medigraphic.com
ISSN 0185-3325 (Impreso)
Órgano Oficial del Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz

2012, Número 5

<< Anterior Siguiente >>

Salud Mental 2012; 35 (5)


La abstinencia al GABA: 20 años de un modelo de hiperexcitabilidad neuronal

Calixto E

Idioma: Español
Referencias bibliográficas: 55
Paginas: 427-434
Archivo PDF: 182.72 Kb.


RESUMEN

La interrupción abrupta del incremento de la concentración en el espacio sináptico del neurotransmisor inhibitorio de la corteza cerebral, el ácido γ-amino butírico (GABA), condiciona un incremento en la actividad de las neuronas. La abstinencia al GABA es una analogía heurística con los síndromes de abstinencia desarrollados por otros agonistas del receptor GABAA como: las benzodiacepinas, los barbitúricos, los neuroesteroides y el alcohol.
La abstinencia a GABA es un modelo de hiperexcitabilidad neuronal validado en animal íntegro por medio del EEG, en el cual aparecen complejos espigas-onda de amplia frecuencia y amplitud. En rebanadas de cerebro se identifica por incremento en la sincronización de disparo de neuronas piramidales y por cambios en las propiedades activas de la membrana neuronal.
El incremento de la excitabilidad neuronal de este modelo es la consecuencia de cambios dinámicos y consecutivos en los componentes presinápticos y postsinápticos como son: a) la disminución en la síntesis/liberación de GABA; b) la disminución en la expresión y la composición de receptores GABAA asociado al incremento en la entrada de calcio a la célula.
Este modelo es un excelente bioensayo para estudiar epilepsias parciales, epilepsias refractarias a tratamiento farmacológico y un modelo para revertir o prevenir la generación de la abstinencia de diferentes drogas.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Brailowsky S. Myoclonus in Papio papio. Mov Disord 1991;6:98-104.

  2. Brailowsky S, Silva-Barrat C, Menini C, Riche D et al. Effects of localized, chronic GABA infusions into different cortical areas of the photosensitive baboon, Papio papio. Electroencephalographic Clin Neurophysiol 1989;72:147-156.

  3. Brailowsky S, Kunimoto M, Menini C, Silva-Barrat C et al. The GABA withdrawal syndrome: a new model of focal epileptogenesis. Brain Res 1988;442:175-179.

  4. Brailowsky S, Kunimoto M, Silva-Barrat C, Menini C et al. Electroencephalographic study of the GABA-Withdrawal syndrome in rats. Epilepsia 1990;31:369-377.

  5. Brailowsky S. The GABA-withdrawal syndrome. Proc West Pharmacol Soc 1991;34:227-228.

  6. Fukuda H, Brailowsky S, Menini C, Silva-Barrat C et al. Anticonvulsant effect of intracortical, chronic infusion of GABA in kindled rats: focal seizures upon withdrawal. Exp Neurol 1987;98:120-129.

  7. Menini C, Mraovitch S, Calando Y, De La Sayette V et al. Metabolic anatomy of the focal epilepsy produced by cessation of chronic intracortical GABA infusion in the rat. Neuroscience 1991;41:607-615.

  8. Morrow Al, Vandoren MJ, Penland SN, Matthews DB. The role of GABAergic neuroactive steroids in ethanol action, tolerance and dependence. Brain Res Rev 2001;37:98-109.

  9. O´Brien CP. Benzodiazepine use, abuse and dependence. J Clin Psychiatry 2005;66:28-33.

  10. Olmedo R, Hoffman RS. Withdrawal syndromes. Emerg Med Clin North Am 2000;18:273-288.

  11. Salazar P, Montiel T, Brailowsky S, Tapia R. Decrease of glutamate decarboxylase activity after in vivo cortical infusion of gamma-amino butyric acid. Neurochem Int 1994;24:363-368.

  12. Kumar S, Porcu P, Warner D, Mattews D et al. The role GABAA receptor in the acute and chronic effect of ethanol: a decade of progress. Psychopharmacol 2009;205:1-54.

  13. Silva-Barrat C, Champagnat J, Brailowsky S, Menini C et al. Relationship between tolerance to GABAA agonist and bursting properties in neocortical neurons during GABA-withdrawal syndrome. Brain Res 1989;498:289-298.

  14. Calixto E, Thiels E, Klann E, Barrionuevo G. Early maintenance of hippocampal Mossy Fiber–Long-Term Potentiation depends on protein and RNA synthesis and presynaptic granule cell integrity. J Neuroscience 2003;23:4842-4849.

  15. Silva-Barrat C, Champagnat J. A potassium current controls burst termination in rat neocortical neurons after GABA withdrawal. Neurosci Lett 1995;189:105-108.

  16. Calixto E, López-Colomé AM, Casasola C, Montiel T et al. Neocortical hyperexcitability after GABA withdrawal in vitro. Epilepsy Res 2000;39:13-26.

  17. Casasola C, Bargas J, Arias-Montaño JA, Calixto E et al. Hippocampal hyperexcitability induced by GABA withdrawal is due to down-regulation of GABA(A) receptors. Epilepsy Res 2001;47:257-271.

  18. García-Ugalde G, Galarraga E, Bargas J, Brailowsky S. Hyperexcitability of hippocampal CA1 region in brain slices after GABA withdrawal. Neurosci Lett 1992;147:229-232.

  19. Wirsen A, Stenberg G, Rosen I, Ingvar DH. Quantified EEG and cortical evoked responses in patients with chronic traumatic frontal lesions. Electroencephalographic Clin Neurophysiol 1992;84:127-138.

  20. Krystal J, Staley J, Mason G, Petrakis I et al. Gamma-amino butyric acid type A receptors and alcoholism. Arch Gen Psychiatry 2006;63:957-968.

  21. Liang J, Suryanarayanan A, Abriam A, Olsen R et al. Mechanism of reversible GABAA receptor plasticity after ethanol intoxication. J Neuroscience 2007;27:12367-12377.

  22. Licata S, Rowlett J. Abuse and dependence liability of benzodiazepine type drugs: GABAA receptor modulation and beyond. Pharmacol Biochem Behavior 2008;90:74-89.

  23. Kelly T, Church J. pH modulation of currents that contribute to the medium and slow after hyper polarizations in rat CA1 pyramidal neurons. J Physiol 2004;554:449-466.

  24. Valverde O, Maldonado R, Mico JA, Gibert-Rahola J. Study of the mechanisms involved in behavioral changes induced by flunitrazepam in morphine withdrawal. Prog Neuropsychopharmacol Biol Psychiatry 1995;19:973-991.

  25. Valverde O, Mico JA, Maldonado R, Gibert-Rahola J. Changes in benzodiazepine- receptor activity modify morphine withdrawal syndrome in mice. Drug Alcohol Depend 1992;(3):293-300.

  26. Yang L, Long C, Evans MS, Faingold C. Ethanol withdrawal results in aberrant membrane properties and synaptic responses in periaqueductal gray neurons associated with seizure susceptibility. Brain Res 2002;957:99-108.

  27. Golan H, Mikenberg K, Greenberger V, Segal M. GABA withdrawal modifies network activity in cultured hippocampal neurons. Neural Plast 2000;7:31-42.

  28. Casasola C, Montiel T, Calixto E, Brailowsky S. Hyperexcitability induced by GABA withdrawal facilitates hippocampal long-term potentiation. Neuroscience 2004;126:163-171.

  29. Montiel T, Almeida D, Arango I, Calixto E et al. Long-lasting effects of GABA infusion into the cerebral cortex of the rat. Neural Plast 2000;7:1-8.

  30. Calixto E, Montiel T, Lemini C, Brailowsky S. Allopregnanolone potentiates a GABA-withdrawal syndrome in the rat cerebral cortex. Neurosci Lett 1995;195:73-76.

  31. Strzelec JS, Czarnecka E. Influence of clonazepam and carbamazepine on alcohol withdrawal syndrome, preference and development of tolerance to ethanol in rats. Pol J Pharmacol 2001;53:117-124.

  32. Nelson TE, Ur CL, Gruol DL. Chronic intermittent ethanol exposure enhances NMDA-receptor-mediated synaptic responses and NMDA receptor expression in hippocampal CA1 region. Brain Res 2005;1048:69-79.

  33. Smith SS, Shen H, Gong H, Zhou X. Neurosteroids regulation of GABAA receptor. Focus on the 4 and  subunit. Pharmacol Ther 2007;116:58-76.

  34. Smith SS, Gong QH. Neurosteroid administration and withdrawal alter GABAA receptor kinetics in CA1 hippocampus of female rats. J Physiol 2005;564:421-436.

  35. Cagetti E, Liang J, Spigelman I, Olsen Rw. Withdrawal from chronic intermittent ethanol treatment changes subunit composition, reduces synaptic function, and decreases behavioral responses to positive allosteric modulators of GABAA receptors. Mol Pharmacol 2003;63:53-64.

  36. Cagetti E, Franco M, Trapani G, Biggio G. Changes in GABA (A) receptor gene expression induced by withdrawal of, but not by long-term exposure to zaleplon or zolpidem. Neuropharmacology 2002,42:191-198.

  37. Follesa P, Mancuso L, Biggio F. Diazepam during prior ethanol withdrawals does not alter seizure susceptibility during a subsequent withdrawal. Pharmacol Biochem Behav 2001;68:339-346.

  38. Follesa P, Biggio F, Mancuso L, Cabras S et al. Ethanol withdrawal-induced up-regulation of the alpha2 subunit of the GABAA receptor and its prevention by diazepam or gamma-hydroxy butyric acid. Brain Res Mol Brain Res 2004;120:130-137.

  39. Izzo E, Auta J, Impagnatiello F, Pesold C et al. Glutamic acid decarboxylase and glutamate receptor changes during tolerance and dependence to benzodiazepines. PNAS 2001;98:3483–3488.

  40. Gulinello M, Gong Qh, Li X, Smith SS. Short-term exposure to a neuroactive steroid increases alpha4 GABA(A) receptor subunit levels in association with increased anxiety in the female rat. Brain Res 2000;910:55-66.

  41. Griffiths J, Lovick T. Withdrawal from progesterone increases expression of alpha4, beta1, and delta GABA(A) receptor subunits in neurons in the periaqueductal gray matter in female Wistar rats. J Comp Neurol 2005;486:89-97.

  42. Oh S, Ho IK. Changes of [3H] muscimol binding and GABA (A) receptor beta2-subunit mRNA level by tolerance to and withdrawal from pentobarbital in rats. Neurochem Res 1999;24:1603-1609.

  43. Crews Ft, Bucklry T, Dodd PR, Ende G et al. Alcoholic neurobiology: changes in dependence and recovery. Alc Clin Exp Res 2005;29:1504-1513.

  44. Mhatre MC, Ticku MK. Chronic GABA treatment down-regulatesthe GABAA receptor alpha 2 and alpha 3 subunit mRNAS as well as polypeptide expression in primary cultured cerebral cortical neurons. Brain Res Mol Brain Res 1994;(1-4):159-165.

  45. Hui S, Sabaliauskas N, Sherpa A, Fenton A et al. A critical role for 4β GABAA receptors in shaping learning deficits at puberty in mice. Science 2010;327(5972):1515-1518.

  46. Jang CG, Oh S, Ho IK. Changes in NMDAR2 subunit mRNA levels during pentobarbital tolerance/withdrawal in the rat brain: an in situ hybridization study. Neurochem Res 1998;23:1371-1377.

  47. Silva-Barrat C, Velluti J, Szente M, Batini C et a. Exaggeration of epileptic- like patterns by nicotine receptor activation during the GABA withdrawal syndrome. Brain Res 2005;1042:133-143.

  48. Silva-Barrat C, Szente M, Menini C, Velluti JC et al. Muscarinic depression of synaptic transmission in the epileptogenic GABA withdrawal syndrome focus. J Neurophysiol 2001;85:2159-2165.

  49. Araneda S, Silva-Barrat C, Menini C, Naquet R. High expression of noradrenaline, choline acetyltransferase and glial fibrillary acid protein in the epileptic focus consecutive to GABA withdrawal. An immunocytochemical study. Brain Res 1994;655:135-146.

  50. Suzuki T, Tsuda M, Narita M, Funada M et al. Diazepam pretreatment suppresses morphine withdrawal signs in the mouse. Life Sci 1996;58: 349-357.

  51. Heberlein A, Bleich S, Kornhuber J, Hillemacher T. Benzodiazepine dependence: causalities and treatment options. Fortschr Neurol Psychiatry 2009;77:7-15.

  52. Sanna E, Mostallino Mc, Busonero F, Talani G et al. Changes in GABA(A) receptor gene expression associated with selective alterations in receptor function and pharmacology after ethanol withdrawal. J Neurosci 2003;23:11711-11724.

  53. Martin ED, Araque A, Buno W. Synaptic regulation of the slow Ca2+- activated K+ current in hippocampal CA1 pyramidal neurons: implication in epileptogenesis. J Neurophysiol 2001;86:2878-2886.

  54. Reddy DS, Kulkarni SK. Neurosteroid co-administration prevents development of tolerance and augments recovery from benzodiazepine withdrawal anxiety and hyperactivity in mice. Methods Find Exp Clin Pharmacol 1997;19:395-405.

  55. Behr J, Gloveli T, Heinemann U. Kindling induces a transient suppression of after hyperpolarization in rat subicular neurons. Brain Res 2000;867:259-264.




2020     |     www.medigraphic.com