UMLS:C0036572 - FACTA Search

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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epileptiform potentials, consisting of spontaneous, generalized bursts frequently assuming a 3/sec spike-wave form and tonic clonic electrographic seizures were produced in 32 lightly anesthetized cats by parenteral injections of penicillin. The activity of 83 identified pyramidal tract cells and 207 cortical non-pyramidal tract cells was correlated with the surface EEG. The majority of both cell types generated depolarizations and action potentials with the EEG spike. Hyperpolarizations, during which cells were inhibited, followed the depolarizations. The depolarizations responded to injected current as if they were generated by excitatory synapses; and hyperpolarizations to injected current and chloride ions as if generated by proximal inhibitory synapses. Attempts to identify a class of neurons firing during the surface-negative wave (presumed inhibitory interneurons) were unsuccessful. Forty-two units were recorded during tonic-clonic seizures. Intracellular records disclosed tonic oscillations of membrane potential, phased bursting with "depolarization shifts", abortive action potentials and post-ictal hyperpolarizations. Cell somata often depolarized to the point of inactivation, but axons continued to fire at high rates. These results emphasize the role of EPSP-IPSP sequences in the generation of spike-wave rhythms.
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PMID:Spike-wave rhythms in cat cortex induced by parenteral penicillin. II. Cellular features. 6 23

Intracellular recordings were obtained from the basolateral amygdala in in vitro rat brain slice preparations to examine whether gamma-aminobutyric acid (GABA)B receptors are altered after in vivo kindling-induced epileptogenesis. Stimulating the stria terminalis evoked excitatory (EPSPs) and inhibitory (IPSPs) postsynaptic potentials in control neurons, and epileptiform bursting or enhanced EPSPs, but no IPSPs, in neurons from animals, 4 to 8 weeks after the last kindled seizure. Baclofen (0.1 nM-100 microM) depressed EPSPs in control and kindled basolateral amygdala neurons, but the EC50 appeared to be shifted 100-fold from 5 nM in control to 500 nM in kindled neurons. Further analysis suggested a high-affinity component may be affected in kind led neurons. The absence of IPSPs in kindled neurons could not account for this shift, because effects of baclofen on EPSP amplitude were reduced in kindled animals even when GABAA receptors were blocked with bicuculline methiodide (30 microM) and postsynpatic GABAB receptors with intracellular guanosine 5'-O-3-thiotriphosphate (10 mM); 6-cyano-2,3-dihydroxy-7-nitroquinoxaline (10 microM) was also present to block bicuculline methiodide-induced bursting. Membrane responses to exogenously applied N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid were not affected by baclofen. Baclofen also hyperpolarized basolateral amygdala neurons and reduced membrane input resistance with an EC50 of 1 microM in control and kindled neurons. Post- but not presynaptic effects of baclofen were blocked by 2-hydroxy-saclofen (100 microM) and pertussis toxin pretreatment. In conclusion, kindling-induced epileptogenesis reduces the sensitivity of presynaptic GABAB receptors, an effect which may contribute to the enhancement of excitatory transmission in kindled animals. Furthermore, different pharmacological properties of pre- and postsynaptic receptors in the amygdala suggest two distinct populations of GABAB receptors whose long-lasting responses to kindling-induced seizures are different.
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PMID:Epileptogenesis reduces the sensitivity of presynaptic gamma-aminobutyric acidB receptors on glutamatergic afferents in the amygdala. 132 20

Recent studies with kindling and convulsant drug models of epilepsy suggest that the piriform (primary olfactory) cortex may be particularly susceptible to generation of epileptiform activity. The present study has examined the generation of interictal epileptiform events in the piriform cortex of kindled rats in vivo, taking advantage of special features of this system that facilitate physiological analysis. The investigation included analysis of extracellular and intracellular potentials, and membrane currents computed by current source density (CSD) analysis. In pyramidal cells, epileptiform events consisted of an initial EPSP that occurred in all-or-none fashion and a long-lasting IPSP with Cl(-)- and K(+)-mediated components. Onset of the IPSP was sufficiently fast that firing evoked by the EPSP was consistently limited to single action potentials. CSD analysis revealed the presence of two distinctly different excitatory epileptiform currents: an initial inward current of unknown origin that is widely distributed over depth, and a second much larger inward current at the depths of proximal apical and basal dendrites of pyramidal cells. It was concluded that this second component is mediated by the associational projections of pyramidal cells excited by the first component. Since these heavy associational projections also extend to neighboring areas including the amygdala, entorhinal cortex, and insular and orbitofrontal areas of neocortex, this second component could be widely propagated within the basal forebrain. An important finding was that the EPSP generated by this associational pathway was completely blocked in cell bodies of pyramidal cells in piriform cortex by the IPSP during most events. This IPSP may therefore play a critical role in limiting seizure activity by preventing reverberating positive feedback in the pyramidal cell population. It can be speculated that compromise of this IPSP, as by repetitive activation by the shock trains used for kindling, leads to prolonged epileptic activity in the piriform cortex and the many limbic structures to which it projects.
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PMID:Neuronal processes that underlie expression of kindled epileptiform events in the piriform cortex in vivo. 160 37

The effects of prenatal protein malnutrition upon the efficacy of excitatory synaptic transmission at the level of the perforant path/dentate granule cell synapse were examined during development of perforant path kindling in chronically implanted adults rats. Rats born to dams fed a low protein (6% casein) or control protein (25% casein) diet were fostered to lactating dams fed the 25% casein diet 24 h after birth and were maintained on this diet throughout life following weaning. Beginning at 90-120 days of age, animals received daily kindling stimulations applied to the perforant path. Extracellular field potentials recorded from the granule cell layer of the dentate gyrus in response to single-pulse stimulation of the perforant path were analyzed to determine the effects of prenatal protein malnutrition on the efficacy of synaptic transmission during the kindling process. Measures used for these analyses included the EPSP slope, an indicator of the level of synaptic drive, the population spike amplitude which is a measure of postsynaptic activation and cellular firing, and the ratio of the population spike amplitude relative to the corresponding EPSP slope value, which was used to evaluate the overall efficacy of synaptic transmission. animals of the 6%/25% diet group were found to have significantly lower afterdischarge thresholds, yet required significantly more daily kindling stimulations to develop generalized motor convulsions (stage 5 seizure) than control animals. Examination of dentate field potentials obtained prior to kindling revealed no significant between group differences in measures of EPSP slope or population spike amplitude. Statistically significant increases in measures of both the population EPSP slope and population spike amplitude were observed in both diet groups 24 h after the first kindled afterdischarge. The degree of increase in both of these measures was significantly greater in animals of the 6%/25% group. Evaluation of input/output measures obtained during kindling revealed a steady increase in the population EPSP slope for both diet groups with animals of the 6%/25% group showing significantly greater levels of enhancement in this measure than controls. Enhancement of population spike amplitudes reached maximal values in animals of the 25%/25% group within the first few kindling stimulations and these levels remained unchanged until the first stage 5 seizure. In contrast, animals of the 6%/25% group showed a continuous increase in the population spike amplitude measure during the entire kindling process. Appearance of the first generalized motor convulsion (stage 5 seizure) resulted in a decrease in population spike amplitudes in both diet groups, with animals of the 6%/25% group showing a significantly greater decrease in this measure than controls.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of prenatal protein malnutrition on kindling-induced alterations in dentate granule cell excitability. I. Synaptic transmission measures. 164 74

To determine if electrophysiological properties of hippocampal pathways are altered after medial septal area (MSA) destruction, extracellular recordings were made from hippocampal slices of rats 30 days following lesion and compared with those from unoperated controls. The preparation of slices, data accumulation and data analyses were done under the same conditions. The electrophysiological parameters of interest were the population spike (PS) and the field EPSP, produced in the CA1 pyramidal layer by stimulation of the Schaffer collaterals. The principal finding of this study was that neuronal excitability in slices from MSA-lesioned rats was altered. The most striking abnormalities were an epileptiform activity, which consisted of multiple PSs, and multiple seizure-like after discharges with a delayed onset to low stimulation intensities. In the CA1 region of the slices collected from lesioned rats the input-output curve of field EPSP versus PS showed a leftward shift as compared with their counterparts in normal slices. These changes may be related to relative reduction of inhibitory processes in interneuronal circuits of CA1 region.
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PMID:[Changes in the neuronal excitability of rat hippocampal slices isolated after destruction of the medial septal area]. 164 80

Antagonism of NMDA-mediated transmission by MK-801 has been shown to block long-term potentiation (LTP) in vitro and delay electrical kindling of the amygdala. The present experiment sought to examine the relationship between synaptic potentiation of the perforant path-granule cell synapse and development of perforant path kindling. MK-801 (0.1 and 1.0 mg/kg) blocked induction of LTP of the perforant path in the unanesthetized animal measured 24 h after train delivery. The 1.0 mg/kg dosage also increased afterdischarge (AD) thresholds, delayed kindling development from daily stimulation of the perforant path (means = 8.82 +/- 1.19 and 22.9 +/- 3.66 sessions to the first stage 5 seizure), and increased AD durations. Kindling produced a significant potentiation of the EPSP (47%) and population spike (49%) after the first evoked AD in control animals. No significant enhancement of either component of the field potential was observed in MK-801-treated animals. Animals treated with this dosage of MK-801, did, however, kindle in the absence of potentiation at this synapse. It was concluded that although NMDA-mediated potentiation may facilitate kindling, synaptic potentiation does not appear to be a critical requirement for kindling to develop. These findings support the notion that development of the burst response and not synaptic enhancement may be the critical physiological alteration that underlies the kindling phenomenon.
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PMID:The NMDA antagonist, MK-801, suppresses long-term potentiation, kindling, and kindling-induced potentiation in the perforant path of the unanesthetized rat. 220 70

The basis for the hyperexcitability and seizure activity associated with enflurane anaesthesia was investigated using extracellular and intracellular recording in rat hippocampal brain slices. Enflurane produced seizure-like burst discharges in CA1 pyramidal neurones, accompanied by depressed field potential amplitudes and a reduced threshold for synaptically evoked population spikes. However, threshold for action potentials evoked by intracellular current injection did not change, nor did action potential amplitude, duration or spike frequency accommodation in single neurones. Enflurane 2.0 vol% hyperpolarized CA1 neurones (3.1 (SD 1.3)mV), decreased membrane conductance (12 (6)% below control), and depressed EPSP amplitudes (34% of control) (P less than 0.01). Enflurane appeared to enhance both intrinsic and synaptically mediated inhibitory potentials. The N-methyl-D-aspartate (NMDA) receptor antagonist amino-phosphonovalerate (APV) 5-20 mumol litre-1 completely blocked seizure-like burst discharge of CA1 neurones in the presence of enflurane, and the enflurane-induced reduction of population spike threshold; it did not alter anaesthetic depression of EPSP amplitude. Thus enflurane-induced burst discharge of CA1 neurones appeared to involve an enhancement of excitatory synaptic transmission rather than depression of intrinsic or synaptic inhibition.
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PMID:Enflurane-induced burst discharge of hippocampal CA1 neurones is blocked by the NMDA receptor antagonist APV. 257 47

Synaptic transmission was studied during the development of kindling in the pathway from entorhinal cortex (EC) to dentate gyrus (DG) of unrestrained unanesthetized rats using chronic neurophysiological techniques. Extracellular field potentials were recorded from the DG in response to activation of the perforant pathway with 0.1-ms constant current square-wave pulses. The evoked field potentials consisted of a population EPSP (a reflection of excitatory synaptic activation) and a population spike (a measure of synchronous postsynaptic discharge of granule cells). Synaptic efficacy was quantitated in this pathway by measurement of the population EPSP slope and population spike amplitude across a range of stimulus intensities from threshold to maximal evoked response. Input-output relationships for population EPSP and population spike were determined at regular intervals during the course of kindling, corresponding to the stages of evoked behavioral seizures. Increases in the population EPSP and population spike were observed after a single kindling stimulus that evoked afterdischarge (AD) when behavioral seizures were minimal. Evaluation of the input-output relationships for the group of kindled animals at the various stages of evoked behavioral seizure activity revealed that increases in the population EPSP continued to slowly evolve with repeated stimulations but that increases in the population spike were maximal after one or at most a few stimulations that evoked AD. The increases in both population EPSP and population spike persisted for the duration of the recording, i.e., through induction of generalized motor convulsions. To evaluate the translation of synaptic activation into cell discharge during kindling, we made use of the population spike/population EPSP ratio across a range of stimulus intensities. The spike/EPSP ratios revealed a dissociation of the population spike and population EPSP early in the course of kindling during class 1 seizures. Specifically, after induction of an AD, an extracellular population EPSP of a given size evoked a larger population spike than an EPSP of comparable size before the induction of an AD by kindling stimulation. The development of generalized motor convulsions (class 5 seizures) was associated with a reduction in the spike/EPSP ratio. The mechanism of this reduction in spike/EPSP ratio is uncertain, but since synaptic activation (as reflected by population EPSP) did not decline during class 5 seizures, the reduction in the spike/EPSP ratio could be consistent with increased inhibition after generalized motor convulsions, or could reflect a decrease in granule cell excitability.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Quantitative analysis of synaptic potentiation during kindling of the perforant path. 302 61

The effect of Mg2+-free medium on neuronal activity in the basolateral nucleus of the rat amygdala slice was studied using intracellular recording techniques. Removal of Mg2+ from perfusate resulted in the development of three types of spontaneous activity, EPSP-like, ictal-like, and interictal-like events. The ictal-like events consisted of a long-duration depolarizing potential with several recurrent interictal bursts riding on it. The tonic and clonic firing phases seen in ictal-like events closely resembled the tonic and clonic phases of seizures which may provide a new model for studying the mechanisms underlying the generation of ictal seizures. The duration of interictal-like events induced in Mg2+-free solution is 10- to 30-fold longer than that produced by a convulsant. Two factors, a small or absent epileptiform afterhyperpolarization and a high density of NMDA receptor binding sites within the basolateral amygdala nucleus, may account for this difference.
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PMID:Characterization of the epileptiform activity induced by magnesium-free solution in rat amygdala slices: an intracellular study. 339 43

The effects of kainic acid (KA, 0.05-1.0 microM), and penicillin (PN, 3.4 mM) were studied in the CA1 region of rat hippocampal slices. Three components of the overall input/output function were taken: (1) the amplitude of the presynaptic compound action potential (prevolley) vs stimulation current applied to Schaffer collaterals, (2) the magnitude of the focally recorded synaptic potential (population EPSP) vs prevolley amplitude; and (3) the amplitude of the focally recorded population spike vs population EPSP magnitude. Recurrent inhibition was measured using the antidromic-orthodromic paired pulse method. KA caused a significant and reversible enhancement of all 3 component input/output functions while having no effect on paired pulse inhibition. PN caused a left shift in the EPSP-population spike relationship and decreased or abolished paired pulse inhibition; the other two measures of excitability were not changed. These results suggest that PN and KA differ fundamentally in the mechanisms by which they produce seizures: PN by removing inhibition while not affecting neuronal excitability per se; KA by exerting a generalized excitatory effect on neural membranes and on synaptic function while leaving recurrent inhibition unchanged.
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PMID:Kainic acid and penicillin: differential effects on excitatory and inhibitory interactions in the CA1 region of the hippocampal slice. 388 88

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