Chapter 43 Models for generalized seizures

Supplements to Clinical Neurophysiology

Volumn 57, Issue C, 2004, Pages 415-424

  Holmes, Gregory L ^a  

^a DARTMOUTH MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

4 AMINOBUTYRIC ACID A RECEPTOR; CALCIUM CHANNEL;

ABSENCE; ANIMAL; DISEASE MODEL; GENETICS; HUMAN; MOUSE; MOUSE MUTANT; RAT; RAT STRAIN; REVIEW; SEIZURE;

ANIMALS; CALCIUM CHANNELS; DISEASE MODELS, ANIMAL; EPILEPSY, ABSENCE; HUMANS; MICE; MICE, MUTANT STRAINS; RATS; RATS, MUTANT STRAINS; RECEPTORS, GABA-A; SEIZURES;

EID: 25144499063     PISSN: 1567424X     EISSN: None     Source Type: Book Series    
DOI: 10.1016/S1567-424X(09)70379-4     Document Type: Article

References (49)

1. Barclay J., Balaguero N., Mione M., Ackerman S.L., Letts V.A., Brodbeck J., Canti C., Meir A., Page K.M., Kusumi K., Perez-Reyes E., Lander E.S., Frankel W.N., Gardiner R.M., Dolphin A.C., and Rees M. Ducky mouse phenotype of epilepsy and ataxia is associated with mutations in the Cacna2d2 gene and decreased calcium channel current in cerebellar Purkinje cells. J. Neurosci. 21 (2001) 6095-6104
2. Ben-Ari Y., and Cossart R. Kainate a double agent that generates seizures; two decades of progress. Trends Neurosci. 23 (2001) 580-587
3. Ben-Ari Y., Tremblay E., Richie D.A., Ghilini G., and Naquet R. Electrographic, clinical and pathological alterations following systemic administration of kainic acid, bicuculline or pentetrazole: metabolic mapping using the deoxyglucose method with special reference to the pathology of epilepsy. Neuroscience 6 (1981) 1361-1391
4. Berg A.T., Shinnar S., Levy S.R., and Testa F.M. Newly diagnosed epilepsy in children: presentation at diagnosis. Epilepsia 40 (1999) 445-452
5. Brodbeck J., Davies A., Courtney J.M., Meir A., Balaguero N., Canit C., Moss F.J., Page K.M., Pratt W.S., Hunt S.P., Barclay J., Rees M., and Dolphin A.C. The ducky mutation in Cacna2d2 results inaltered Purkinje cell morphology and is associated with the expression of a truncated alpha 2 delta-2protein with abnormal function. J. Biol. Chem. 277 (2002) 7684-7693
6. 2+ channel beta subunit gene Cchb4 is associated with ataxia and seizures in the lethargic (lh) mouse. Cell 88 (2002) 385-392
7. Cavalheiro E.A., Silva D.F., Turski W.A., Calderazzo-Filho L.S., Bortolotto Z.A., and Turski L. The susceptibility of rats to pilocarpine-induced seizures is age- dependent. Brain Res. 465 (1987) 43-58
8. Cavalheiro E.A., Leite J.P., Bortolotto Z.A., Turski W.A., Ikonomidou C., and Turski L. Long-term effects of pilocarpine in rats: structural damage of the brain triggers kindling and spontaneous recurrent seizures. Epilepsia 32 (1991) 778-782
9. Chen L., Chetkovich D.M., Petralia R.S., Sweeney N.T., Kawasaki Y., Wenthold R.J., Bredt D.S., and Nicoll R.A. Stargazin regulates synaptic targeting of AMPA receptors by two distinct mechanims. Nature 408 (2000) 936-943
10. Coenen A.M., Drinkenburg W.H., Inoue M., and Van Luijtelaar E.L. Genetic models of absence epilepsy, with emphasis on the WAG/Rij strain of rats. Epilepsy Res. 12 (1992) 75-86
11. Coenen A.M., Blezer E.H., and Van Luijtelaar E.L. Effects of the GABA-uptake inhibitor tiagabine on elecetroencephalogram, spike-wave discharges and behaviour of rats. Epilepsy Res. 21 (1995) 89-94
12. Cortez M.A., McKerlie C., and Snead O.C. III A model of atypical absence seizures: EEG, pharmacology, and developmental characterization. Neurology 56 (2001) 341-349
13. Cortez M.A., Cunnane S.C., and Snead O.C. III Brain sterols in the AY-9944 rat model of atypical absence seizures. Epilepsia 43 (2002) 3-8
14. Cox G.A., Lutz C.M., Yang C.L., Biemesderfer D., Bronson R.T., Fu A., Aronson P.S., Noebels J.L., and Frankel W.N. Sodium/hydrogen exchanger gene defect in slow-wave epilepsy mutant mice. Cell 91 (1997) 139-148
15. Crunelli V., and Leresche N. Childhood absence epilepsy: genes, channels, neurons and networks. Nat. Rev. Neurosci. 3 (2002) 371-382
16. Denier C., Ducros A., Vahedi K., Joutel A., Thierry P., Ritz A., Castelnovo G., Deonna T., Gerald P., Devoize J.L., Gayou A., Perrouty B., Soisson T., Autret A., Warter J.M., Vighetto A., Van Bogaert P., Alamowitch S., Roullet E., and Tournier-Lasserve E. High prevalence of CACNA1A truncations and broader clinical spectrum in episodic ataxia type 2. Neurology 52 (1999) 1816-1821
17. Dudek F.E., Hellier J.L., Williams P.A., Ferraro D.J., and Staley K.J. The course of cellular alterations associated with the development of spontaneous seizures after status epilepticus. Prog. Brain Res. 135 (2002) 53-65
18. Fisher R.S. Animal models of the epilepsies. Brain Res. Rev. 14 (1989) 245-278
19. Fletcher C.F., Lutz C.M., O'Sullivan T.N., Shaughnessy Jr. J.D., Hawkes R., Frankel W.N., Copeland N.G., and Jenkins N.A. Absence epilepsy in tottering mutant mice is associated with calcium channel defects. Cell 87 (1996) 607-617
20. Fletcher C.F., Tottene A., Lennon V.A., Wilson S.M., Dubel S.J., Paylor R., Hosford D.A., Tessarollo L., MeEnery N.W., Pietrobon D., Copeland N.G., and Jenkins N.A. Dystonia and cerebellar atrophy in Cacnala null mice lacking P/A calcium channel activity. FASEB 15 (2001) 1288-1290
21. Frankel W.N. Detecting genes in new and old mouse models for epilepsy: a prospectus through the magnifying glass. Epilepsy Res. 36 (1999) 97-110
22. Hauser W.A. Incidence and prevalence. In: Engel Jr. J., and Pedley T.A. (Eds). Epilepsy: A Comprehensive Textbook (1997), Lippincott-Raven, Philadelphia 47-57
23. Hellar A.H., Dichter M.A., and Sidman R.L. Anticonvulsant sensitivity of absence seizures in the tottering mutant mouse. Epilepsia 24 (1983) 25-34
24. Holmes G.L., Gaiarsa J.-L., Chevassus-Au-Louis N., and Ben-Ari Y. Consequences of neonatal seizures in the rat morphological and behavioral effects. Ann. Neurol. 44 (1998) 845-857
25. B receptor activation in absence seizures of lethargic (lh/lh) mice. Science 257 (1992) 398-401
26. Jouvenceau A., Eunson L.H., Spauschus A., Ramesh V., Zuberi S.M., Kullmann D.M., and Hanna M.G. Human epilepsy associated with dysfunction of the brain P/Q-type calcium channel. Lancet 358 (2001) 801-807
27. Jun K., Piedras-Renteria E.S., Smith S.M., Wheeler D.B., Lee S.B., Lee T.G., Chin H., Adams M.E., Scheller R.H., Tsien R.W., and Shin H.S. Ablation of P/Q type Ca(2+) channel currents, altered synaptic transmission, and progressive ataxia in mice lacking the alpha (1A)-subunit. Proc. Nat. Acad. Sci. USA 96 (1999) 15245-15250
28. Levitt P., and Noebels J.L. Mutant mouse tottering: selective increase of locus ceruleus axons in a defined single-locus mutation. Proc. Natl. Acad. Sci. USA 78 (1981) 4630-4634
29. B neurotransmission in the control of abscence seizures in the rat. Neuroscience 48 (1992) 87-93
30. Marescaux C., Vergnes M., and Depaulis A. Genetic absence epilepsy in rats from Strabourg - a review. J. Nerual Transm. 35 Suppl. (1992) 37-69
31. Meeren H.K.M., Pijn J.P.M., Van Luijtelaar E.L.J.M., Coenen A.M.L., and Lopes da Silva F.H. Cortical focus drives widespread corticothalamic networks during spontaneous absence seizures in rats. J. Neurosci. 22 (2002) 1480-1495
32. Nadler J.V. Kainic acid as a tool for the study of temporal lobe epilepsy. Life Sci. 29 (1981) 2031-2042
33. Noebels J.L., and Sidman R.L. Inherited epilepsy: spike-wave and focal motor seizures in the mutant mouse tottering. Science 204 (1979) 1334-1336
34. 2+ channel gene CACNLlA4. Cell 87 (1996) 543-552
35. Persad V., Cortez M.A., and Snead O.C. III A chronic modelof atypical absence seizures: studies of development and gender sensitivity. Epielpsy Res. 48 (2002) 111-119
36. Sarkisian M.R. Overview of the current animal models for human seizure and epileptic disorders. Epilepsy Behav. 2 (2001) 201-216
37. Silveira D.C., Sogawa Y., and Holmes G.L. The expression of Fos following kainic acid-induced seizures is age- dependent. Eur. J. Neurosci. 15 (2002) 329-344
38. Snead O.C. III Basic mechanisms of generalized absence seizures. Ann. Neurol. 37 (1995) 146-157
39. Song I., Kim D., Jun K., and Shin H.S. Role of T-type calcium channels in the genesis of absence seizure in the mutant mice for α1A, the pore-forming subunit of the P/Q-type calcium channel. Soc. Neurosci. Abstr. 27 (2001) 121-151
40. Sperber E.F., Haas K.Z., Romero M.T., and Stanton P.K. Flurothyl status epilepticus in developing rats: behavioral, electographic, histological and electrophysiological studies. Develop. Brain Res. 116 (1999) 59-68
41. Stafstrom C.E., and Holmes G.L. Infantile spasms: criteria for an animal model. Int. Rev. Neurobiol. 49 (2002) 391-411
42. Stafstrom C.E., Thompson J.L., and Holmes G.L. Kainic acid seizures in the developing brain: status epilepticus and spontaneous recurrent seizures. Dev. Brain Res. 65 (1992) 227-236
43. Tremblay E., Represa A., and Ben-Ari Y. Autoradiographic localization of kainic acid binding sites in the human hippocampus. Brain Res. 343 (1985) 378-382
44. Tsakiridou E., Bertollini L., DeCurtis M., Avanzini G., and Pape H.-C. Selective increase in T-type calcium conductance of reticular thalamic neurons in a rat model of absence epilepsy. J. Neurosci. 15 (1995) 3110-3117
45. Villeneuve N., Ben-Ari Y., Holmes G.L., and Gaiarsa J.-L. Neonatal seizures induced persistent changes in intrinsic properties of CA1 rat hippocampal cells. Ann. Neurol. 47 (2000) 729-738
46. Wallace R.H., Marini C., Petrou S., Harkin L.A., Bowser D.N., Panchal R.G., Williams D.A., Sutherland G.R., Mulley J.C., Scheffer I.E., and Berkovic S.F. Mutant GABA(A) receptor gamma2-subunit in childhood absence epilepsy and febrile seizures. Nat. Genet. (2001) 49-52
47. White H.S., Woodhead J.H., Wilcox K.S., Stables J.P., Kupferberg H.J., and Wolf H.H. Discovery and preclinical development of antiepileptic drugs. In: Levy R.H., Mattson R.H., Meldrum B.S., and Perucca E. (Eds). Antiepileptic Drugs, 5th edn. (2002), Lippincott Williams and Williams, Philadephia 36-48
48. Wong M., Wozniak D.F., and Yamada K.A. An animal model of generalized nonconvulsive sttus epilepticus: immediate characteristics and long-term effects. Exp. Neurol. 183 (2003) 87-99
49. Zhang Y., and Noebels J.L. Altered calcium currents in thalamocortical relay cells of mouse absence models with mutations of α1A and β4 caclium channel subunits. Soc. Neurosci. Abstr. 27 (2002) 116-151