Generalized Epileptic Disorders: An Update
Massimo Avoli,
Michael A. Rogawski,
Giuliano Avanzini,
Massimo Avoli
Montreal Neurological Institute and Departments of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada;
Search for more papers by this authorMichael A. Rogawski
Epilepsy Research Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.; and
Search for more papers by this authorGiuliano Avanzini
Istituto Nazionale Neurologico C. Besta, Milan, Italy
Search for more papers by this authorMassimo Avoli,
Michael A. Rogawski,
Giuliano Avanzini,
Massimo Avoli
Montreal Neurological Institute and Departments of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada;
Search for more papers by this authorMichael A. Rogawski
Epilepsy Research Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, U.S.A.; and
Search for more papers by this authorGiuliano Avanzini
Istituto Nazionale Neurologico C. Besta, Milan, Italy
Search for more papers by this authorAddress correspondence and research requests to Dr. M. Avoli at 3801 University Street, Montreal, Quebec, H3A 2B4, Canada. E-mail: [email protected]

REFERENCES
- 1
ILAE Commission on Classification and Terminology. Proposal for revised clinical and electroencephalographic classification of epileptic seizures.
Epilepsia
1981; 22: 489–501.
10.1111/j.1528-1157.1981.tb06159.x Google Scholar
- 2 Rogawski MA. KCNQ2/KCNQ3 K+ channels and the molecular pathogenesis of epilepsy: implications for therapy. Trends Neurosci 2000; 23: 393–8.DOI: 10.1016/s0166-2236(00)01629-5
- 3 Steinlein OK & Noebels JL. Ion channels and epilepsy in man and mouse. Curr Opin Genet Dev 2000; 10: 286–91.DOI: 10.1016/s0959-437x(00)00079-4
- 4 ILAE Commission on Classification and Terminology. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989; 301: 389–99.
- 5 Shoffner JM, Lott MT, Lezza AM, et al. Myoclonic epilepsy and ragged-red fiber disease (MERRF) is associated with a mitochondrial DNA tRNA(Lys) mutation. Cell 1990; 61: 931–7.
- 6 Reiner O, Carrozzo R, Shen Y, et al. Isolation of a Miller-Dieker lissencephaly gene containing G protein β-subunit-like repeats. Nature 1993; 364: 717–21.
- 7 Hattori M, Adachi H, Tsujimoto M, et al. Miller-Dieker lissencephaly gene encodes a subunit of brain platelet-activating factor acetylhydrolase. Nature 1994; 370: 216–8.
- 8 Pennacchio LA, Lehesjoki AE, Stone NE, et al. Mutations in the gene encoding cystatin B in progressive myoclonus epilepsy. Science 1996; 271: 1731–4.
- 9 Lehesjoki AE & Koskiniemi M. Progressive myoclonus epilepsy of Unverricht-Lundborg type. Epilepsia 1999; 40(suppl 3): 23–8.
- 10 Serratosa JM, Gardiner RM, Lehesjoki AE, et al. The molecular genetic bases of the progressive myoclonus epilepsies. Adv Neurol 1999; 79: 383–98.
- 11 Pennacchio LA, Bouley DM, Higgins KM, et al. Progressive ataxia, myoclonic epilepsy and cerebellar apoptosis in cystatin B-deficient mice. Nat Genet 1998; 20: 251–8.DOI: 10.1038/3059
- 12 Minassian BA, Lee JR, Herbrick JA, et al. Mutations in a gene encoding a novel protein tyrosine phosphatase cause progressive myoclonus epilepsy. Nat Genet 1998; 20: 171–4.DOI: 10.1038/2470
- 13 Serratosa JM, Gomez-Garre P, Gallardo ME, et al. A novel protein tyrosine phosphatase gene is mutated in progressive myoclonus epilepsy of the Lafora type (EPM2). Hum Mol Genet 1999; 8: 345–52.DOI: 10.1093/hmg/8.2.345
- 14
Mole SE,
Mitchison HM,
Munroe PB.
Molecular basis of the neuronal ceroid lipofuscinoses: mutations in CLN1, CLN2, CLN3, and CLN5.
Hum Mutat
1999; 14: 199–215.DOI: 10.1002/(sici)1098-1004(1999)14:3<199::aid-humu3>3.0.co;2-a
10.1002/(sici)1098-1004(1999)14:3<199::aid-humu3>3.0.co;2-a CAS PubMed Web of Science® Google Scholar
- 15 Mole S & Gardiner M. Molecular genetics of the neuronal ceroid lipofuscinoses. Epilepsia 1999; 40(suppl 3): 29–32.
- 16 Bennett MJ & Hofmann SL. The neuronal ceroid-lipofuscinoses (Batten disease): a new class of lysosomal storage diseases. J Inherit Metab Dis 1999; 22: 535–44.
- 17 Jiang Y, Lev-Lehman E, Bressler J, et al. Genetics of Angelman syndrome. Am J Hum Genet 1999; 65: 1–6.DOI: 10.1086/302473
- 18 DeLorey TM & Olsen RW. GABA and epileptogenesis: comparing BABRB3 gene-deficient mice with Angelman syndrome in man. Epilepsy Res 1999; 36: 123–32.DOI: 10.1016/s0920-1211(99)00046-7
- 19 Minassian BA, DeLorey TM, Olsen RW, et al. Angelman syndrome: correlations between epilepsy phenotypes and genotypes. Ann Neurol 1998; 43: 485–93.
- 20 DeLorey TM, Handforth A, Homanics GE, et al. Mice lacking the β3 subunit of the GABAA receptor have the epilepsy phenotype and many of the behavioral characteristics of Angelman syndrome. J Neurosci 1998; 18: 8505–14.
- 21 Lehmann-Horn F & Jurkat-Rott K. Voltage-gated ion channels and hereditary disease. Physiol Rev 1999; 79: 1317–72.
- 22 Lennox WG & Lennox MA. Epilepsy and related disorders. Boston: Little, Brown, 1960.
- 23 Cargill M, Altshuler D, Ireland J, et al. Characterization of single-nucleotide polymorphisms in coding regions of human genes. Nat Genet 1999; 22: 231–8.DOI: 10.1038/10290
- 24 Leppert MF & Singh N. Benign familial neonatal epilepsy with mutations in two potassium channel genes. Curr Opin Neurol 1999; 12: 143–7.DOI: 10.1006/csla.1998.0044
- 25 Biervert C, Schroeder BC, Kubisch C, et al. A potassium channel mutation in neonatal human epilepsy. Science 1998; 279: 403–6.DOI: 10.1126/science.279.5349.403
- 26 Charlier C, Singh NA, Ryan SG, et al. A pore mutation in a novel KQT-like potassium channel gene in an idiopathic epilepsy family. Nat Genet 1998; 18: 53–5.
- 27 Schroeder BC, Kubisch C, Stein V, Jentsch TJ. Moderate loss of function of cyclic-AMP-modulated KCNQ2/KCNQ3 K+ channels causes epilepsy. Nature 1998; 396: 687–90.DOI: 10.1038/25367
- 28 Leppert MF & Singh N. Susceptibility genes in human epilepsy. Semin Neurol 1999; 19: 397–405.
- 29 Biervert C & Steinlein OK. Structural and mutational analysis of KCNQ2, the major gene locus for benign familial neonatal convulsions. Hum Genet 1999; 104: 234–40.DOI: 10.1007/s004390050941
- 30 Wang HS, Pan Z, Shi W, et al. KCNQ2 and KCNQ3 potassium channel subunits: molecular correlates of the M-channel. Science 1998; 282: 1890–3.
- 31 Selyanko AA, Hadley JK, Wood IC, et al. Two types of K+ channel subunit, Erg1 and KCNQ2/3, contribute to the M-like current in a mammalian neuronal cell. J Neurosci 1999; 19: 7742–56.
- 32 Brown DA. M-currents. In: T Narahashi, ed. Ion channels. Vol 1. New York: Plenum, 1998: 55–94.
- 33
Wallace RH,
Wang DW,
Singh R, et al. Febrile seizures and generalized epilepsy associated with a mutation in the Na+-channel β1 subunit gene SCN1B.
Nat Genet
1998; 19: 366–70.DOI: 10.1038/1252
10.1038/1252 Google Scholar
- 34 Escayg A, MacDonald BT, Meisler MH, et al. Mutations of SCN1A, encoding a neuronal sodium channel, in two families with GEFS+2. Nat Genet 2000; 24: 343–5.DOI: 10.1038/74159
- 35 Mantegazza M, Franceschetti S, Avanzini G. Anemone toxin (ATX II) induced increase in persistent sodium current: effects on the firing properties of neocortical pyramidal neurones. J Physiol 1998; 507: 105–16.
- 36 Steinlein OK, Stoodt J, Biervert C, et al. The voltage gated potassium channel KCNQ2 and idiopathic generalized epilepsy. Neuroreport 1999; 10: 1163–6.
- 37 Coetzee WA, Amarillo Y, Chiu J, et al. Molecular diversity of K+ channels. Ann N Y Acad Sci 1999; 868: 233–85.
- 38 Juhng KN, Kokate TG, Yamaguchi S, et al. Induction of seizures by the potent K+ channel-blocking scorpion venom peptide toxins tityustoxin-Kα and pandinustoxin-Kα. Epilepsy Res 1999; 34: 177–86.DOI: 10.1016/s0920-1211(98)00111-9
- 39 Signorini S, Liao YJ, Duncan SA, et al. Normal cerebellar development but susceptibility to seizures in mice lacking G protein-coupled, inwardly rectifying K+ channel GIRK2. Proc Natl Acad Sci U S A 1997; 94: 923–7.DOI: 10.1073/pnas.94.3.923
- 40 Smart SL, Lopantsev V, Zhang CL, et al. Deletion of the KV1.1 potassium channel causes epilepsy in mice. Neuron 1998; 20: 809–19.
- 41 Zuberi SM, Eunson LH, Spauschus A, et al. A novel mutation in the human voltage-gated potassium channel gene (Kv1.1) associates with episodic ataxia type 1 and sometimes with partial epilepsy. Brain 1999; 122: 817–25.DOI: 10.1093/brain/122.5.817
- 42
Gibbs FA,
Gibbs EL,
Lennox WG.
The electroencephalogram in epilepsy and in conditions of impaired consciousness.
Arch Neurol Psychiatry
1935; 34: 1135–48.
10.1001/archneurpsyc.1935.02250240002001 Google Scholar
- 43 Jasper H & Droogleever-Fortuyn J. Experimental studies on the functional anatomy of petit mal epilepsy. Res Publ Assoc Res Nerv Ment Dis 1946; 26: 272–98.
- 44 Marcus EM & Watson CW. Bilateral synchronous spike wave electrographic patterns in the cat: interaction of bilateral cortical foci in the intact, the bilateral cortical-callosal, and a diencephalic preparation. Arch Neurol 1966; 14: 601–10.
- 45 Marcus EM & Watson CW. Symmetrical epileptogenic foci in monkey cerebral cortex: mechanisms of interaction and regional variations in capacity for synchronous discharges. Arch Neurol 1968; 19: 99–116.
- 46 Menini C & Naquet R. Les myoclonies: des myoclonies du Papio papio a certaines myoclonies humaines. Rev Neurol (Paris) 1986; 142: 3–28.
- 47
Naquet R,
Menini C,
Catier J.
Photically-induced epilepsy in Papio papio: the initiation of discharges and the role of the frontal cortex and of the corpus callosum. In: MAB Brazier,
H Petsche, eds. Synchronization of the EEG in the epilepsies. Vienna: Springer, 1972: 347–67.
10.1007/978-3-7091-8306-9_22 Google Scholar
- 48 Gloor P. Generalized cortico-reticular epilepsies: some considerations on the pathophysiology of generalized bilaterally synchronous spike and wave discharge. Epilepia 1968; 9: 249–63.
- 49 Gloor P. Neurophysiological bases of generalized seizures termed centrencephalic. In: H Gastaut, H Jasper, J Bancaud, et al., eds. The physiopathogenesis of the epilepsies. Springfield, IL: Charles C Thomas, 1969: 209–36.
- 50 Fisher RS & Prince DA. Spike-wave rhythms in cat cortex induced by parenteral penicillin. I. Electroencephalographic features. Electroencephalogr Clin Neurophysiol 1977; 42: 608–24.
- 51 Fisher RS & Prince DA. Spike-wave rhythms in cat cortex induced by parenteral penicillin. II. Cellular features. Electroencephalogr Clin Neurophysiol 1977; 42: 625–39.
- 52
Avoli M,
Gloor P,
Kostopoulos G, et al. Generalized epilepsy: neurobiological approaches. Boston: Birkhauser, 1990.
10.1007/978-1-4684-6767-3 Google Scholar
- 53 Avoli M, White HS, Zona C, et al. D. Sites of action for conventional and newer anti-epileptic drugs; focus on valproate, lamotrigine and topiramate. In: G Avanzini, G Regesta, P Tanganelli, M Avoli, eds. Models of epileptic disorders: molecular and cellular targets for anti-epileptic drugs. London: John Libbey, 1997: 199–205.
- 54 Danober L, Deransart C, Deapulis A, et al. Pathophysiological mechanisms of genetic absence epilepsy in the rat. Progr Neurobiol 1998; 55: 27–57.
- 55 Seidenbecher T, Staak R, Pape H-C. Relations between cortical and thalamic cellular activities during absence seizures in rats. Eur J Neurosci 1998; 10: 1103–12.DOI: 10.1046/j.1460-9568.1998.00123.x
- 56 Inoue M, Van Luijtelaar ELJM, Vossen JMH, et al. Visual evoked potentials during spontaneously occurring spike-wave discharges in rats. Electroencephalogr Clin Neurophysiol 1992; 84: 172–9.
- 57 Kellaway P. Sleep and epilepsy. Epilepsia 1985; 26: S15–30.
- 58 Gloor P, Avoli M, Kostopoulos G. Thalamocortical relationships in generalized epilepsy with bilaterally synchronous spike-and-wave discharge. In: M Avoli, P Gloor, G Kostopoulos, R Naquet, eds. Generalized epilepsy: neurobiological approaches. Boston: Birkhauser, 1990: 190–212.
- 59 Avoli M. Mechanisms of generalized spike-wave epilepsy. In: RJ Porter, D Chadwick, eds. The epilepsies II. Boston: Butterworth-Heinemann, 1997: 31–48.
- 60 Avoli M & Gloor P. The effects of transient functional depression of the thalamus on spindles and on bilateral synchronous epileptic discharges of feline generalized penicillin epilepsy. Epilepsia 1981; 22: 443–52.
- 61 Avoli M & Gloor P. Role of the thalamus in generalized penicillin epilepsy: observations on decorticated cats. Exp Neurol 1982; 77: 386–402.
- 62 Avoli M & Gloor P. Interaction of cortex and thalamus in spike and wave discharges of feline generalized penicillin epilepsy. Exp Neurol 1982; 76: 196–217.
- 63 Buzsaki G, Laszlovski I, Lajthma A, et al. Spike-and-wave neocortical patterns in rats: genetic and aminergic control. Neuroscience 1990; 38: 323–33.
- 64 Kandel A & Buzsaki G. Cellular-synaptic generation of sleep spindles, spike-and-wave discharges, and evoked thalamocortical responses in the neocortex of the rat. J Neurosci 1997; 17: 6783–97.
- 65 Avoli M, Gloor P, Kostopoulos G, et al. An analysis of penicillin-induced generalized spike and wave discharges using simultaneous recording of cortical and thalamic single units. J Neurophysiol 1983; 50: 819–37.
- 66 McLachlan RS, Avoli M, Gloor P. Transition from spindles to generalized spike and wave discharges in the cat: simultaneous single-cell recordings in cortex and thalamus. Exp Neurol 1984; 85: 413–25.
- 67 McLachlan RS, Gloor P, Avoli M. Differential participation of some 'specific' and 'non-specific' thalamic nuclei in generalized spike and wave discharges of feline generalized penicillin epilepsy. Brain Res 1984; 307: 277–87.
- 68 Inoue M, Duysens J, Vossen JM, et al. Thalamic multiple-unit activity underlying spike-wave discharges in anesthetized rats. Brain Res 1993; 612: 35–40.
- 69 Pinault D, Leresche N, Charpier S, et al. Intracellular recordings in thalamic neurones during spontaneous spike and wave discharges in rats with absence epilepsy. J Physiol (Lond) 1998; 509: 449–56.
- 70 Charpier S, Leresche N, Deniau JM, et al. On the putative contribution of GABAB receptors to the electrical events occurring during spontaneous spike and wave discharges. Neuropharmacology 1999; 38: 1699–706.DOI: 10.1016/s0028-3908(99)00139-2
- 71 Steriade M, McCormick DA, Sejnowski TJ. Thalamocortical oscillations in the sleeping and aroused brain. Science 1993; 262: 679–85.
- 72 Steriade M, Deschenes M, Domich L, et al. Abolition of spindle oscillations in thalamic neurons disconnected from nucleus reticularis thalami. J Neurophysiol 1985; 54: 1473–97.
- 73 Steriade M, Domich M, Oakson G. The deafferented RT nucleus generates spindle rhythmicity. J Neurophysiol 1987; 57: 260–73.
- 74 Avanzini G, De Curtis M, Franceschetti S, et al. Cortical versus thalamic mechanisms underlying spike and wave discharges in GAERS. Epilepsy Res 1996; 26: 37–44.DOI: 10.1016/s0920-1211(96)00037-x
- 75 Tsakiridou E, Bertolloni L, De Curtis M, et al. Selective increase in T-type calcium conductance of reticular thalamic neurons in a rat model of absence epilepsy. J Neurosci 1995; 15: 3110–7.
- 76 Jahnsen H & Llinas R. Electrophysiological properties of guinea-pig thalamic neurones: an in vitro study. J Physiol (Lond) 1984; 349: 205–26.
- 77 Jahnsen H & Llinas R. Ionic basis for the electro-responsiveness and oscillatory properties of guinea-pig thalamic neurones in vitro. J Physiol (Lond) 1984; 349: 227–47.
- 78 Deschenes M, Paradis M, Roy JP, et al. Electrophysiology of neurons of lateral thalamic nuclei in cat: resting properties and burst discharges. J Neurophysiol 1984; 51: 1196–219.
- 79 Suzuki S & Rogawski MA. T-type calcium channels mediate the transition between tonic and phasic firing in thalamic neuron. Proc Natl Acad Sci U S A 1989; 86: 7228–32.
- 80 Huguenard JR & Prince DA. Intrathalamic rhythmicity studied in vitro: nominal T-current modulation causes robust antioscillatory effects. J Neurosci 1994; 14: 5485–502.
- 81 Parri HR & Crunelli V. Sodium current in rat and cat thalamocortical neurons: role of a non-inactivating component in tonic and burst firing. J Neurosci 1998; 18: 854–67.
- 82 Huntsman MM, Porcello DM, Homanics GE, et al. Reciprocal inhibitory connections and network synchrony in the mammalian thalamus. Science 1999; 283: 541–43.DOI: 10.1126/science.283.5401.541
- 83 Snead OC. Basic mechanisms of generalized absence seizures. Ann Neurol 1995; 37: 146–57.
- 84 Snead OC. Antiabsence seizure activity of specific GABAB and γ-hydroxybutyric acid receptor antagonists. Pharmacol Biochem Behav 1996; 53: 73–9.DOI: 10.1016/0091-3057(95)00200-6
- 85 Williams SR, Turner JP, Crunelli V. Gamma-hydroxybutyrate promotes oscillatory activity of rat and cat thalamocortical neurons by a tonic GABAB receptor-mediated hyperpolarization. Neuroscience 1995; 66: 133–41.DOI: 10.1016/0306-4522(94)00604-4
- 86 Destexhe A. Spike and wave oscillations based on the properties of GABAB receptors. J Neurosci 1998; 18: 9099–111.
- 87 Destexhe A. Can GABAA conductances explain the fast oscillation frequency of absence seizures in rodents. Eur J Neurosci 1999:2175–81.
- 88 Hosford DA, Clark S, Cao Z, et al. The role of GABAB receptor activation in absence seizures of lethargic (lh/lh) mice. Science 1992; 257: 398-401.
- 89 Spreafico R, Mennini T, Danober L, et al. GABAA receptor impairment in the genetic absence epilepsy rats from Strasbourg (GAERS): an immunocytochemical and receptor binding autoradiographic study. Epilepsy Res 1993; 15: 229–38.
- 90 Knight AR & Bowery NG. GABA receptors in rats with spontaneous generalized nonconvulsive epilepsy. J Neural Transm Suppl 1992; 35: 189–96.
- 91 Leresche N, Parri HR, Erdemli G, et al. On the action of the anti-absence drug ethosuximide in the rat and cat thalamus. J Neurosci 1998; 18: 4842–53.
- 92 Blumenfeld H & McCormick D.A. Corticothalamic inputs control the pattern of activity generated in thalamocortical networks. J. Neurosci 2000; 20: 5153–62.
- 93 Luhmann HJ, Mittmann T, Van Luijtelaar G, et al. Impairment of intracortical GABAergic inhibition in a rat model of absence epilepsy. Epilepsy Res 1995; 22: 43–51.DOI: 10.1016/0920-1211(95)00032-6
- 94 Williams D. Study of thalamic and cortical rhythms in petit mal. Brain 1953; 76: 50–69.
- 95 Steriade M & Contreras D. Spike-wave complexes and fast components of cortically generated seizures. I. Role of neocortex and thalamus. J Neurophysiol 1998; 80: 1439–55.
- 96 Steriade M, Amzica F, Neckelmann D, et al. Spike-wave complexes and fast components of cortically generated seizures. II. Extra- and intracellular patterns. J Neurophysiol 1998; 80: 1456–79.
- 97 Neckelmann D, Amzica F, Steriade M. Spike-wave complexes and fast components of cortically generated seizures. III. Synchronizing mechanisms. J Neurophysiol 1998; 80: 1480–94.
- 98 Timofeev I, Grenier F, Steriade M. Spike-wave complexes and fast components of cortically generated seizures. IV. Paroxysmal fast runs in cortical and thalamic neurons. J Neurophysiol 1998; 80: 1495–513.
- 99 Avoli M, Louvel J, Drapeau C, et al. GABAA-mediated inhibition and in vitro epileptogenesis in the human neocortex. J Neurophysiol 1995; 73: 468–84.
- 100 Kostopoulos G, Avoli M, Gloor P. Participation of cortical recurrent inhibition in the genesis of spike and wave discharges in feline generalized penicillin epilepsy. Brain Res 1983; 267: 101–12.
- 101 Ben-Ari Y, Krnjevic K, Reiffenstein RJ, et al. Inhibitory conductance changes and action of gamma-aminobutyrate in rat hippocampus. Neuroscience 1981; 6: 2445–63.
- 102 Galvan M, Grafe P, Ten Bruggencate G. Convulsant actions of 4-aminopyridine on the guinea-pig olfactory cortex slice. Brain Res 1982; 241: 75–86.
- 103 Rogawski MA & Porter RJ. Antiepileptic drugs: pharmacological mechanisms and clinical efficacy with consideration of promising developmental stage compounds. Pharmacol Rev 1990; 42: 223–86.
- 104 Ragsdale DS & Avoli M. Sodium channels as molecular targets for antiepileptic drugs. Brain Res Rev 1998; 26: 16–28.
- 105 Zona C & Avoli M. Effects induced by the antiepileptic drug valproic acid upon the ionic currents recorded in rat neocortical neurons in cell culture. Exp Brain Res 1990; 81: 313–7.
- 106 Zona C & Avoli M. Lamotrigine reduces voltage-gated sodium currents in rat central neurons in culture. Epilepsia 1997; 38: 522–5.
- 107 Xie X, Lancaster B, Peakman T, et al. Interaction of the antiepileptic drug lamotrigine with recombinant rat brain type IIA Na+ channels and with native Na+ channels in rat hippocampal neurones. Pflugers Arch Eur J Physiol 1995; 430: 437–46.
- 108 Zona C, Ciotti MT, Avoli M. Topiramate attenuates voltage-gated sodium currents in rat cerebellar granule cells. Neurosci Lett 1997; 231: 123–6.DOI: 10.1016/s0304-3940(97)00543-0
- 109 Kawasaki H, Tancredi V, D'Arcangelo G, et al. Multiple actions of the novel anticonvulsant drug topiramate in the rat subiculum in vitro. Brain Res 1998; 807: 125–34.DOI: 10.1016/s0006-8993(98)00785-9
- 110 Taverna S, Mantegazza M, Franceschetti S, et al. Valproate selectively reduces the persistent fraction of Na+ current in neocortical neurons. Epilepsy Res 1998; 32: 304–8.DOI: 10.1016/s0920-1211(98)00060-6
- 111 Taverna S, Sancini G, Mantegazza M, et al. Inhibition of transient and persistent Na+ current fractions by the new anticonvulsant topiramate. J Pharmacol Exp Ther 1999; 288: 960–8.
- 112 Coulter DA, Huguenard JR, Prince DA. Specific petit mal anticonvulsants reduce calcium currents in thalamic neurons. Neurosci Lett 1989; 98: 74–8.
- 113 Coulter DA, Huguenard JR, Prince DA. Differential effects of petit mal anticonvulsants and convulsants on thalamic neurones: calcium current reduction. Br J Pharmacol 1990; 100: 800–6.
- 114 Huguenard JR & Prince DA. Clonazepam suppresses GABAB-mediated inhibition in thalamic relay neurons through effects in nucleus reticularis. J Neurophysiol 1994; 71: 2576–81.
- 115 Pfrieger FW, Veselovsky NS, Gottmann K, et al. Pharmacological characterization of calcium currents and synaptic transmission between thalamic neurons in vitro. J Neurosci 1992; 12: 4347–57.
- 116 Sayer RJ, Brown AM, Schwindt PC, et al. Calcium currents in acutely isolated human neocortical neurons. J Neurophysiol 1993; 69: 1596–606.
- 117 Gloor P & Fariello R. Generalized epilepsy: some of its cellular mechanisms differ from those of focal epilepsy. Trends Neurosci 1988; 11: 63–8.
- 118 Guberman A, Gloor P, Sherwin AL. Response of generalized penicillin epilepsy in the cat to ethosuximide and diphenylhydantoin. Neurology 1975; 25: 785–864.
- 119 Giaretta D, Avoli M, Gloor P. Intracellular recordings in pericruciate neurons during spike and wave discharges of feline generalized penicillin epilepsy. Brain Res 1987; 405: 68–79.