HE ROLE OF CORTICAL SPREADING DEPRESSION ON INDUCTION OF SEIZURES IN THE HIPPOCAMPUS OF MALE RATS

Spreading depression is a pathophysiological phenomenon that is initiated by a selfpropagating

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
m
thick ) containing the hippocampus
region were prepared and perfused with GABA
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
A
after induction of spreading
depression a significant reduction in the amplitude of excitatory field potentials was observed in test groups,
),( AMPANMDA
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