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Pavel Mareš – One of the best experts on this subject based on the ideXlab platform.

  • A1 not A2A adenosine receptors play a role in cortical epileptic Afterdischarges in immature rats
    Journal of Neural Transmission, 2014
    Co-Authors: Pavel Mareš
    Abstract:

    Endo- as well as exogenous adenosine exhibits anticonvulsant action. Participation of individual types of adenosine receptors was studied in present experiments in immature rats. Cortical epileptic Afterdischarges were used as a model in rat pups 12, 18 and 25 days old. CCPA, an agonist of A1 adenosine receptors, decreased markedly duration of Afterdischarges whereas DPCPX, an antagonist of A1 receptors, exhibited strong proconvulsant action. Action of either drug was best expressed in 12-day-old rats and it decreased with age. Drugs influencing A2A adenosine receptors (agonist CGS21680 and antagonist ZM241385) did not exhibit systematic effects in our model. Motor phenomena accompanying cortical stimulation or epileptic Afterdischarge were never influenced by any of the four drugs studied. A1 adenosine receptors are important in the model of cortical seizures, especially in the youngest group studied.

  • Antagonists of group I metabotropic glutamate receptors and cortical Afterdischarges in immature rats
    Epilepsia, 2009
    Co-Authors: Denisa Lojková-janečková, Pavel Mareš
    Abstract:

    Summary Purpose:  Antagonists of group I metabotropic glutamate receptors (mGluRs) are known to exhibit anticonvulsant action without serious side effects. Recently we found anticonvulsant effects of specific antagonists of mGluR subtypes 1 and 5 (AIDA and MTEP) against pentetrazol-induced convulsions in developing rats. In order to determine if the effects of these two antagonists are not exclusively restricted to pentetrazol-induced seizures, we studied their action in a novel seizure model involving immature rats. Methods:  Epileptic Afterdischarges were elicited by low-frequency stimulation of sensorimotor cortical region in 12-, 18-, and 25-day-old rats with implanted electrodes. Drugs were administered intraperitoneally after the first Afterdischarge: AIDA in doses from 5 to 40 mg/kg; MTEP in doses from 2.5 to 40 mg/kg. The stimulation was then repeated five more times with the same current intensity. Electrocorticographic and motor phenomena were recorded and evaluated. Results:  AIDA did not significantly influence movements during stimulation, Afterdischarges as well as clonic seizures accompanying Afterdischarges. In contrast, MTEP was able to significantly shorten Afterdischarges without changes in the two motor phenomena. The effect of MTEP was best expressed in 12-day-old rats; in 25-day-old rats the trials exhibited only a transient shortening of Afterdischarges after high doses of MTEP. Discussion:  In contrast to similar action against pentetrazol-induced seizures, AIDA and MTEP substantially differ in their action on cortical epileptic Afterdischarges. The anticonvulsant action of MTEP in the present model diminishes with age.

  • Interaction of excitatory amino acid agonists with cortical Afterdischarges in developing rats.
    Epilepsia, 2002
    Co-Authors: Pavel Mareš, R Haugvicová, H Kubová
    Abstract:

    Summary:  Purpose: To determine the role of excitatory aminamino acids (EAAs) in genesis of two types of epileptic Afterdischarges. Methods: Cortical stimulation and recording electrodes were implanted in 12-, 18-, and 25-day-old rats. Epileptic Afterdischarges were induced by rhythmic stimulation of sensorimotor cortex. The stimulation was repeated 6 times with 20-min intervals. Ten minutes after the first Afterdischarge, N-methyl-d-aspartate, homocysteine, or kainic acid was injected. The doses were chosen individually for different age groups to be subconvulsive. Type and duration of Afterdischarges as well as type and severity of motor correlates were evaluated. Results: N -methyl- d -aspartate prolonged Afterdischarges only in 12-day-old rats, whereas two other drugs did it in all age groups. Motor correlates of Afterdischarges were changed to flexion seizures in 12-day-old rats after N -methyl- d -aspartate and homocysteine; in 25-day-old rats homocysteine led to generalized tonic–clonic seizures (i.e., both patterns seen after substantially higher doses of these drugs in nonstimulated rats). Seizures lasted tens of minutes. Kainic acid did not change the motor pattern in any age group, but nonconvulsive EEG seizures were recorded in the interstimulation periods mainly in 18- and 25-day-old rats. Increased transition into the limbic type of Afterdischarges appeared only after homocysteine in 18- and 25-day-old rats. Conclusions: A mutual potentiation of epileptic phenomena was induced by two agents. The actions of N-methyl-d-aspartate and kainic acid differ in all age groups; the effects of homocysteine were identical with those of N-methyl-d-aspartate in 12-day-old rats but not later. Only homocysteine augmented transition into the limbic type of Afterdischarges.

Nancy L. Wayne – One of the best experts on this subject based on the ideXlab platform.

György Buzsáki – One of the best experts on this subject based on the ideXlab platform.

  • Ultra-slow oscillation (0.025 Hz) triggers hippocampal Afterdischarges in Wistar rats.
    Neuroscience, 1999
    Co-Authors: Markku Penttonen, N Nurminen, Riitta Miettinen, Jouni Sirviö, Darrell A. Henze, Jozsef Csicsvari, György Buzsáki
    Abstract:

    Abstract Oscillations in neuronal networks are assumed to serve various physiological functions, from coordination of motor patterns to perceptual binding of sensory information. Here, we describe an ultra-slow oscillation (0.025 Hz) in the hippocampus. Extracellular and intracellular activity was recorded from the CA1 and subicular regions in rats of the Wistar and Sprague–Dawley strains, anesthetized with urethane. In a subgroup of Wistar rats (23%), spontaneous Afterdischarges (4.7±1.6 s) occurred regularly at 40.8±15.7 s. The Afterdischarge was initiated by a fast increase of population synchrony (100–250 Hz oscillation; “tonic” phase), followed by large-amplitude rhythmic waves and associated action potentials at gamma and beta frequency (15–50 Hz; “clonic” phase). The Afterdischarges were bilaterally synchronous and terminated relatively abruptly without post-ictal depression. Single-pulse stimulation of the commissural input could trigger Afterdischarges, but only at times when they were about to occur. Commissural stimulation evoked inhibitory postsynaptic potentials in pyramidal cells. However, when the stimulus triggered an Afterdischarge, the inhibitory postsynaptic potential was absent and the cells remained depolarized during most of the Afterdischarge. Afterdischarges were not observed in the Sprague–Dawley rats. Long-term analysis of interneuronal activity in intact, drug-free rats also revealed periodic excitability changes in the hippocampal network at 0.025 Hz. These findings indicate the presence of an ultra-slow oscillation in the hippocampal formation. The ultra-slow clock induced Afterdischarges in susceptible animals. We hypothesize that a transient failure of GABAergic inhibition in a subset of Wistar rats is responsible for the emergence of epileptiform patterns.

  • Termination of Epileptic Afterdischarge in the Hippocampus
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997
    Co-Authors: Anatol Bragin, Markku Penttonen, György Buzsáki
    Abstract:

    The mechanism of Afterdischarge termination in the various hippocampal regions was examined in the rat. Stimulation of the perforant path or the commissural system was used to elicit Afterdischarges. Combination of multiple site recordings with silicon probes, current source density analysis, and unit recordings in the awake animal allowed for a high spatspatial resolution of the field events. Interpretation of the field observations was aided by intracellular recordings from anesthetized rats. Irrespective of the evoking conditions, Afterdischarges always terminated first in the CA1 region. Termination of the Afterdischarge was heralded by a large DC shift initiated in dendritic layers associated with a low amplitude “Afterdischarge termination oscillation” (ATO) at 40 to 80 Hz in the cell body layer. ATOs were also observed in the CA3 region and the dentate gyrus. The DC shift spread at the same velocity (0. 1-0.2 mm/sec) in all directions and could cross the hippocampal fissure. All but 1 of the 25 putative interneurons in the CA1 and dentate regions ceased to fire before the onset of ATO. Intracellularly, ATO and the emerging DC potential were associated with fast depolarizing potentials and firing of pyramidal cells and depolarization block of spike initiation, respectively. Both field ATO and the intracellular depolarization shift were replicated by focal microinjection of potassium. We hypothesize that [K+]o lost by the intensely discharging neurons during the Afterdischarge triggers propagating waves of depolarization in the astrocytic network. In turn, astrocytes release potassium, which induces a depolarization block of spike generation in neurons, resulting in “postictal depression” of the EEG.

  • epileptic Afterdischarge in the hippocampal entorhinal system current source density and unit studies
    Neuroscience, 1997
    Co-Authors: A. Bragina, Markku Penttonen, Jozsef Csicsvari, György Buzsáki
    Abstract:

    The contribution of the various hippocampal regions to the maintenance of epileptic activity, induced by stimulation of the perforant path or commissural system, was examined in the awake rat. Combination of multiple-site recordings with silicon probes, current source density analysis and unit recordings allowed for a high spatspatial resolution of the field events. Following perforant path stimulation, seizures began in the dentate gyrus, followed by events in the CA3-CA1 regions. After commissural stimulation, rhythmic bursts in the CA3-CA1 circuitry preceded the activation of the dentate gyrus. Correlation of events in the different subregions indicated that the sustained rhythmic Afterdischarge (2-6 Hz) could not be explained by a cycle-by-cycle excitation of principal cell populations in the hippocampal-entorhinal loop. The primary Afterdischarge always terminated in the CA1 region, followed by the dentate gyrus, CA3 region and the entorhinal cortex. The duration and pattern of the hippocampal Afterdischarge was essentially unaffected by removal of the entorhinal cortex. The emergence of large population spike bursts coincided with a decreased discharge of interneurons in both CA1 and hilar regions. The majority of hilar interneurons displayed a strong amplitude decrement prior to the onset of population spike phase of the Afterdischarge. These findings suggest that (i) Afterdischarges can independently arise in the CA3-CA1 and entorhinal dentate gyrus circuitries, (ii) reverberation of excitation in the hippocampal-entorhinal loop is not critical for the maintenance of Afterdischarges and (iii) decreased activity of the interneuronal network may release population bursting of principal cells.

Wolfgang Löscher – One of the best experts on this subject based on the ideXlab platform.

  • Phenytoin’s effect on the spread of seizure activity in the amygdala kindling model.
    Naunyn-Schmiedeberg's archives of pharmacology, 1997
    Co-Authors: U. Ebert, Sybille Cramer, Wolfgang Löscher
    Abstract:

    Phenytoin is a major antiepileptic drug for treatment of limbic seizures. The effect of phenytoin on the generation and spread of seizure activity was studied in a rat model of this type of seizures. Sprague-Dawley and Wistar rats were implanted with a stimulation and recording electrode in the basolateral amygdala. Naive Sprague-Dawley rats showed an increase in current intensity necessary for eliciting Afterdischarges (Afterdischarge threshold) of about 200% after administration of phenytoin (75 mg/kg i.p.), while seizure severity at threshold was increased compared to controls. Afterdischarge and seizure durations were significantly prolonged under phenytoin. This result suggests that phenytoin can exert a potent anticonvulsant effect on the generation of focal seizure activity, but it does not suppress or may even increase on-going Afterdischarge activity once it occurs. Following amygdala kindling in Wistar rats, administration of phenytoin again resulted in an increase in the Afterdischarge threshold. However, all rats still showed generalized seizures, and epileptic Afterdischarges could be recorded in various limbic brain regions at threshold current. This result suggests that phenytoin can increase the threshold for generation of epileptic discharges in kindled rats, but is not able to prevent the development of generalized seizure activity and the spread of Afterdischarges within the limbic system when focal activity is initiated. We conclude that phenytoin is able to suppress focal seizure activity in the amygdala kindling model of the rat. However, it does not prevent the spread of seizure activity originating in the limbic system. Therefore, a decrease in focal seizure susceptibility seems to be the primary target for phenytoin’s anticonvulsant action.

  • susceptibility of different cell layers of the anterior and posterior part of the piriform cortex to electrical stimulation and kindling comparison with the basolateral amygdala and area tempestas
    Neuroscience, 1995
    Co-Authors: Wolfgang Löscher, U. Ebert, Ulrich Wahnschaffe, Chris Rundfeldt
    Abstract:

    Abstract Several lines of evidence suggest that the piriform cortex functions as a generator in the development and propagation of forebrain (limbic type) seizures, particularly in the kindling model of epilepsy. It is, however, not clear where, within the rather large piriform cortex region, the generator resides, and how much tissue is involved. Highly sensitive loci to chemical or electrical stimstimulation have been described both in the deep anterior and posterior parts of the piriform cortex. Furthermore, data from piriform cortex slice preparations indicated that epileptiform potentials originate in deep structures, particularly the endopiriform nucleus that underlies the piriform cortex. In the present study, in rats, we implanted stimulation and recording electrodes in various rostrocaudal locations of the piriform cortex and endopiriform nucleus, including the “area tempestas” i.e., a structure in the anterior part of the piriform cortex previously proposed to be critically involved in the generation of convulsive seizures of limbic origin. Within the piriform cortex, electrodes were aimed at different cellular layers of this structure. For comparison, additional animals received electrodes in different parts of the basolateral amygdala. A total of 19 different locations was obtained in this way. The susceptibility of these locations to electrical stimstimulation was characterized by determining the threshold for induction of Afterdischarges. The Afterdischarge threshold was lowest in layer III of the posterior piriform cortex and some locations in the endopiriform nucleus, whereas amygdala and “area tempestas” displayed higher values. In several animals, particularly those with electrodes in layer III of the posterior piriform cortex, spontaneous spiking was seen in prestimulation recordings, whereas this was never observed in recordings from the amygdala. Subsequent kindling by repeated stimstimulation of the various locations demonstrated marked differences in Afterdischarge threshold reduction and kindling rate. The most marked decreases in Afterdischarge threshold were seen in locations within layer III of the piriform cortex, whereas several other locations, including the “area tempestas”, exhibited only moderate decreases or no decrease at all. In contrast to previous observations with only few locations in the piriform cortex region, the posterior piriform cortex was not in general slower to kindle than the anterior piriform cortex, although some locations in the posterior piriform cortex exhibited significantly lower kindling rates than the amygdala. The highest kindling rate was seen in the dorsal endopiriform nucleus. When the stepwise progression of kindling was studied, several locations in the piriform cortex stayed for long periods in the early and middle, i.e. focal stages of the kindling process, thus refuting previous suggestions that the piriform cortex generally proceeds rapidly through these stages. Behavioral characteristics of seizures kindled from the diverse sites did not differ. In conclusion, within the amygdala-piriform cortex region, the most sensitive cells to electrical induction of Afterdischarge and reduction of Afterdischarge threshold by repeated electrical stimstimulation reside in layer III of the posterior piriform cortex, while the anterior part of the piriform cortex, including the locus previously termed “area tempestas”, is less susceptible in this regard. In contrast to the marked decrease in Afterdischarge threshold, several locations in the posterior piriform cortex kindle only slowly, thus demonstrating a separation between decrease in seizure threshold and increase in seizure severity in response to repeated electrical stimstimulation.

  • Development and pharmacological suppression of secondary Afterdischarges in the hippocampus of amygdala-kindled rats.
    The European journal of neuroscience, 1995
    Co-Authors: U. Ebert, Chris Rundfeldt, Wolfgang Löscher
    Abstract:

    The development and spread of Afterdischarges in the ipsilateral limbic system during amygdala kindling, a model of complex partial seizures, was studied in male and female rats. Kindling stimulation was performed in the basolateral amygdala, and Afterdischarges were recorded from the stimulation electrode and electrodes in the nucleus accumbens, the posterior piriform cortex and the ventral hipphippocampus, all implanted on the right side of the brain. All structures showed primary Afterdischarges already after the first stimulation, indicating a close anatomical and physiological connection to the epileptogenic focus. The development of robust secondary Afterdischarges, which occurred after the end of the primary Afterdischarges in the amygdala and which always originated in the hippocampus but also spread to one or more of the other recording sites, is described. The secondary Afterdischarges initially occurred after about nine kindling stimulations in both male and female rats, and were associated with an increase in primary Afterdischarge duration and a progression from focal to motor seizures. In order to test the effect of common antiepileptic drugs on the secondary Afterdischarges, a group of female rats were treated with valproate, carbamazepine or phenytoin. All drugs suppressed the secondary Afterdischarges, although they had a different anticonvulsant efficacy on motor seizures and Afterdischarge duration after amygdala stimulation. While valproate and carbamazepine dose-dependently reduced all parameters of the kindled seizure, including the secondary Afterdischarges in the hippocampus, phenytoin suppressed the secondary Afterdischarges also in the absence of any anticonvulsant effect, suggesting that recurrent hippocampal activation is not crucial for the kindled state. Recording of secondary Afterdischarges in the hippocampus may offer the possibility of studying the conditions for development and pharmacological suppression of recurrent hippocampal activation in amygdala-kindled rats.

Markku Penttonen – One of the best experts on this subject based on the ideXlab platform.

  • Frequency bands and spatiotemporal dynamics of β burst stimulation induced Afterdischarges in hippocampus in vivo
    Neuroscience, 2005
    Co-Authors: J.e. Mikkonen, Markku Penttonen
    Abstract:

    Temporal and spatial characteristics of hippocampal neuronal network activation are modified during epileptiform Afterdischarges. We developed a beta burst stimulation protocol to investigate subregional variations and substrates of rhythmic population spike discharges in vivo in urethane anesthetized Wistar rat hippocampus with a 14-electrode recording array and extracellular single electrode recordings. Our 64 pulse beta burst stimulation protocol was constructed from electrical pulses delivered at intervals corresponding to beta (14-25 Hz), Delta (2 Hz), and slow (0.5 Hz) frequencies. In each experiment these interleaved pulses were all repeated four times with unchanged intervals. Stimulation of either perforant path or fimbria fornix induced a prolonged Afterdischarge pattern peaking at 200 Hz fast, 20 Hz beta, and 2 Hz Delta frequencies. Analysis of variance confirmed that the response pattern of the discharges remained constant regardless of the stimulation beta frequency. Within the Afterdischarge the fast frequencies were restricted to independent hippocampal subfields whereas beta and slow frequencies correlated across the subfields. Current source density (CSD) analysis revealed that the original signal propagation through subfields of the hippocampus was compromised during the beta burst stimulation induced Afterdischarge. In addition, the CSD profile of the epileptiform Afterdischarge was consistently similar across the different experiments. Time-frequency analysis revealed that the beta frequency Afterdischarge was initiated and terminated at higher gamma (30-80 Hz) frequencies. However, the alterations in the CSD profile of the hippocampus coincided with the beta frequency dominated discharges. We propose that hippocampal epileptiform activity at fast, beta and Delta frequencies represents coupled oscillators at respectively increasing spatial scales in the hippocampal neuronal network in vivo.

  • Ultra-slow oscillation (0.025 Hz) triggers hippocampal Afterdischarges in Wistar rats.
    Neuroscience, 1999
    Co-Authors: Markku Penttonen, N Nurminen, Riitta Miettinen, Jouni Sirviö, Darrell A. Henze, Jozsef Csicsvari, György Buzsáki
    Abstract:

    Abstract Oscillations in neuronal networks are assumed to serve various physiological functions, from coordination of motor patterns to perceptual binding of sensory information. Here, we describe an ultra-slow oscillation (0.025 Hz) in the hippocampus. Extracellular and intracellular activity was recorded from the CA1 and subicular regions in rats of the Wistar and Sprague–Dawley strains, anesthetized with urethane. In a subgroup of Wistar rats (23%), spontaneous Afterdischarges (4.7±1.6 s) occurred regularly at 40.8±15.7 s. The Afterdischarge was initiated by a fast increase of population synchrony (100–250 Hz oscillation; “tonic” phase), followed by large-amplitude rhythmic waves and associated action potentials at gamma and beta frequency (15–50 Hz; “clonic” phase). The Afterdischarges were bilaterally synchronous and terminated relatively abruptly without post-ictal depression. Single-pulse stimulation of the commissural input could trigger Afterdischarges, but only at times when they were about to occur. Commissural stimulation evoked inhibitory postsynaptic potentials in pyramidal cells. However, when the stimulus triggered an Afterdischarge, the inhibitory postsynaptic potential was absent and the cells remained depolarized during most of the Afterdischarge. Afterdischarges were not observed in the Sprague–Dawley rats. Long-term analysis of interneuronal activity in intact, drug-free rats also revealed periodic excitability changes in the hippocampal network at 0.025 Hz. These findings indicate the presence of an ultra-slow oscillation in the hippocampal formation. The ultra-slow clock induced Afterdischarges in susceptible animals. We hypothesize that a transient failure of GABAergic inhibition in a subset of Wistar rats is responsible for the emergence of epileptiform patterns.

  • Termination of Epileptic Afterdischarge in the Hippocampus
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997
    Co-Authors: Anatol Bragin, Markku Penttonen, György Buzsáki
    Abstract:

    The mechanism of Afterdischarge termination in the various hippocampal regions was examined in the rat. Stimulation of the perforant path or the commissural system was used to elicit Afterdischarges. Combination of multiple site recordings with silicon probes, current source density analysis, and unit recordings in the awake animal allowed for a high spatial resolution of the field events. Interpretation of the field observations was aided by intracellular recordings from anesthetized rats. Irrespective of the evoking conditions, Afterdischarges always terminated first in the CA1 region. Termination of the Afterdischarge was heralded by a large DC shift initiated in dendritic layers associated with a low amplitude “Afterdischarge termination oscillation” (ATO) at 40 to 80 Hz in the cell body layer. ATOs were also observed in the CA3 region and the dentate gyrus. The DC shift spread at the same velocity (0. 1-0.2 mm/sec) in all directions and could cross the hippocampal fissure. All but 1 of the 25 putative interneurons in the CA1 and dentate regions ceased to fire before the onset of ATO. Intracellularly, ATO and the emerging DC potential were associated with fast depolarizing potentials and firing of pyramidal cells and depolarization block of spike initiation, respectively. Both field ATO and the intracellular depolarization shift were replicated by focal microinjection of potassium. We hypothesize that [K+]o lost by the intensely discharging neurons during the Afterdischarge triggers propagating waves of depolarization in the astrocytic network. In turn, astrocytes release potassium, which induces a depolarization block of spike generation in neurons, resulting in “postictal depression” of the EEG.