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

Hippocampal slices, from which the entorhinal cortex had been removed, were exposed to artificial cerebrospinal fluid containing no magnesium (0-Mg ACSF) to elicit interictal bursts (IIBs) and electrographic seizures (EGSs). In 0-Mg ACSF, IIBs and EGSs occurred in both area CA1 and area CA3. The IIBs in CA3 led the IIBs in CA1 by several milliseconds. The epileptiform bursts occurring during the EGSs seemed to have the opposite relationship, with bursts in CA1 leading those in CA3 by several milliseconds. When the connections between CA1 and CA2-3 were cut, the IIBs ceased in CA1 and continued in CA3. To further characterize the local differences in epileptiform activity, totally separate minislices of area CA1 and area CA2-3 were prepared. In the CA2-3 minislices, a few EGSs occurred and thereafter only persistent IIBs prevailed. Conversely, in the CA1 minislices, many spontaneous EGSs occurred for long periods of time and no IIBs were seen. Periodic stimulation of the CA1 minislices triggered IIBs that suppressed the recurrent EGSs. In the hippocampal slice exposed to low magnesium, IIBs originate in CA2-3 and are propagated to CA1, where they can have a suppressant effect on EGSs. Furthermore, unlike IIBs, the bursts making up the EGSs seem to start in CA1 and invade CA2-3.
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PMID:Hippocampal epileptiform activity induced by magnesium-free medium: differences between areas CA1 and CA2-3. 238 88

Spontaneous and evoked field potentials and cellular discharges were studied in the subcortically denervated hippocampus of the freely moving rat. The fimbria fornix, the ventral hippocampal commissure, and the supracallosal afferent fibers were removed by aspiration, and recordings were made 3-5 months after the lesion. Two types of spontaneous interictal spikes were observed. Type 1 interictal spike had identical depth distribution to physiological sharp waves but they were shorter in duration (less than 40 ms), larger in amplitude (greater than 2.5 mV) and population spikes were riding on the main deflection. Type 2 interictal spikes were negative in the stratum oriens and positive in the pyramidal layer and stratum radiatum of both CA1 and CA3. The amplitude of both types of interictal spikes could exceed 6 mV. We suggest that interictal spikes were initiated randomly in different subpopulations of the CA2-3 region and the location of the initiating population burst determined the polarity and amplitude of the extracellular interictal spike. Repetitive stimulation of the perforant path (5 Hz, 6 s) evoked markedly uniform afterdischarges in both intact and fimbria fornix-deprived rats. The threshold of afterdischarges was significantly lower, the seizure spread to the contralateral hippocampus was slower, and secondary afterdischarges lasted significantly longer in the lesioned rats. We suggest that under physiological conditions the electrical stability of the hippocampus is ensured by the feed-forward inhibitory action of subcortical afferents. Removal of tonic inhibitory influences and/or sprouting of local axon collaterals allows extreme synchronization and reverberation of information in the entorhinal-hippocampal-entorhinal cortex circuitry. The presence of interictal spikes and increased susceptibility to seizures for several months after the lesion offers the fimbria-fornix-deprived hippocampus a useful chronic preparation to study the mechanisms of limbic epilepsy.
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PMID:Neuronal activity in the subcortically denervated hippocampus: a chronic model for epilepsy. 271 Mar 28

Two neuronal calcium-binding proteins, calbindin-D28k (CaBP) and parvalbumin (PV), were localized in the normal rat hippocampus by using immunocytochemical methods to determine 1) their location and 2) whether a correlation exists between the presence of these two calcium-binding proteins and the selective vulnerability of different hippocampal neuronal populations to experimental seizure activity. CaBP-like immunoreactivity (CaBP-LI) is present in all dentate granule cells and some, but not all, CA1 and CA2 pyramidal cells. Some CA1 pyramidal cells lack CaBP-LI, and those that do are lightly stained compared to the dentate granule cells. CA3 pyramidal cells appear to contain neither CaBP- nor PV-LI, and no granule or pyramidal cells exhibit PV-LI. CaBP-LI is present in distinct populations of dentate and hippocampal interneurons but absent from others. In area dentata, CaBP-LI is present in a small number of interneurons of the molecular and granule cell layers and in a small population of presumed basket cells in or below the granule cell layer. Conversely, more presumed dentate basket cells exhibit PV-LI than CaBP-LI. In the hilus of area dentata, few cells are CaBP- or PV-immunoreactive. The hilar somatostatin/neuropeptide Y (NPY)-immunoreactive cells and hilar mossy cells, two distinct and large populations, lack CaBP- and PV-LI. In the CA3 region, CaBP-LI is present in a relatively small number of interneurons in each stratum. PV-immunoreactive interneurons in area CA3 are more numerous. In area CA1, CaBP-LI is present in many interneurons in strata radiatum and lacunosum-moleculare. Some, but relatively fewer, CaBP-positive interneurons are present in strata pyramidale and oriens. Conversely, PV-immunoreactive interneurons are numerous in strata pyramidale and oriens but rare in strata radiatum and lacunosum-moleculare. Staining with the particulate chromagen benzidine hydrochloride revealed a previously undescribed dense band of CaBP-LI in the inner dentate molecular layer, a lamina enriched with kainate-displaceable glutamate-binding sites and innervated by the apparently excitatory ipsilateral associational/commissural (IAC) pathway that originates in the CaBP-negative hilar mossy cells. Bilateral electrical stimulation of the perforant path was performed in order to destroy the hilar mossy cells and to determine if this band of CaBP-LI is normally present within the mossy cell terminals. Perforant path stimulation that destroyed hilar mossy cells throughout the dorsal portions of both hippocampi did not abolish the dense CaBP-like immunoreactivity in the inner molecular layer.
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PMID:Calcium-binding protein (calbindin-D28k) and parvalbumin immunocytochemistry: localization in the rat hippocampus with specific reference to the selective vulnerability of hippocampal neurons to seizure activity. 292 92

Regional differences in Na,K-ATPase activity, and development of Na,K-ATPase activity were examined in rabbit hippocampus using a histochemical marker of enzyme activity. Stratum lucidum of CA3/CA2, corresponding to the mossy fiber terminal field, showed high Na,K-ATPase activity compared to stratum radiatum of CA1. A significant increase in Na,K-ATPase activity was found between 8 and 15 days postnatal. Tissues with limited Na,K-ATPase activity (immature hippocampus, the mature CA1 region) appear particularly prone to seizure-like abnormalities, perhaps reflecting an inability to regulate extracellular potassium.
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PMID:Developmental and regional differences in the localization of Na,K-ATPase activity in the rabbit hippocampus. 299 29

To determine if electrophysiological properties of hippocampal pathways are altered in kindled rats, extracellular recordings were made from hippocampal slices of rats kindled in the lateral entorhinal cortex and compared with those from implanted but unstimulated controls. Studies were made either 24 h or 28 days after the last kindled seizure and done in normal (3.5 mM) or elevated (7 mM) K+. The preparation of slices, data accumulation, and data analyses were done blind. One day or 28 days after the last kindled seizure, the proportion of slices with spontaneous epileptiform bursts recorded from the CA2/3 region in elevated K+ was significantly (P less than 0.001) increased in the kindled animals. The frequency of spontaneous burst firing was also increased and reached significance (P less than 0.02) at 28 days following the last kindling stimulus. One day after the last kindling stimulus, paired-pulse (GABAergic) inhibition in the CA1 region was decreased (P less than 0.001). Several measures suggested an increased synaptic inhibition in the dentate gyrus of slices from the kindled groups 1 day after kindling. Paired-pulse inhibition was increased (P less than 0.01), the current required to evoke a near-threshold population spike was increased (P less than 0.05), and the population spike amplitude was reduced for a given field excitatory postsynaptic potential (EPSP) (P less than 0.01). Twenty-eight days after the last kindling stimulus, however, paired-pulse inhibition in the dentate was slightly less in slices from kindled rats (P less than 0.005). In other respects the CA1 and dentate regions did not differ between kindled and control groups within 24 h of the last stage V seizure. Thus the maximum amplitudes of presynaptic fiber volley, population spike, and field-excitatory postsynaptic potential (EPSP) slope, and the number of population spikes evoked by a near-maximally effective afferent stimulus, were unchanged. In the CA1 region the input-output curve of field EPSP versus population spike, and the current intensity required to evoke a near-threshold population spike were also unchanged. In addition, no spontaneous bursts were recorded from CA1 in 3.5 mM K+. We conclude that either synapses or neurons intrinsic to the hippocampus are altered by kindling stimuli applied outside this brain area. The transient increase in inhibition in the dentate gyrus suggests that it may reflect a compensatory reaction to kindled seizures. In contrast, the long-lasting (at least 28 days) increase in burst firing in CA2/3 may represent a mechanism for the initiation or propagation of kindled seizures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Abnormal neuronal excitability in hippocampal slices from kindled rats. 300 Dec 36

Recent studies have shown that opioid peptide levels are altered in hippocampal formation of kindled animals. We therefore studied the distributions of mu and delta opioid binding sites in hippocampal formation of kindled and control rats using quantitative in vitro autoradiography. Animals received daily stimulations of the amygdala until they experienced 3 class 5 seizures. Paired control animals underwent implantation of electrodes but were not stimulated. Mu binding sites were labeled with 125I-FK-33824. Twenty-four hours after the last kindled seizure, mu binding was decreased by 32% in stratum pyramidale of CA1 and stratum radiatum of CA2 and by 17-27% throughout most of the rest of CA1, CA2, and CA3. Few, if any, differences were seen between kindled and control animals at 7 or 28 days after the last kindled seizure. Delta binding sites were labeled with 125I-[D-Ala2,D-Leu5]enkephalin in the presence of the morphiceptin analog PL-032. Twenty-four hours after the last kindled seizure, delta binding was decreased only in stratum moleculare of the dentate gyrus. Seven days after the last kindled seizure, delta binding was decreased by 11-17% throughout CA1, CA3, and the dentate gyrus. At 28 days after the last seizure, however, no differences were found between kindled and control animals. Since the decreases in mu and delta opioid binding are transient, they are unlikely to be the molecular basis of the permanent kindling phenomenon. Rather, these changes in opioid binding may represent responses to repeated seizures.
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PMID:An in vitro autoradiographic analysis of mu and delta opioid binding in the hippocampal formation of kindled rats. 303 68

Kindling is an animal model of epilepsy induced by periodic focal electrical stimulation of the brain. The network of brain structures responsible for this permanent abnormal excitability is unknown. We hypothesized that the hippocampal formation serves a facilitatory role in lateral entorhinal cortex kindling. We therefore investigated the effect of dentate granule cell destruction induced by the neurotoxin, colchicine into entorhinal cortex kindling development. We found that injection of colchicine into the hippocampal formation, but not frontal cortex, resulted in a 31% increase in the number of stimulations required to establish kindling in comparison with vehicle-injected controls. The effect of intrahippocampal colchicine was due to a 95% increase in the number of stimulations required to attain a class 2 seizure. Based on these and other data, we propose that elimination of granule cells reduces activation of CA2/3 neurons, thereby impairing development of entorhinal kindling.
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PMID:Evidence implicating dentate granule cells in development of entorhinal kindling. 395 61

Electroencephalographic, behavioral, and neuropathologic changes were monitored after infusions of the endogenous excitatory amino acid, quinolinic acid (QUIN), into the dorsal hippocampus of unanesthetized, freely moving rats. A dose of 120 nmol QUIN was required to reliably precipitate seizures although EEG changes were observed with doses as small as 3 nmol. Seizure episodes were characterized by repetitive periods of high-voltage spiking typically lasting 20 s but occasional longer multicomponent episodes (60 s) were also observed. The latency of specific QUIN-induced seizures was similar for all doses tested (19 to 32 min); however, the total number of seizures and total time in seizures increased in a dose-dependent fashion from 30 to 300 nmol QUIN. Seizure episodes were often associated with a frozen appearance of the animal and intermittent "wet dog shakes". Ataxia was apparent in animals receiving 120 and 300 nmol QUIN. Using light microscopic analyses, pyramidal cell degeneration was observed in the QUIN-injected hippocampus (CA3 and CA1 cells more susceptible than CA2 cells); dentate granule cells showed signs of degeneration only at the largest QUIN dose. No neuropathologic changes were found outside the injected hippocampus. Seizures and neuropathologic changes induced by 120 nmol QUIN were completely blocked by pre- or cotreatment with 12 nmol (-)2-amino-7-phosphonoheptanoic acid. Experiments with [3H]QUIN indicated that only 3% of the injected radioactivity was present in the dorsal hippocampus at the average time of seizure onset (25 min), and consisted entirely of unmetabolized QUIN. The potent convulsant properties of QUIN, an endogenous metabolite, may prove to be of relevance for the etiology of human temporal lobe epilepsy.
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PMID:Seizure activity and lesions after intrahippocampal quinolinic acid injection. 670 78

Sustained electrical stimulation of the perforant path in urethane-anesthetized rats evoked hippocampal granule cell population spikes and epileptiform discharges. After stimulation, recurrent inhibition in the granule cell layer was abolished. Light microscopic analysis revealed a highly reproducible pattern of hippocampal damage to dentate pyramidal basket cells, hilar cells in general and CA3 and CA1 pyramidal cells. CA2 pyramidal cells and dentate granule cells were relatively unaffected. When perforant path stimulation on one side of the brain evoked bilateral granule cell discharges, damage was bilateral. Unilateral hippocampal seizures were associated with unilateral hippocampal damage. Rapid Golgi-stained hippocampi exhibited spherical dendritic swellings at the sites of termination of excitatory entorhinal afferents to the hippocampus and in the mossy fiber region. Electrical stimulation of a single excitatory afferent to the hippocampus appears to reproduce the "epileptic" pattern of hippocampal damage without using convulsant drugs and without causing motor convulsions. It is suggested that seizure-associated brain damage is caused by excessive pre-synaptic release of excitatory transmitter that induces intracellular post-synaptic changes that lead to dendritic swelling and cell death.
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PMID:"Epileptic" brain damage in rats induced by sustained electrical stimulation of the perforant path. I. Acute electrophysiological and light microscopic studies. 687 37

In unrestrained rabbits with generalized epileptic seizures induced by systemic application of convulsant drugs, regional changes in blood-brain barrier (BBB) permeability to macromolecules were investigated using Evans Blue (EB) as indicator. BBB leakage due to seizures was present only in animals in which the mean arterial blood pressure rose about 50 mm Hg with the onset of convulsive motor activity. However, a blood pressure increase was not necessarily associated with the occurrence of BBB opening. Pentylenetetrazole-induced seizures resulted in bilateral EB leakage mainly in the hypothalamus, with exception of the mammillary bodies, and the preoptic area, and they were associated, in most cases, with an intensive staining of the cerebellum and also of the midbrain tegmentum. In contrast, seizures due to the GABA receptor blocker bicuculline brought about a penetration of the dye in the region of the pallidum, whereas the GABA synthesis inhibitor methoxypyridoxine produced BBB breakdown in the hippocampus. Methionine-sulfoximine convulsions resulted in a selective stain of the corpora mammillaria, and kainic acid induced a diffuse leakage in neocortical brain areas. As a rule, BBB breakdown was bilateral and confined to anatomically limited brain areas, suggesting that BBB integrity was not only disturbed by abrupt increases in the intraluminal pressure, but was also influenced from the brain tissue. The fluorescence microscopic observations revealed that the tracer penetrated into the neuropil through larger vessels. It had the tendency to accumulate in neurons. In case of the hippocampus, CA2 pyramidal cells revealed more intense uptake of EB than those of the adjacent fields.
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PMID:Regional patterns of blood-brain barrier breakdown during epileptiform seizures induced by various convulsive agents. 687 4


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