ABSTRACT
Background and Purpose: Spreading depression [SD] is a neuronal-glyal depolarization, with a possible role in different neurological disorders including epilepsy and migraine aura. Initiation and propagation of SD modulate excitability of neuronal network. The aim of the present study was to investigate electrophysiological characteristics of neurons of the lateral amygdala in the late phase of excitability during SD
Methods and Materials: In this experimental study, 6 male rats were used. We used horizontal amygdala-hippocampusneocortex slice in which SD was induced by KCl application in each brain structure. After superfusion of these slices with GABAA receptor antagonist bicuculline [1.25 micromol/L] for 45 min, initiation of SD evoked ictal epileptic activity in all tested slices. The induction of SD in the lateral amygdala resulted in presence of interictal and ictal epileptiform field potentials and intracellular paroxysmal shift [PDS] For data analysis, paired ttest and one-way ANOVA were used in Sigma Stat 3 software
Results: The results demonstrated that SD moved the resting membrane potential [before -60.3 +/- 0.5 and after -52.8 +/- 0.78] towards depolarization after inducing the spreading depression in lateral Amygdale [P<0.001]. Likewise, the threshold for action potential before induction [5.5 +/- 0.2] and after induction [3.3 +/- 0.1] increased [P<0.001], together with the frequency of spontaneous activity of neurons before [164.1 +/- 40.2] and after [227.2 +/- 45.1] induction [P<0.05]. Most cells became slow adapting after SD induction
Conclusion: The results imply a possible role for SD as an underlying mechanism of epilepsy in predisposed neural tissue with increased excitation or decreased inhibition