Neurological Sciences

, Volume 34, Issue 4, pp 537–538 | Cite as

Relationship between thresholds to convulsions induced by a benzodiazepine inverse agonist and [3H]-l-glutamate binding in the membranes of brain regions

  • Marcos Brandão Contó
  • José Gilberto Barbosa de Carvalho
  • Marco Antonio Campana Venditti
Brief Communication

Abstract

Although some studies have investigated the influence of kindling model of epilepsy on the glutamatergic neurotransmission, the relation between glutamatergic receptors and seizure susceptibility remains unclear. The present study sought to determine if rats with high (HTR) and low (LTR) thresholds to clonic convulsions induced by the benzodiazepine inverse agonist DMCM differed in the [3H]-l-glutamate binding to membranes from discrete brain regions. Compared to the HTR subgroup, the LTR subgroup presented a lower binding of [3H]-l-glutamate in the hippocampus, frontal cortex and amygdala plus limbic cortex, suggesting that glutamatergic receptors in these brain regions may underlie the susceptibility to DMCM-induced convulsions.

Keywords

Convulsion Seizure [3H]-l-glutamate Binding Benzodiazepine inverse agonist DMCM 

Notes

Acknowledgments

This research was supported by Associação Fundo de Incentivo à Pesquisa (AFIP). M.B. Contó was the recipient of a fellowship from Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Capes).

References

  1. 1.
    Berkovic SF, Howell RA, Hay DA, Hopper JL (1998) Epilepsies in twins: genetics of the major epilepsy syndromes. Ann Neurol 43:435–445PubMedCrossRefGoogle Scholar
  2. 2.
    Bradford HF (1995) Glutamate, GABA and epilepsy. Prog Neurobiol 47:477–511PubMedCrossRefGoogle Scholar
  3. 3.
    Ngur DO, Rosenberg HC, Chiu TH (1990) Modulation of GABA-stimulated Cl flux by a benzodiazepine agonist and “inverse agonist” after chronic flurazepam treatment. Eur J Pharmacol 176:351–356PubMedCrossRefGoogle Scholar
  4. 4.
    Ferrarese C, Cogliati C, Tortorella R, Zucca C, Bogliun G, Beghi E (1998) Diazepam binding inhibitor (DBI) in the plasma of pediatric and adult epileptic patients. Epilepsy Res 29:129–134PubMedCrossRefGoogle Scholar
  5. 5.
    Polc P, Jahromi SS, Facciponte G, Pelletier MR, Zhang L, Carlen PL (1996) Benzodiazepine antagonists reduce epileptiform discharges in rat hippocampal slices. Epilepsia 37(10):1007–1014PubMedCrossRefGoogle Scholar
  6. 6.
    Van Rijn C, Meinardi H (2009) Neurochemistry and epileptology. Epilepsia 50(3):17–29PubMedCrossRefGoogle Scholar
  7. 7.
    Contó MB, Hipólide DC, Carvalho JGB, Venditti MAC (2012) Rats with different thresholds for DMCM-induced clonic convulsions differ in the sleep-time of diazepam and [3H]-Ro 15-4513 binding. Epilepsy Res 98:216–222PubMedCrossRefGoogle Scholar
  8. 8.
    Rössler AS, Schröder H, Dodd RH, Chapouthier G, Greecksch G (2000) Benzodiazepine receptor inverse agonist-induced kindling of rats alters learning and glutamate binding. Pharmacol Biochem Behav 67:169–175PubMedCrossRefGoogle Scholar
  9. 9.
    Schröeder H, Becker A, Schröeder U, Hoellt V (1999) 3H-l-glutamate binding and 3H-d-aspartate release from hippocampal tissue during the development of pentylenetetrazole kindling in rats. Pharmacol Biochem Behav 62(2):349–352PubMedCrossRefGoogle Scholar
  10. 10.
    March PA (1998) Seizures: classification, etiologies, and pathophysiology. Clin Tech Small Anim Pract 13(3):119–131PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 2012

Authors and Affiliations

  • Marcos Brandão Contó
    • 1
  • José Gilberto Barbosa de Carvalho
    • 1
  • Marco Antonio Campana Venditti
    • 1
  1. 1.Departamento de PsicobiologiaUniversidade Federal de São Paulo, Escola Paulista de Medicina (UNIFESP/EPM)São PauloBrazil

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