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

[Effects of transient and permanent inhibition of the amygdala on acquisition of piriform cortex kindled seizures in rats]

Epilepsy is one of the most common neuronal disorders in man. The amygdala is one of the important locations for seizures originated from piriform cortex. Neverthless, its role in development of such seizures has not been reported so far. Therefore in this study, the effects of amygdala inhibition on kindling rate of piriform cortex was investigated. Under two study protocols, thirty male Wistar rats[300-350 g] in 5 groups [n=6] were studied. In the first protocol animals were divided into three groups; first group only were canulated without any treatment, second group received artificial CSF and third group received 0.5 micro l of 2% lidocaine intra amygdaloid. The second protocol, included two groups; in the first group the amygdala was lesioned by electrical DC current and animals were stimulated 24 h later and in the second group animals canulated but amygdala was not lesioned In this study, intra amygdala injection of 2% lidocaine and electrical lesion of it increased number of stimulation to receive S4 and S5 stages of seizure, but had no effects on number of stimulations to receive S1, S2, S3 stages cumulative after discharge duration [ADD], after discharge threshold and ADD after the first duration. We concluded that the amygdala has a critical role in the development of epileptic seizures from piriform cortex to other regions and this role is significantly affected by transient and permanent inhibition of neuronal activity of amygdala

role of adenosine A1 receptor activity of piriform cortex neurons on amygdala kindled seizures in rats

Considering the anticonvulsant effects of A1 Adenosine Receptors and the anatomical connections between piriform Cortex and Amygdala, in this study, the role of A1 adenosine receptors activity of piriform cortex neurons on amygdala kindled seizures was investigated in rats. The rats were fully kindled by daily electrical stimulation of amygdala. N6-cyclohexyleadenosine [CHA; 1,10 and 100 mM], as a selective A1 agonist and 1,3-dimethyl-8-cyclohexylexantine [CPT; 20 and 10 mM], as a selective A1 antagonist were microinjected [0.5ml, 0.25 ml/min] into the piriform cortex. Animals were stimulated at 5, 15 or 90 min after drug microinjection and seizure parameters were measured. Intra-piriform CHA [10 or 100 mM] reduced afterdischarge duration and stage 5 seizure duration and prolonged stage 4 latency significantly. Pretreatment with CPT [10 mM] 5 min before CHA [100 mM] eliminated the effects of CHA. These observations suggest that A1 adenosine receptors activity in piriform cortex reduced the seizure severity and attenuated the distribution of seizure activity to other brain regions

Adenosine Al receptors of amygdala has not anticonvulsant effects on piriform cortex kindled seizures in rats

Adenosine is an endogenous anticonvulsant which exerts its anticonvulsant effects through adenosine Al receptors. As the piriform/amygdala is a critical circuit for limbic seizure propagation, in this study the role of amygdala Al receptors on piriform cortex kindled seizures was investigated. Rats were kindled by daily electrical stimulation of piriform cortex. In the first experiment fully kindled animals received intra-amygdala N6-cyclohexyladenosine [CHA; 10-500 micro M, a selective Al receptor] or 2% lidocaine [for reversal neuronal inhibition] bilaterally. 5 min later, animals were stimulated and seizure parameters were measured. In the second experiment, the effect of daily microinjection of CHA [100 microM] into the amygdala on piriform cortex kindling rate was investigated. Different doses of CHA had no effect on kindled seizure parameters. On the other hand, intra-amygdala 2% lidocaine reduced the kindled seizures severity. There were significant increase in stage 4 latency and decrease in stage 5 duration. Also, daily intra-amygdala CHA had no significant effect on kindling rate. The amygdala neuronal activity has a role in propagation of epileptic seizures from piriform cortex. Elimination of this activity by lidocaine decreases the severity of piriform cortex kindled seizures. However, the amygdala Al receptors have no role in this regard