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

Does whole body exposure to GSM-950 MHz electromagnetic fields affect acquisition and consolidation of spatial information in rats?

This study was planned to examine the effects of whole-body exposure to GSM-950 MHz electromagnetic fields [EMFs] on acquisition and consolidation of spatial memory in rats using a water maze task. In experiment 1, the animals were given two blocks of five trials per day for three consecutive days in a water maze task. The interval between blocks was 4h. Before each training session, the animals were exposed to 950 MHz EMFs for 45 min with lower-[0.835 mW/cm[2]] or higher-power [1.166 mW/cm[2]] densities. In experiment 2, the animals were given two blocks of 5 trials with a 3 min interval between blocks. Immediately after the last trial, they were exposed to EMFs for 45 min with lower-or higher-power densities. In both experiments, 48 h after the last training day a 60 s probe test was done. Results from experiment1 [pre-training exposure to EMFs] indicated no significant differences in performances of exposed and non-exposed groups either during acquisition [learning] or during probe test [memory retention]. Results from experiment 2 [post training exposure to EMFs] also indicated no significant differences among groups during acquisition or probe test. In these experiments, no effect of exposure to 950 MHz on acquisition or consolidation of spatial navigation of rats in a water maze was detected

Low-power density of 950 MHz rediation does not affect long-term potentiation in rat dentate gyrus

Over the last decade, exposure to non-ionizing electromagnetic waves due to base station antenna has increased. This in vivo study was planned for evaluating the effects of whole-body exposure to 950 MHz field of GSM mobile phone system on rat dentate gyrus long-term potentiation. 24 naive male Wistar rats [3 month old, 225 +/- 25 g] were randomly divided in the three groups [sham-exposed, GSM and continuous field exposed]. The exposure program was planned for 10 sessions at 3 days. Animals were exposed to electromagnetic field for 45 minutes in a circular plastic chamber [mean power density=0.835 mW/cm[2]]. Immediately after end exposure, anesthesia was induced for long term potentiation [LTP] induction. Field potentials were recorded and analyzed using the population spike amplitude and EPSP slope for 60- min. There were no significant differences in population spike amplitude, EPSP slope and EPSP slope maintenance among the three groups. This study provides no evidence indicating that long-term potentiation can be affected by the whole-body exposure to low-power density of 950 MHz field of GSM mobile phone system

Facilitating effects of morphine dependence on spatial learning and memory in rat

The effect of morphine on spatial learning and memory is controversial. In the present study, the male rats were used to evaluate the effect of morphine dependence and cold water swimming on spatial learning and memory. Dependent animals received morphine sulfate in drinking water for 25 days. Animals were divided into four groups in simple randomized manner. The first control and dependent groups, were studied in normal water [20 +/- 2 °C], and the second control and dependent groups were studied in cold water [10-12 °C]. Morris Water Maze [MWM] experimentations were begun from 21st to 25th days of morphine administration. In each group of animals, spatial learning and memory parameters were analyzed. The results showed that morphine dependence may facilitates spatial learning and memory in MWM, and cold water reduces swimming speed but facilitating the formation of spatial memory. On the other hand, cold water swimming abolished the effects of morphine on spatial learning but facilitated its effect on spatial memory. The underling mechanism[s] to these phenomenon remains to be elucidated

[Effects of corticosterone injections after training and memory reactivation on recall of fear memory in rats]

Recent evidence indicated that when a stabilized memory is recalled or reactivated, it again becomes labile and initiates a time-dependent process referred to "reconsolidation". Considering the documented role of stress hormones on emotional memory, the purpose of this study was to compare the effects of glucocorticoids on consolidation and reconsolidation of a fear conditioning memory. Adult male Wistar rats were trained in fear conditioning system. In experiment 1, rats were placed into context and after 180 s were given two 2 s, 0.4 mA shocks with an interval of 120 s. Twenty seconds after the final shock, rats removed from the context box and were injected with different doses of corticosterone or vehicle. In reconsolidation experiments, rats received 2 s, 0.4 mA shocks with an interval of 120 s [moderate memory] or given eight 2 s, 1.5 mA shocks with an interval of 62 s [strong memory]. Thirty seconds after the final shock, rats removed from the context box. For reactivation, 24 h later rats were returned to the chamber for 90s. Immediately after reactivation, rats were injected with different doses of corticosterone or vehicle. Twenty-four hours after training or memory reactivation, rats were returned to the context box for 5 min. Seconds of freezing [defined as the absence of all visible movement oxcept respiration] during the retrieval testing were scored for each rat. The findings indicated that injections of corticosterone after training enhanced memory consolidation at dose of 3 mg/kg. Injections of the drug after memory reactivation did not change recall of moderate memory, but impaired recall of strong memory at dose of 3 mg/kg. The data indicate that glucocorticoids have opposite effects on consolidation and reconsolidation of contextual fear conditioning memory. Further studies are needed to determine the underlying mechanisms

[ effect of GSM mobile phone base station waves on hippocampus synaptic plasticity]

Over the last decade, exposure to electromagnetic waves due to base station antenna has increased. This in vivo study was planned for evaluating the effects of 950 MHz waves of GSM mobile phone system on dentate gyrus long-term potentiation. 32 naive male Wistar rats [3 months old, 220 +/- 15 g] were randomly divided into four groups [sham-exposed, continuous 950 MHz, 950 MHz with modulation and 950 MHz GSM field exposed]. The exposure program was planned for 10 sessions at 3 days. Animals were exposed to electromagnetic field for 45min in a circular plastic chamber [mean electric field = 50.4 V/m]. Immediately after ending exposure, anesthesia was induced for LTP induction. Field potentials were recorded and analyzed using the population spike amplitude, EPSP slope, EPSP slope maintenance and EPSP duration for 60-min. There were no significant differences in population spike amplitude, EPSP slope and EPSP slope maintenance and EPSP duration among the four groups. This experiment provides no evidence indicating that rat's long-term potentiation can be affected by the whole-body exposure to 950 MHz field of GSM mobile phone system

[Verapamil enhances the impairing effects of stress on retrieval of long-term memory in rats]

This study investigated an interaction between acute restraint stress and verapamil, as a blocker of L-type voltage sensitive channels on retrieval of long-term memory. Young adult male rats were trained in one trial inhibitory avoidance task [1mA, 1.5s footshock]. On retention test given 48 hr after training, the latency to re-enter dark compartment and time spent in light chamber of the apparatus were recorded. Thirty min before retention test, the rats were exposed to a 10 min of restraint stress in a Plexiglass with or without prior treatment of verapamil [5, 10, 20 mg/kg]. The results showed verapamil pretreatment enhanced the impairing effect of stress on memory retrieval. The applied stress increased circulating corticosterone levels as assessed immediately after the retention test, indicating that stress-induced impairment of memory retrieval is mediated, in part, by increased plasma levels of glucocorticoids. Verapamil did not affect on this response. These findings indicate that acute restraint stress impair retrieval of long-term memory, and provide evidence for the existence of an interaction between stress and L-type voltage calcium channels on this process

Responsiveness of paragigantocellularis nucleus neurons in morphine dependent rats to forskolin in vivo single unit recording

Although tolerance to and dependence on opioids are characterized by excessive activity of cAMP pathway in some brain stem nuclei, the impact of morphine dependence on activity of cAMP pathway in paragigantocellularis nucleus [PGi], located in the rostral ventrolateral medulla, remains unclear. Therefore, the effect of adenyl cyclase activator forskolin on spontaneous firing rate of PGi neurons and precipitation of withdrawal signs in morphine dependent rats was studied. Electrophysiologic extracellular single unit activity was recorded from PGi of urethane anesthetized NMRI male rats [200-350 g]. Forskolin [100 nM /300-400 nL / 3-4 min] was microinjected into PGi. To assess behavioral signs, frequency analysis was used. The results showed that spontaneous PGi neuronal firing rate in morphine dependent rats was lower than that of control ones, which confirms the tolerance to morphine. Forskolin caused an increase in PGi neuronal firing rate in control rats and completely suppressed spontaneous firing rate of PGi neurons in morphine dependent ones [p<0.001]. In freely moving control rats, forskolin induced wet-dog shake and chewing sings but not in morphine dependent ones. It is concluded that adaptive change in activity of cAMP pathway in PGi neurons following chronic morphine exposure may play a role in the development of tolerance to and dependence on morphine

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

Examination of theta pulse effect on CA1 synaptic transmission in hippocampal slices of pentylenetetrazol - kindled rats

Effects of theta pulse stimulation [TPS] on CA1 synaptic transmission in pentylenetetrazol [PTZ] kindled rats were studied. PTZ [45 mg/kg] was injected every 48 hours to NMRI male rats. Hippocampal slices were prepared from control, partially and fully kindled rats. Theta pulse was delivered to Schaffer collaterals and recording was made from strata radiatum and pyramidale of CA1 region of hippocampal slices. PTZ kindling resulted in an enduring increase in fEPSP slope, but not OPS amplitude, in CA1 region of hippocampus. TPS decreased the amplitude of population spikes [PS] of partially and fully kindled rats which was significant in the latter as compared to controls. It is concluded that repeated administration of PTZ can change susceptibility of CA1 synapses to TPS

effect of morphine injection in the priaqueductal gray matter on the neuronal responsiveness of nucleus reticularis paragigantocellularis to formalin

Nucleus reticularis paragigantocellularis [PGi] has a very effective role in the supraspinal pain modulation. PGi as a rostroventromedial medulla [RVM] structure receives a major input from periaqueductal gray matter [PAG].Formalin as a peripheral noxious stimulus has biphasic nociception and behavioural manifestations. To assess morphine injection in the priaqueductal gray matter[PAG] on the neuronal responsiveness of nucleus reticularis paragigantocellularis [PGi] to formalin. The experimental subjects were male NMRI rats. Diluted formulin [2.5%] as a chemical noxious stimulus and morphine as an analgesic drug were used. Using single unit recording [an extracelluar recording electrophysiologic method] the research was done. Findings indicate that the responses of the PGi inhibitory neurons evoked by formalin were disinhibited by morphine microinjection in the FAG. In the excitatory neurons, morphine decreased the firing rate to the baseline activity. PGi inhibitory neurons are affected by the PAG's GABAergic interneurons. Morphine blocks GABA released from these intenneurons and results to off- cell disinhibition. On- cells suppressions are probably related to morphine effects directly

Effects of formalin as a peripheral noxious stimulus on the nucleus reticularis paragigantocellularis neurons of ansethetized rats

In the present study, the effects of formalin as a peripheral noxious stimulus on spontaneously active units of the nucleus reticularis paragigantocellularis [PGi], a narrow region of the ventral pontine reticular formation, was examined in urethane anesthetized rats. Spontaneous discharge of the PGi neurons was variable, ranging from I to 37 spikes per second. Formalin as a chemical irritant and prolonged noxious stimulus induced changes in the firing of spontaneously active PGi neurons. There were three neuronal subpopulations in the PGi that responded to formalin: excited [19.35%], inhibited [45.16%] and unchanged [35.48%]. Thus we suggest that PGi neurons may be involved in the processing of information related to formalin as a chemical irritant