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2012, Number 5

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Rev Fac Med UNAM 2012; 55 (5)

Temporal lobe epilepsy and hippocampal neurons from areas CA1 and CA3

López-Hernándeza E, Solísa H

Language: Spanish
References: 66
Page: 16-25
PDF size: 165.50 Kb.


ABSTRACT

Temporal Lobe Epilepsy is the most common form of human epilepsy. Hippocampal sclerosis, neuronal loss, gliosis and hippocampal volume reduction are the representative changes of this pathology. Also some other near areas like amygdala, gyrus parahipocampal and entorrinal cortex are affected. Furthermore the neural circuits undergo activitydependent reorganization during epileptogenesis. This brain circuits remodeling include neuronal loss (acute and delayed), neurogenesis, gliosis, plasticity (axonal and dendritic), inflammation and molecular reorganization. Two significant changes are evident, aberrant sprouting of granule cell axons in the dentate gyrus and hilar ectopic granular cells. Because temporal lobe epilepsy commonly develops after brain injury, most experimental animal models involve use of this factor. The pilocarpine-induced status epilepticus rat model may be the most widely used model of temporal lobe epilepsy. In the present work, we review the experimental support for seizure-induced plasticity in neural circuits, and then turn to evidence that seizure-induced plasticity occurs in human temporal-lobe.


REFERENCES

  1. International League against Epilepsy (ILAE)/ International Bureau for Epilepsy (IBE)/ World Health Organization (WHO) Global Campaign Against Epilepsy out of the shadows. Annual Report 2001.

  2. Organización Panamericana de la Salud, Departamento de Salud Mental y Abuso de Sustancias de la Organización Mundial de la Salud (OMS), Liga Internacional Contra la Epilepsia (ILAE), Buró Internacional para la Epilepsia (IBE). INFORME SOBRE LA EPILEPSIA EN LATINOAMERICA. Panamá. 2008.

  3. López E, Bravo J, Solís H. Epilepsia y antiepilépticos de primera y segunda generación. Aspectos básicos útiles en la práctica clínica. Rev Fac Med UNAM. 2005;48(5):201-9.

  4. Carpio A, Lisanti N, Calle H, Borrero I, Toral AM, Vasquez I. Validación de un cuestionario para el diagnóstico de la epilepsia en servicios de atención primaria. Rev Panam Salud Pública. 2006;2006;19(3):157-62.

  5. Medina HMT, Chaves SF, Chinchilla CN, Gracia GF. Las Epilepsias en Centroamérica. Tegucigalpa, Honduras. 2001.

  6. Engel J Jr. Introduction to temporal lobe epilepsy. Epilepsy Res. 1996;26:141-50.

  7. Engel J Jr. Mesial Temporal Lobe Epilepsy: What Have We Learned? NEUROSCIENTIST. 2001; 7(4):340–352.

  8. Rabadán AT, Zanniello G, Baccanelli M, Rosler RJ, Ogresta F, Pietrani M, et al. Cirugía de la Epilepsia Mesial Temporal. Rev Neurológica Argentina. 2002;27:45-54.

  9. Pereno GL. Fisiopatología de la Epilepsia del Lóbulo Temporal: Revisión del Proceso de Muerte Neuronal a la Neuroplasticidad. Rev Argentina de Ciencias del Comportamiento. 2010;2(1):46-57.

  10. Stables JP, Bertram EH, White HS, Coulter DA, Dichter MA, Jacobs MP, Loscher W, Lowenstein DH, Moshe SL, Noebels JL, Davis M. Epilepsia. 2002; 43(11):1410-20.

  11. Solís OH, Arauz CJ. Modelos experimentales de epilepsia. En: Feria VA, Martínez MD y Rubio DF. Eds. Epilepsia Un enfoque multidisciplinario. México: Trillas. 1986: 74-97.

  12. Turski WA, Cavalheiro EA, Schwarz M, Czuczwar SJ, Kleinrok Z, Turski L. Limbic seizures produced by pilocarpine in rats: behavioural, electroencephalographic and neuropathological study. Behav Brain Res. 1983; 9(3):315-35.

  13. Curia G, Longo D, Biagini G, Jones RS, Avoli M. The pilocarpine model of temporal lobe epilepsy. J Neurosci Methods. 2008;172(2):143-57.

  14. Jeong KH, Lee KE, Kim SY, Cho KO. Upregulation of Krüppel-like factor 6 in the mouse hippocampus after pilocarpine-induced status epilepticus. Neuroscience. 2011. doi:10.1016/j.neuroscience.2011.02.046.

  15. Sano K. 1 Hippocampus and Epilepsy Surgery. Epilepsia. 1997; 38(Suppl. 6):4

  16. Lado FA, Laureta E, Moshé SL. Seizure-induced hippocampal damage in the mature and immature brain. Epileptic Disord. 2002;4(2):83-97.

  17. Campanille V, Moschini J. Epilepsia del Lóbulo Temporal con Esclerosis Mesial Temporal. Rev. Neurológica Argentina. 2004; 29:30-41.

  18. Valdivieso COF, Mota GV, Velasco MAL, Figueroa PE, Criales CJL. Esclerosis temporal mesial. Gac Méd Méx. 2005; 141(6):541-2.

  19. Pitkänen A, Sutula TP. Is epilepsy a progressive disorder? Prospects for new therapeutic approaches in temporal-lobe epilepsy. Lancet Neurol. 2002; 1(3):173-81.

  20. Sutula TP. Mechanisms of epilepsy progression: current theories and perspectives from neuroplasticity in adulthood and development. Epilepsy Res. 2004; 60(2-3):161-71.

  21. Thom M. Hippocampal sclerosis: progress since Sommer. Brain Pathol. 2009;19(4):565-72.

  22. Mueller SG, Laxer KD, Barakos J, Cheong I, Garcia P, Weiner MW. Subfield atrophy pattern in temporal lobe epilepsy with and without mesial sclerosis detected by high-resolution MRI at 4 Tesla: preliminary results. Epilepsia. 2009; 50(6):1474-83.

  23. Murphy BL, Pun RY, Yin H, Faulkner CR, Loepke AW, Danzer SC. Heterogeneous integration of adult-generated granule cells into the epileptic brain. J Neurosci. 2011;31(1):105-17.

  24. Solís H, Bravo J, Galindo-Morales JA, López E. Participación de la inhibición recurrente en algunos modelos de convulsiones generalizadas. En: Feria VA, Martínez MD y Rubio DF. eds. Epilepsia aspectos neurobiológicos, médicos y sociales. México: Ediciones del Instituto Nacional de Neurología. 1997: 66-84

  25. Pierce JP, McCloskey DP, Scharfman HE. Morphometry of hilar ectopic granule cells in the rat. J Comp Neurol. 2011; 519(6):1196-218.

  26. Sbai O, Khrestchatisky M, Esclapez M, Ferhat L. Drebrin A expression is altered after pilocarpine-induced seizures: Time course of changes is consistent for a role in the integrity and stability of dendritic spines of hippocampal granule cells. Hippocampus. 2011 Jan 14. doi: 10.1002/hipo.20914.

  27. Ribak CE, Tran PH, Spigelman I, Okazaki MM, Nadler JV. Status epilepticus-induced hilar basal dendrites on rodent granule cells contribute to recurrent excitatory circuitry. J Comp Neurol. 2000;428(2):240-53.

  28. Bentivoglio M, Jones EG, Mazzarello P, Ribak CE, Shepherd GM, Swanson LW. Camillo Golgi and modern neuroscience. Brain Res Rev. 2011;66(1-2):1-4.

  29. De Carlos JA, Borrell J. A historical reflection of the contributions of Cajal and Golgi to the foundations of neuroscience. Brain Res Rev. 2007;55(1):8-16.

  30. Fairén A. Cajal and Lorente de Nó on cortical interneurons: coincidences and progress. Brain Res Rev. 2007;55(2): 430-44.

  31. Spencer WA, Kandel ER. Hippocampal neuron responses to selective activation of recurrent collaterals of hippocampofugal axons. Experimental Neurology. 1961;4(2):149-61

  32. Lacaille JC, Schwartzkroin PA. Stratum lacunosum-moleculare interneurons of hippocampal CA1 region. I. Intracellular response characteristics, synaptic responses, and morphology. J Neurosci. 1988;8(4):1400-10.

  33. Lacaille JC, Schwartzkroin PA. Stratum lacunosum-moleculare interneurons of hippocampal CA1 region. II. Intrasomatic and intradendritic recordings of local circuit synaptic interactions. J Neurosci. 1988;8(4):1411-24.

  34. Ishizuka N, Cowan WM, Amaral DG. A quantitative analysis of the dendritic organization of pyramidal cells in the rat hippocampus. J Comp Neurol. 1995;362(1):17-45.

  35. Sik A, Penttonen M, Ylinen A, Buzsáki G. Hippocampal CA1 interneurons: an in vivo intracellular labeling study. J Neurosci. 1995;15(10):6651-65.

  36. Perez Y, Morin F, Beaulieu C, Lacaille JC. Axonal sprouting of CA1 pyramidal cells in hyperexcitable hippocampal slices of kainate-treated rats. Eur J Neurosci. 1996;8(4):736-48.

  37. Scorza CA, Araujo BH, Leite LA, Torres LB, Otalora LF, Oliveira MS, et al. Morphological and electrophysiological properties of pyramidal-like neurons in the stratum oriens of Cornu ammonis 1 and Cornu ammonis 2 area of Proechimys. Neuroscience. 2011;177:252-68.

  38. Epónimos médicos Galvanismo, galvanización. http://www.historiadelamedicina.org/Galvani.html

  39. Scanziani M, Häusser M. Electrophysiology in the age of light. Nature. 2009; 461(7266):930-9.

  40. Buckmaster PS, Dudek FE. Neuron loss, granule cell axon reorganization, and functional changes in the dentate gyrus of epileptic kainate-treated rats. J Comp Neurol. 1997; 385(3):385-404.

  41. Bragin A, Azizyan A, Almajano J, Wilson CL, Engel J Jr. Analysis of chronic seizure onsets after intrahippocampal kainic acid injection in freely moving rats. Epilepsia. 2005; 46(10):1592-8.

  42. Jiruska P, Finnerty GT, Powell AD, Lofti N, Cmejla R, Jefferys JG. Epileptic high-frequency network activity in a model of non-lesional temporal lobe epilepsy. Brain. 2010; 133(Pt 5):1380-90.

  43. Sloviter RS. Hippocampal epileptogenesis in animal models of mesial temporal lobe epilepsy with hippocampal sclerosis: the importance of the “latent period” and other concepts. Epilepsia. 2008;49 Suppl 9:85-92.

  44. López E, Parra L, Bravo J, Téllez- Girón RJ, Solís H. Cambios en la excitabilidad neuronal y alteraciones en la densidad neuronal del hipocampo inducidos por isquemia focal. Arch Neurocien Mex. 1997;2(2):61-6.

  45. Solís H, López E, Parra L, Bravo J, Escobar A. Morphological and electrophysiological changes after cerebral ischemia in the rat hippocampus. Experimental Neurology. 1998;151(1):170-1.

  46. Eccles JC. Conduction and synaptic transmission in the nervous system. Annu Rev Physiol. 1948;10:93-116.

  47. Hunt CC, Kuffler SW. Pharmacology of the neuromuscular junction. J Pharmacol Exp Ther. 1950;98(4:2):96-120.

  48. Fatt P, Katz B. An analysis of the end-plate potential recorded with an intracellular electrode. J Physiol. 1951; 115(3):320-70.

  49. Hodking AL, Huxley AF. Movement of sodium and potassium ions during nervous activity. Cold Spring Harb Symp Quant Biol. 1952;17:43-52.

  50. Wong RK, Prince DA, Basbaum AI. Intradendritic recordings from hippocampal neurons. Proc Natl Acad Sci U S A. 1979;76(2):986-90.

  51. Schwartzkroin PA. Further characteristics of hippocampal CA1 cells in vitro. Brain Res. 1977;128(1):53-68.

  52. Benardo LS, Masukawa LM, Prince DA. Electrophysiology of isolated hippocampal pyramidal dendrites. J Neurosci. 1982;2(11):1614-22.

  53. Mason A. Electrophysiology and burst-firing of rat subicular pyramidal neurons in vitro: a comparison with area CA1. Brain Res. 1993;600(1):174-8.

  54. Csicsvari J, Hirase H, Czurkó A, Mamiya A, Buzsáki G. Oscillatory coupling of hippocampal pyramidal cells and interneurons in the behaving Rat. J Neurosci. 1999; 19(1):274-87.

  55. Dudek FE, Spitz M. Hypothetical mechanisms for the cellular and neurophysiologic basis of secondary epileptogenesis: proposed role of synaptic reorganization. J Clin Neurophysiol. 1997;14(2):90-101.

  56. Esclapez M, Hirsch JC, Khazipov R, Ben-Ari Y, Bernard C. Operative GABAergic inhibition in hippocampal CA1 pyramidal neurons in experimental epilepsy. Proc Natl Acad Sci U S A. 1997; 94(22):12151-6.

  57. Houser CR, Esclapez M. Vulnerability and plasticity of the GABA system in the pilocarpine model of spontaneous recurrent seizures. Epilepsy Res. 1996; 26(1):207-18.

  58. Esclapez M, Hirsch JC, Ben-Ari Y, Bernard C Newly formed excitatory pathways provide a substrate for hyperexcitability in experimental temporal lobe epilepsy. J Comp Neurol. 1999; 408(4):449-60.

  59. Smith BN, Dudek FE. Short- and long-term changes in CA1 network excitability after kainate treatment in rats. J Neurophysiol. 2001;85(1):1-9.

  60. Lehmann TN, Gabriel S, Kovacs R, Eilers A, Kivi A, Schulze K, et al. Alterations of neuronal connectivity in area CA1 of hippocampal slices from temporal lobe epilepsy patients and from pilocarpine-treated epileptic rats. Epilepsia. 2000; 41 Suppl 6:S190-4.

  61. Cossart R, Dinocourt C, Hirsch JC, Merchan-Perez A, De Felipe J, Ben-Ari Y, et al. Dendritic but not somatic GABAergic inhibition is decreased in experimental epilepsy. Nat Neurosci. 2001;4(1):52-62.

  62. Tang FR, Loke WK. Cyto-, axo- and dendro-architectonic changes of neurons in the limbic system in the mouse pilocarpine model of temporal lobe epilepsy. Epilepsy Res. 2010; 89(1):43-51.

  63. McAuliffe JJ, Bronson SL, Hester MS, Murphy BL, Dahlquist-Topalá R, Richards DA, et al. Altered patterning of dentate granule cell mossy fiber inputs onto CA3 pyramidal cells in limbic epilepsy. Hippocampus. 2011; 21(1):93-107. doi: 10.1002/hipo.20726.

  64. Pearce JMS. Bromide, the first effective antiepileptic agent. Historical note. J Neurol Neurosurg Psychiatry. 2002;72:412 doi:10.1136/jnnp.72.3.412.

  65. López-Muñoz F, Ucha-Udabe R, Alamo C. The history of barbiturates a century after their clinical introduction. Neuropsychiatr Dis Treat. 2005; 1(4): 329–343.

  66. Sebe JY, Baraban SC. The promise of an interneuron-based cell therapy for epilepsy. Dev Neurobiol. 2011;71(1):107- 17. doi: 10.1002/dneu.20813.




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