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Instituto Nacional de Neurología y Neurocirugía

2018, Número 4

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Arch Neurocien 2018; 23 (4)


Microglía y neurodegeneración en el núcleo talámico dorsomedial de la rata infante después del Estado Epiléptico

García-Martínez A, Quiroz-Vergara F, Véliz-Castillo I, Álvarez- Croda M, López-Meraz María-Leonor

Idioma: Español
Referencias bibliográficas: 64
Paginas: 6-15
Archivo PDF: 817.13 Kb.


RESUMEN

Introducción: El estado epiléptico (EE) produce extensa muerte neuronal en el cerebro en desarrollo. Entre las estructuras cerebrales afectadas es de relevancia el tálamo, al ser el centro de relevo e integración de la información hacia la corteza cerebral. La microglía es un sistema especializado de inmunidad celular que se activa o sobre-expresa cuando existe daño al tejido cerebral.
Objetivo: Determinar cambios en la cantidad y morfología de la microglía en el núcleo dorsomedial del tálamo de ratas en desarrollo después del EE y su relación con la neurodegeneración.
Método: El EE se produjo con el modelo de litio-pilocarpina en ratas de 14 días de edad; las ratas control no convulsionaron. La microglía se identificó utilizando el marcador Iba1 y se determinó la microglía total, así como la microglía con características morfológicas de no-activada y activada en condiciones control y 2, 6, 24 y 48 h después del EE. La presencia de células en degeneración se evaluó con el colorante Fluoro-Jade C.
Resultados: La microglía total después del EE fue similar al control, mientras que la microglía activada aumentó 6-48 h después del EE, efecto que coincidió con el tiempo al cual se observaron neuronas en degeneración.
Conclusión: Estos hallazgos demuestran que la microglía se activa en respuesta al EE y sugiere que su activación podría estar implicada en los mecanismos que promueven neurodegeneración en el tálamo en desarrollo.


REFERENCIAS (EN ESTE ARTÍCULO)

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  2. Trinka E, Cock H, Hesdorffer D, Rossetti AO, Scheffer IE, Shinnar S, et al. A definition and classification of status epilepticus-Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia 2015; 56(10):1515-23.

  3. DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. Epidemiology of status epilepticus. J Clin Neurophysiol 1995; 12(4):316-25.

  4. DeLorenzo, Hauser WA, Towne AR, Boggs JG, Pellock JM, Penberthy L, Garnett L, et al. A prospective, population-based epidemiologic study of status epilepticus in Richmond, Virginia. Neurol 1996; 46:1029-35.

  5. Hauser, W. The prevalence and incidence of convulsive disorders in children. Epilepsia 1994; 35 Suppl2: S1–6.

  6. Sankar R, Shin DH, Liu H, Mazarati A, Pereira de Vasconcelos A, Wasterlain CG. Patterns of status epilepticus-induced neuronal injury during development and long-term consequences. J Neurosci 1998; 18(20):8382-93.

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  9. López-Meraz ML, Wasterlain CG, Rocha LL, Allen S, Niquet J. Vulnerability of postnatal hippocampal neurons to seizures varies regionally with their maturational stage. Neurobiol Dis 2010; 37(2): 394-402.

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  13. Vezzani A , C onti M , D e L uigi A , R avizza T, M oneta D , M archesi F, e t a l. I nterleukin- 1beta i mmunoreactivity a nd microglia are enhanced in the rat hippocampus by focal kainate application: functional evidence for enhancement of electrographic seizures. J Neurosci 1999; 19(12): 5054-65.

  14. Wang N, Mi X, Gao B, Gu J, Wang W, Zhang Y, et al. Minocycline inhibits brain inflammation and attenuates spontaneous recurrent seizures following pilocarpine-induced status epilepticus. Neuroscience 2015; 287:144–56.

  15. Haas KZ, Sperber EF, Moshe SL. Kindling in developing animals: expression of severe seizures and enhanced development of bilateral foci. Brain Res Dev Brain Res 1990; 56(2): 275-80.

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  22. Eyo U, Peng J, Swiatkowski P, Mukherjee A, Bispo A, Wu LJ. Neuronal hyperactivity recruits microglial processes via neuronal NMDA receptors and microglial P2Y12 receptors after status epilepticus. J Neurosci 2014; 34(32):10528-40.

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  25. Järvelä JT, Lopez-Picon FR, Plysjuk A, Ruohonen S, Holopainen IE. Temporal profiles of age-dependent changes in cytokine mRNA expression and glial cell activation after status epilepticus in postnatal rat hippocampus. J Neuroinflammation 2011; 8:29.

  26. Kaur C, Rathnasamy G, Ling EA. Biology of microglia in the developing brain. J Neuropathol Exp Neurol. 2017; 76(9):736-43.

  27. Álvarez-Croda DM, Santiago-García J, Medel-Matus JS, Martínez-Quiroz J, Puig-Lagunes AA, Beltrán-Parrazal L, et al. Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat. An Acad Bras Cienc 2016; 88 Suppl 1:653-63.

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  29. Merrill JE, Benveniste EN. Cytokines in inflammatory brain lesions: helpful and harmful. Trends Neurosci 1996; 19(8):331–8.

  30. Denker SP, Ji S, Dingman A, Lee SY, Derugin N, Wendland MF, et al. Macrophages are comprised of resident brain microglia not infiltrating peripheral monocytes acutely after neonatal stroke. J Neurochem 2007; 100(4): 893-904.

  31. Ravizza T, Gagliardi B, Noé F, Boer K, Aronica E, Vezzani A. Innate and adaptive immunity during epileptogenesis and spontaneous seizures: evidence from experimental models and human temporal lobe epilepsy. Neurobiol Dis 2008; 29(1):142-60.

  32. Fabene PF, Navarro MG, Martinello M, Rossi B, Merigo F, Ottoboni L, et al. A role for leukocyte-endothelial adhesion mechanisms in epilepsy. Nat Med. 2008; 14(12):1377-83.

  33. Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, et al. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia 2005; 46(4):470-2.

  34. Trinka E, Cock H, Hesdorffer D, Rossetti AO, Scheffer IE, Shinnar S, et al. A definition and classification of status epilepticus-Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia 2015; 56(10):1515-23.

  35. DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. Epidemiology of status epilepticus. J Clin Neurophysiol 1995; 12(4):316-25.

  36. DeLorenzo, Hauser WA, Towne AR, Boggs JG, Pellock JM, Penberthy L, Garnett L, et al. A prospective, population-based epidemiologic study of status epilepticus in Richmond, Virginia. Neurol 1996; 46:1029-35.

  37. Hauser, W. The prevalence and incidence of convulsive disorders in children. Epilepsia 1994; 35 Suppl2: S1–6.

  38. Sankar R, Shin DH, Liu H, Mazarati A, Pereira de Vasconcelos A, Wasterlain CG. Patterns of status epilepticus-induced neuronal injury during development and long-term consequences. J Neurosci 1998; 18(20):8382-93.

  39. Kubová H, Druga R, Lukasiuk K, Suchomelova L, Haugvicova R, Jirmanova I, et al. Status epilepticus causes necrotic damage in the mediodorsal nucleus of the thalamus in immature rats. J Neurosci 2001; 21(10):3593–9.

  40. Nairismägi J, Pitkänen A, Kettunen MI, Kauppinen RA, Kubova H. Status epilepticus in 12-day-old rats leads to temporal lobe neurodegeneration and volume reduction: a histologic and MRI study. Epilepsia 2006; 47(3): 479-88.

  41. López-Meraz ML, Wasterlain CG, Rocha LL, Allen S, Niquet J. Vulnerability of postnatal hippocampal neurons to seizures varies regionally with their maturational stage. Neurobiol Dis 2010; 37(2): 394-402.

  42. Nakajima M, Halassa MM. Thalamic control of functional cortical connectivity. Curr Opin Neurobiol 2017; 44:127-31.

  43. Hanisch UK, KettenmannH. Microglia: active sensor and versatile effector cells in the normal and pathologic brain. Nat Neurosci 2007; 10(11):1387–94.

  44. Vezzani A, Ravizza T, Balosso S, Aronica E. Glia as a source of cytokines: Implications for neuronal excitability and survival. Epilepsia 2008; 49 Suppl 2:24–32.

  45. Vezzani A , C onti M , D e L uigi A , R avizza T, M oneta D , M archesi F, e t a l. I nterleukin- 1beta i mmunoreactivity a nd microglia are enhanced in the rat hippocampus by focal kainate application: functional evidence for enhancement of electrographic seizures. J Neurosci 1999; 19(12): 5054-65.

  46. Wang N, Mi X, Gao B, Gu J, Wang W, Zhang Y, et al. Minocycline inhibits brain inflammation and attenuates spontaneous recurrent seizures following pilocarpine-induced status epilepticus. Neuroscience 2015; 287:144–56.

  47. Haas KZ, Sperber EF, Moshe SL. Kindling in developing animals: expression of severe seizures and enhanced development of bilateral foci. Brain Res Dev Brain Res 1990; 56(2): 275-80.

  48. Sherwood NM, Timiras PS. A stereotaxic atlas of the developing rat brain. Berkeley-Los Angeles-London, University of California Press, 1970.

  49. Schindelin J, Arganda-Carreras I, Frise E, Kaynig V, Longair M, Pietzsch T, et al. Fiji: an open-source platform for biologicalimage analysis. Nat Methods 2012; 9 (7):676-82.

  50. Jonas RA, Yuan TF, Liang YX, Jonas JB, Tay DK, Ellis-Behnke RG. The spider effect: morphological and orienting classification of microglia in response to stimuli in vivo. PLoS One 2012; 7(2) p.e30763.

  51. Avignone E, Ulmann L, Levavasseur F, Rassendren F, Audinat E. Status epilepticus induces a particular microglial activation state characterized by enhanced purinergic signaling. J Neurosci 2008; 28 (37): 9133-44.

  52. De Simoni MG, Perego C, Ravizza T, Moneta D, Conti M, Marchesi F, et al. Inflammatory cytokines and related genes are induced in the rat hippocampus by limbic status epilepticus. Eur J Neurosci 2000; 12(7): 2623–33.

  53. Ravizza T, Rizzi M, Perego C. Inflammatory response and glia activation in developing rat hippocampus after status epilepticus. Epilepsia 2005; 46 Suppl 5:113-7.

  54. Eyo U, Peng J, Swiatkowski P, Mukherjee A, Bispo A, Wu LJ. Neuronal hyperactivity recruits microglial processes via neuronal NMDA receptors and microglial P2Y12 receptors after status epilepticus. J Neurosci 2014; 34(32):10528-40.

  55. Ouhaz Z, Ba-M'hamed S, Bennis M. Morphological, structural, and functional alterations of the prefrontal cortex and the basolateral amygdala after early lesion of the rat mediodorsal thalamus. Brain Struct Fun 2017; 222(6): 2527-45.

  56. Rizzi M, Perego C, Aliprandi M, Richichi C, Ravizza T, Colella D, et al. Glia activation and cytokine increase in rat hippocampus by kainic acid-induced status epilepticus during postnatal development. Neurobiol Dis 2003; 14(3): 494-503.

  57. Järvelä JT, Lopez-Picon FR, Plysjuk A, Ruohonen S, Holopainen IE. Temporal profiles of age-dependent changes in cytokine mRNA expression and glial cell activation after status epilepticus in postnatal rat hippocampus. J Neuroinflammation 2011; 8:29.

  58. Kaur C, Rathnasamy G, Ling EA. Biology of microglia in the developing brain. J Neuropathol Exp Neurol. 2017; 76(9):736-43.

  59. Álvarez-Croda DM, Santiago-García J, Medel-Matus JS, Martínez-Quiroz J, Puig-Lagunes AA, Beltrán-Parrazal L, et al. Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat. An Acad Bras Cienc 2016; 88 Suppl 1:653-63.

  60. Medel-Matus JS, Álvarez-Croda DM, Martínez-Quiroz J, Beltrán-Parrazal L, Morgado-Valle C, López-Meraz MC. IL-1β increases necrotic neuronal cell death in the developing rat hippocampus after status epilepticus by activating type 1 IL-1 receptor (IL-1RI). Int J Dev Neurosci 2014; 238: 232-40.

  61. Merrill JE, Benveniste EN. Cytokines in inflammatory brain lesions: helpful and harmful. Trends Neurosci 1996; 19(8):331–8.

  62. Denker SP, Ji S, Dingman A, Lee SY, Derugin N, Wendland MF, et al. Macrophages are comprised of resident brain microglia not infiltrating peripheral monocytes acutely after neonatal stroke. J Neurochem 2007; 100(4): 893-904.

  63. Ravizza T, Gagliardi B, Noé F, Boer K, Aronica E, Vezzani A. Innate and adaptive immunity during epileptogenesis and spontaneous seizures: evidence from experimental models and human temporal lobe epilepsy. Neurobiol Dis 2008; 29(1):142-60.

  64. Fabene PF, Navarro MG, Martinello M, Rossi B, Merigo F, Ottoboni L, et al. A role for leukocyte-endothelial adhesion mechanisms in epilepsy. Nat Med. 2008; 14(12):1377-83.




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