Interrelation of spreading depression and epileptiform burst in the lateral amygdala

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

Neurotoxin effects of Roth 801, dental sealer, on the spontaneous bioelectrical activity of F1 neuronal cells in Helix aspersa: using current-clamp technique

Some dental sealers have neurotoxic effects on neuronaltissues. These effects appear to be mediated through the inhibition of ionicchannels. Intracellular recording was performed on neuronal cells tocharacterize the underlying ionic mechanisms of neurotoxicity induced byRoth 801. Materials and Experiments were carried out on F1 neuronalsoma membrane located in the right parietal ganglion of snail, Helixaspersa. The properties of action potential were analyzed using singleelectrode current clamp method. Roth 801 was applied to the bathingsolution in invasive and gradual forms. In the current clamp experiments, several parameters, including,resting membrane potential [RMP], the peak amplitude of action potential,spike width, frequency, the peak amplitude of after hyperpolarization [AHP]were analyzed. In both invasive and gradual forms Roth 801 decreased thepeak of amplitude and frequency of action potential and the peakamplitude of AHP. But the duration of spike was prolonged. After invasiveapplication of Roth 801, membrane potential was depolarized. However ingradual method, it was initially hyperpolarized and subsequently shiftedtowards depolarized potential. These results suggest that Roth 801 affects shape andfrequency of action potential through inhibition of ionic currents