stereotaxic levels by FluoroJade B staining was most prominent in ipsilateral hippocampal CA3 where it extended from septal to temporal pole. Minor but significant neuronal injury was present in ipsilateral CA1. Extra-hippocampal neuronal damage was generally limited in extent and restricted to the lateral septal nucleus, injected amygdala and select regions of neocortex ipsilateral to the seizure elicitation side. Continuous surface EEG recorded with implanted telemetry units in freely-moving mice detected spontaneous, epileptic seizures by five days post-KA in all mice. Epileptic seizure number averaged 1-4 per day. Hippocampi from epileptic mice 15 days post-KA displayed unilateral CA3 lesions, astrogliosis and increased neuropeptide Y immunoreactivity suggestive of mossy fiber rearrangement. These studies characterize a mouse model of unilatera…

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Research works printed but not linked: 60

  1. Araki, 2002, Characterization of neuronal death induced by focally evoked limbic seizures in the C57BL/6 mouse, J. Neurosci. Res., 69, 614, 10.1002/jnr.10356 · DOI
  2. Baraban, 1997, Knock-out mice reveal a critical antiepileptic role for neuropeptide Y, J. Neurosci., 17, 8927, 10.1523/JNEUROSCI.17-23-08927.1997 · DOI
  3. Ben-Ari, 1980, Injections of kainic acid into the amygdaloid complex of the rat: an electrographic, clinical and histological study in relation to the pathology of epilepsy, Neuroscience, 5, 515, 10.1016/0306-4522(80)90049-4 · DOI
  4. Borges, 2003, Neuronal and glial pathological changes during epileptogenesis in the mouse pilocarpine model, Exp. Neurol., 182, 21, 10.1016/S0014-4886(03)00086-4 · DOI
  5. Bothwell, 2001, Neuronal hypertrophy in the neocortex of patients with temporal lobe epilepsy, J. Neurosci., 21, 4789, 10.1523/JNEUROSCI.21-13-04789.2001 · DOI
  6. Brandt, 2003, N-methyl-d-aspartate receptor blockade after status epilepticus protects against limbic brain damage but not against epilepsy in kainate model of temporal lobe epilepsy, Neuroscience, 118, 727, 10.1016/S0306-4522(03)00027-7 · DOI
  7. Chang, 2003, Epilepsy, N. Engl. J. Med., 349, 1257, 10.1056/NEJMra022308 · DOI
  8. Dawodu, 2005, Quantitative neuropathology of the entorhinal cortex region in patients with hippocampal sclerosis and temporal lobe epilepsy, Epilepsia, 46, 23, 10.1111/j.0013-9580.2005.21804.x · DOI
  9. DeGiorgio, 1992, Hippocampal pyramidal cell loss in human status epilepticus, Epilepsia, 33, 23, 10.1111/j.1528-1157.1992.tb02278.x · DOI
  10. Doherty, 2003, Rapid stereological quantitation of temporal neocortex in TLE, Magn. Reson. Imaging, 21, 511, 10.1016/S0730-725X(03)00078-X · DOI
  11. Du, 1993, Preferential neuronal loss in layer III of the entorhinal cortex in patients with temporal lobe epilepsy, Epilepsy Res., 16, 223, 10.1016/0920-1211(93)90083-J · DOI
  12. Dudek, 1994, Functional significance of hippocampal plasticity in epileptic brain: electrophysiological changes of the dentate granule cells associated with mossy fiber sprouting, Hippocampus, 4, 259, 10.1002/hipo.450040306 · DOI
  13. Engel, 2001, Mesial temporal lobe epilepsy: what have we learned?, Neuroscientist, 7, 340, 10.1177/107385840100700410 · DOI
  14. Fariello, 1989, Potentiation of kainic acid epileptogenicity and sparing from neuronal damage by an NMDA receptor antagonist, Epilepsy Res., 3, 206, 10.1016/0920-1211(89)90025-9 · DOI
  15. Fujikawa, 2000, Status epilepticus-induced neuronal loss in humans without systemic complications or epilepsy, Epilepsia, 41, 981, 10.1111/j.1528-1157.2000.tb00283.x · DOI
  16. Gouder, 2003, Seizure suppression by adenosine A1 receptor activation in a mouse model of pharmacoresistant epilepsy, Epilepsia, 44, 877, 10.1046/j.1528-1157.2003.03603.x · DOI
  17. Harvey, 2005, Hippocampal granule cell activity and c-Fos expression during spontaneous seizures in awake, chronically epileptic, pilocarpine-treated rats: implications for hippocampal epileptogenesis, J. Comp. Neurol., 488, 442, 10.1002/cne.20594 · DOI
  18. Hendriksen, 2001, Altered hippocampal gene expression prior to the onset of spontaneous seizures in the rat post-status epilepticus model, Eur. J. Neurosci., 14, 1475, 10.1046/j.0953-816x.2001.01778.x · DOI
  19. Henshall, 2002, Activation of Bcl-2-associated death protein and counter-response of Akt within cell populations during seizure-induced neuronal death, J. Neurosci., 22, 8458, 10.1523/JNEUROSCI.22-19-08458.2002 · DOI
  20. Henshall, 2000, Spatio-temporal profile of DNA fragmentation and its relationship to patterns of epileptiform activity following focally evoked limbic seizures, Brain Res., 858, 290, 10.1016/S0006-8993(99)02452-X · DOI
  21. Hudson, 1993, Amygdaloid sclerosis in temporal lobe epilepsy, Ann. Neurol., 33, 622, 10.1002/ana.410330611 · DOI
  22. Kasugai, 2007, Differences in two mice strains on kainic acid-induced amygdalar seizures, Biochem. Biophys. Res. Commun., 357, 1078, 10.1016/j.bbrc.2007.04.067 · DOI
  23. Kienzler, 2006, Excitotoxic hippocampal neuron loss following sustained electrical stimulation of the perforant pathway in the mouse, Brain Res., 1085, 195, 10.1016/j.brainres.2006.02.055 · DOI
  24. Klitgaard, 2002, Pilocarpine-induced epileptogenesis in the rat: impact of initial duration of status epilepticus on electrophysiological and neuropathological alterations, Epilepsy Res., 51, 93, 10.1016/S0920-1211(02)00099-2 · DOI
  25. Kubova, 2001, Status epilepticus causes necrotic damage in the mediodorsal nucleus of the thalamus in immature rats, J. Neurosci., 21, 3593, 10.1523/JNEUROSCI.21-10-03593.2001 · DOI
  26. Li, 2008, Adenosine kinase is a target for the prediction and prevention of epileptogenesis in mice, J. Clin. Invest., 118, 571
  27. Liu, 1999, Substance P is expressed in hippocampal principal neurons during status epilepticus and plays a critical role in the maintenance of status epilepticus, Proc. Natl. Acad. Sci. U. S. A., 96, 5286, 10.1073/pnas.96.9.5286 · DOI
  28. Meldrum, 2002, Implications for neuroprotective treatments, Prog. Brain Res., 135, 487, 10.1016/S0079-6123(02)35046-5 · DOI
  29. Menini, 1980, Sustained limbic seizures induced by intraamygdaloid kainic acid in the baboon: symptomatology and neuropathological consequences, Ann. Neurol., 8, 501, 10.1002/ana.410080507 · DOI
  30. Morimoto, 2004, Kindling and status epilepticus models of epilepsy: rewiring the brain, Prog. Neurobiol., 73, 1, 10.1016/j.pneurobio.2004.03.009 · DOI
  31. Murphy, 2007, Bcl-w protects hippocampus during experimental status epilepticus, Am. J. Pathol., 171, 1258, 10.2353/ajpath.2007.070269 · DOI
  32. Narkilahti, 2003, Administration of caspase 3 inhibitor during and after status epilepticus in rat: effect on neuronal damage and epileptogenesis, Neuropharmacology, 44, 1068, 10.1016/S0028-3908(03)00115-1 · DOI
  33. Nissinen, 2000, A new model of chronic temporal lobe epilepsy induced by electrical stimulation of the amygdala in rat, Epilepsy Res., 38, 177, 10.1016/S0920-1211(99)00088-1 · DOI
  34. Nissinen, 2001, Is mossy fiber sprouting present at the time of the first spontaneous seizures in rat experimental temporal lobe epilepsy?, Hippocampus, 11, 299, 10.1002/hipo.1044 · DOI
  35. Parent, 1997, Dentate granule cell neurogenesis is increased by seizures and contributes to aberrant network reorganization in the adult rat hippocampus, J. Neurosci., 17, 3727, 10.1523/JNEUROSCI.17-10-03727.1997 · DOI
  36. Pitkanen, 1998, Amygdala damage in experimental and human temporal lobe epilepsy, Epilepsy Res., 32, 233, 10.1016/S0920-1211(98)00055-2 · DOI
  37. Pitkanen, 2005, Administration of diazepam during status epilepticus reduces development and severity of epilepsy in rat, Epilepsy Res., 63, 27, 10.1016/j.eplepsyres.2004.10.003 · DOI
  38. Pitkanen, 2007, Epileptogenesis in experimental models, Epilepsia, 48, 13, 10.1111/j.1528-1167.2007.01063.x · DOI
  39. Richichi, 2004, Anticonvulsant and antiepileptogenic effects mediated by adeno-associated virus vector neuropeptide Y expression in the rat hippocampus, J. Neurosci., 24, 3051, 10.1523/JNEUROSCI.4056-03.2004 · DOI
  40. Schauwecker, 1997, Genetic determinants of susceptibility to excitotoxic cell death: implications for gene targeting approaches, Proc. Natl. Acad. Sci. U. S. A., 94, 4103, 10.1073/pnas.94.8.4103 · DOI
  41. Schwarzer, 1995, Somatostatin, neuropeptide Y, neurokinin B and cholecystokinin immunoreactivity in two chronic models of temporal lobe epilepsy, Neuroscience, 69, 831, 10.1016/0306-4522(95)00268-N · DOI
  42. Shinoda, 2004, Development of a model of seizure-induced hippocampal injury with features of programmed cell death in the BALB/c mouse, J. Neurosci. Res., 76, 121, 10.1002/jnr.20064 · DOI
  43. Shinoda, 2004, Bim regulation may determine hippocampal vulnerability after injurious seizures and in temporal lobe epilepsy, J. Clin. Invest., 113, 1059, 10.1172/JCI200419971 · DOI
  44. Sloviter, 1983, "Epileptic" brain damage in rats induced by sustained electrical stimulation of the perforant path. I. Acute electrophysiological and light microscopic studies, Brain Res. Bull., 10, 675, 10.1016/0361-9230(83)90037-0 · DOI
  45. Sloviter, 2005, The neurobiology of temporal lobe epilepsy: too much information, not enough knowledge, C. R. Biol., 328, 143, 10.1016/j.crvi.2004.10.010 · DOI
  46. Sloviter, 2007, On the relevance of prolonged convulsive status epilepticus in animals to the etiology and neurobiology of human temporal lobe epilepsy, Epilepsia, 48, 6, 10.1111/j.1528-1167.2007.01335.x · DOI
  47. Tanaka, 1985, Spontaneous secondarily generalized seizures induced by a single microinjection of kainic acid into unilateral amygdala in cats, Electroencephalogr. Clin. Neurophysiol., 61, 422, 10.1016/0013-4694(85)91034-X · DOI
  48. Tanaka, 1988, Long-term observation of rats after unilateral intra-amygdaloid injection of kainic acid, Brain Res., 463, 163, 10.1016/0006-8993(88)90541-0 · DOI
  49. Tu, 2005, Spontaneous release of neuropeptide Y tonically inhibits recurrent mossy fiber synaptic transmission in epileptic brain, J. Neurosci., 25, 1718, 10.1523/JNEUROSCI.4835-04.2005 · DOI
  50. Tuunanen, 1999, Status epilepticus-induced neuronal damage in the rat amygdaloid complex: distribution, time-course and mechanisms, Neuroscience, 94, 473, 10.1016/S0306-4522(99)00251-1 · DOI
  51. Vezzani, 1994, Enhanced neuropeptide Y release in the hippocampus is associated with chronic seizure susceptibility in kainic acid treated rats, Brain Res., 660, 138, 10.1016/0006-8993(94)90847-8 · DOI
  52. Vezzani, 1996, Functional changes in somatostatin and neuropeptide Y containing neurons in the rat hippocampus in chronic models of limbic seizures, Epilepsy Res., 26, 267, 10.1016/S0920-1211(96)00059-9 · DOI
  53. Vezzani, 1999, Interleukin-1beta immunoreactivity and microglia are enhanced in the rat hippocampus by focal kainate application: functional evidence for enhancement of electrographic seizures, J. Neurosci., 19, 5054, 10.1523/JNEUROSCI.19-12-05054.1999 · DOI
  54. Vezzani, 2002, Seizure susceptibility and epileptogenesis are decreased in transgenic rats overexpressing neuropeptide Y, Neuroscience, 110, 237, 10.1016/S0306-4522(01)00581-4 · DOI
  55. Weiergraber, 2005, Electrocorticographic and deep intracerebral EEG recording in mice using a telemetry system, Brain Res. Brain Res. Protoc., 14, 154, 10.1016/j.brainresprot.2004.12.006 · DOI
  56. Williams, 2002, Reassessment of the effects of cycloheximide on mossy fiber sprouting and epileptogenesis in the pilocarpine model of temporal lobe epilepsy, J. Neurophysiol., 88, 2075, 10.1152/jn.2002.88.4.2075 · DOI
  57. Williams, 2007, Development of spontaneous seizures after experimental status epilepticus: implications for understanding epileptogenesis, Epilepsia, 48, 157, 10.1111/j.1528-1167.2007.01304.x · DOI
  58. Woldbye, 1997, Powerful inhibition of kainic acid seizures by neuropeptide Y via Y5-like receptors, Nat. Med., 3, 761, 10.1038/nm0797-761 · DOI
  59. Wuarin, 1996, Electrographic seizures and new recurrent excitatory circuits in the dentate gyrus of hippocampal slices from kainate-treated epileptic rats, J. Neurosci., 16, 4438, 10.1523/JNEUROSCI.16-14-04438.1996 · DOI
  60. Zappone, 2004, Translamellar disinhibition in the rat hippocampal dentate gyrus after seizure-induced degeneration of vulnerable hilar neurons, J. Neurosci., 24, 853, 10.1523/JNEUROSCI.1619-03.2004 · DOI

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Metadata

Authors
Mouri, G., Jimenez-Mateos, E., Engel, T., Dunleavy, M., Hatazaki, S., Paucard, A., Matsushima, S., Taki, W., & Henshall, D. C.
Venue
Brain Research
Publisher
Elsevier BV
Published
2008-06
Volume
1213
Pages
140-151
ISSN
0006-8993
DOI
10.1016/j.brainres.2008.03.061
Cited by
139
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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