Background & Aims : Spreading depression is a pathophysiological phenomenon that is initiated by a self-propagating depolarization wave with a short-term excitability and is followed immediately by an inhibitory phase and then continues with a long-term secondary excitability. Spreading depression has a critical role in many disorders such as migraine and seizures . The purpose of this study was to investigate the role of glutamate receptors and burst activity induced by spreading depression on synaptic plasticity in hippocampus CA1 region .

  Materials & Methods : This study was performed on brain slices of 18 male Wistar rats, weighing between 250- 350 g. The slices were studied at one group as control and two groups as glutamate receptor antagonists ( AP5 and CNQX). After deep anesthesia, the animals were decapitated and the brain was removed from the skull. Horizontal slices (500 thick ) containing the hippocampus region were prepared and perfused with GABA_A antagonist ( bicuculline 1.25). SD was created with KCl and then LTP was indused and excitatory field potentials were recorded.

  Results : Followed by inhibition of glutamate receptors after induction of spreading depression a significant reduction in the amplitude of excitatory field potentials was observed in test groups, CNQX (103.26 3.2), AP5 (102.88 1.1), compared to bicuculine (134 6.7) with Mann Whitney U test . (P <0.001)

  Conclusion : The results of this study emphasize on the role of glutamate receptors in induction of cortical spreading depression, so the antagonists that inhibit these receptors lead to suppression of cortical spreading depression. The study of the phase secondary excitability of SD may help us to understand the mechanism of SD action in associated neurological disorders. This finding can improve the therapeutic strategies for treatment of epilepsy .

  SOURCE: URMIA MED J 2014: 25(4): 318 ISSN: 1027-3727