Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brain biopsy specimens from a 38-year-old woman with adversive seizures and bifrontal mass lesions evident on computed tomographic scans showed extracellular and intracellular deposits of crystallized proteins. These were morphologically identical to the immunoglobulin crystals seen in reactive or neoplastic plasma cells and by peroxidase-antiperoxidase methods were found to contain polyclonal immunoglobulins. In addition, severe angiitis of the intracerebral blood vessels was present.
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PMID:Crystalline encephalopathy: cerebral immunoprotein deposits and isolated angiitis. 398 92

Intracellular recordings from pairs of neurons in slices of rat hippocampus directly demonstrated electronic coupling between CA3 pyramidal cells. When two neurons were impaled simultaneously (as verified by subsequent double staining with horseradish peroxidase), current pulses injected into one cell caused voltage changes in other cells. These interactions were bidirectional. Fast prepotentials, historically thought to represent spike activity in dendrites, resulted from action potentials in other electronically coupled pyramidal cells. These data directly demonstrate electrotonic coupling between neurons in the mammalian brain and indicate that some fast prepotentials are coupling potentials. Coupling between pyramidal cells could mediate synchronization of normal rhythmic activity and of burst discharges during seizures.
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PMID:Electrotonic coupling between pyramidal cells: a direct demonstration in rat hippocampal slices. 626 13

The ultrastructure and the blood-brain-barrier (BBB) permeability were studied in mice suffering from lymphocytic choriomeningitis (LCM). Brains and meninges from mice suffering from LCM virus-induced lymphocytic choriomeningitis were studied by investigating the BBB function and by electron and light microscopy. The cellular exudate in the leptomeninges was located in the subarachnoid space, in arachnoidea and pia, and it was dominated by proliferated pial cells and mononuclear cells, most of which were lymphocytes, while there were only a few neutrophil granulocytes. Many intravascular lymphocytes were seen adhering to as well as penetrating the vessel walls. Many of these lymphocytes were morphologically compatible with T cells. Lymphocytes and larger mononuclear cells were also accumulated in the choroid plexus, and lymphocytes were present in the ventricular system with a tendency to adhere to ependymal epithelial cells. Inspection of the ultrathin sections incubated for horseradish peroxidase (HRP)-activity revealed that the overwhelming part of the peroxidase activity was localized in the extracellular space of the meningeal vessel walls and especially in the abundant intercellular fluid which, like the inflammatory cells, was found in the subarachnoid space in arachnoidea and in pia. In the neuropil, only very small quantities of reaction product were seen intercellularly in the most superficial layers of the cortex. The tight junctions were always intact, but the possibility of a non-demonstrable opening is discussed. Evaluation of the BBB permeability for 2-amino[1-14C]isobutyric acid (AIB) was made by quantitative autoradiography, and it was demonstrated convincingly that AIB concentrations in the subpial and perichorodial tissues were markedly increased in diseased animals as compared to the controls. Our results seem to contradict previous theories on the cause of death resulting from the LCM disease. The findings presented here do not speak in favor of a pronounced brain edema, just as results obtained by us and others do not speak for the possibility of the death being caused by convulsive seizures with subsequent brain anoxia. However, our observations are compatible with the hypothesis that cytotoxic T cells may interact in vivo with virus-infected targets, which are essential for the regulation of the composition of the cerebrospinal fluid. On the other hand, the dysfunction of the BBB demonstrated adds a new element to the pathologic mechanism in a model for the study of virus-induced meningitis.
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PMID:The permeability of the blood-brain barrier in mice suffering from fatal lymphocytic choriomeningitis virus infection. 646 79

Human serum albumin-like immunoreactivity was detected by the peroxidase-antiperoxidase method in histological sections of the hippocampus from epileptic and control brains obtained on routine autopsies. In the hippocampi of epileptic patients immunoreactive astrocytes were found, the number of which was increasing with the severity of the manifest convulsions. The highest numbers of immunoreactive astrocytes were observed in those patients who died in status epilepticus. Hippocampi from control patients with no neurologic disorders in life were devoid of immunoreactive astrocytes. The results are discussed in terms of the breakdown of the blood-brain barrier during epileptic seizures.
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PMID:Immunohistochemical localization of extravasated serum albumin in the hippocampus of human subjects with partial and generalized epilepsies and epileptiform convulsions. 651 99

Edema formation and blood-brain barrier permeability was studied in animals with epileptic seizures induced by subcutaneous injection of kainic acid. Brain edema was most pronounced between 3 and 24 h after kainic acid injection. It was reflected by massive swelling of perineuronal and perivascular astroglia. Three hours after kainic acid perivascular astroglia swelling resulted in disturbance of local microcirculation in the affected brain areas. In addition, compression of drainage veins by the edematous brain induced focal perivenous hemorrhages similar to herniation damage in human brain edema. Tracer studies with sodium fluorescein, Evans blue, albumin and horseradish peroxidase revealed only a mild increase in the permeability of cerebral vessels, topographically unrelated to areas of brain edema. This finding indicates the presence of cytotoxic brain edema in kainic acid-induced epileptic brain damage. Treatment of brain edema with dexamethasone did not influence the incidence and severity of kainic acid-induced epileptic brain damage. However, in 54% of animals injected with kainic acid, lesions were completely prevented by treatment of brain edema with mannitol. The present results indicate that brain edema plays an important role in the pathogenesis of epileptic brain damage following systemic kainic acid intoxication. It is suggested that in this model of limbic epilepsy the brain edema is due to the massive ionic imbalance elicited in the affected brain regions by the kainic acid-induced persistent neuronal excitation.
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PMID:The role of brain edema in epileptic brain damage induced by systemic kainic acid injection. 652 75

We evaluated clinical features of five cases of Toxoplasma encephalitis (TE) occurring in recent Haitian entrants into the United States. None of the patients had any underlying malignancy or known immunosuppressive therapy. Histopathologic findings of TE at autopsy were confirmed by peroxidase-antiperoxidase method. Four patients had an antecedent episode of disseminated tuberculosis and all five were receiving antituberculous therapy when neurologic manifestations of lethargy, seizures, and motor weakness first developed. These symptoms progressed into coma and death within 15 days. Peripheral lymphocytopenia was noted in all patients; three were anergic. Parenchymal lesions were identified by CT brain scans and total proteins were elevated in spinal fluid in all cases. TE appears to be a manifestation of the acquired immune deficiency syndrome in Haitians; it should be suspected in those with a febrile illness and multiple focal lesions of the central nervous system.
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PMID:Toxoplasma encephalitis in recent Haitian entrants. 662 28

Cerebrovascular permeability to protein (CVP-p) was assessed during limbic seizures by injecting unrestrained rats intraperitoneally with kainic acid followed by intravenous horseradish peroxidase (HRP); animals survived approximately 1 h after seizure onset. Brains were processed for the blue HRP reaction product followed by light microscopic examination of sequential sagittal sections. In all cases kainate-induced seizures caused increased CVP-p within the thalamus, temporal hippocampal formation, and neocortex. Somewhat less frequently other limbic structures and the striatum were HRP-positive. A lamina-specific extravasation occurred in the dorsal hippocampus; reaction product occupied the mossy fiber zone of field CA3, a likely focus of kainate action. Extravasation of HRP also occurred within, or juxtaposed to, certain myelinated fiber bundles. Brains from animals treated as blanks (kainate but no HRP) were devoid of peroxidase activity, and in nonseizing animals HRP gained access only to circumventricular organs. Although regions of increased CVP-p partially covary with areas of increased electrical activity and glucose metabolism, neuronal activation occurs over a much greater volume of brain tissue than does CVP-p. A close relationship may exist between these circumscribed areas of protein extravasation and seizure foci. Both vasogenic and cytotoxic edema appear to be simultaneously present during kainate seizures.
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PMID:Increased cerebrovascular permeability to protein during systemic kainic acid seizures. 670 55

Light and electron microscopy and quantitative estimates of pinocytotic activity in cerebral arterioles and capillaries were performed in two different rat models of altered blood-brain barrier permeability in order to determine the side of initially increased vesicular transport. Seizures were produced by 20 consecutive electroshocks, and ischemic neuronal damage was produced by a 30-minute period of combined right common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase was used to evaluate blood-brain barrier permeability. Serial 1micronm.sections showed an ateriole within most foci of horseradish peroxidase extravasation. There were areas of brain in both experimental groups in which the only permeable vessels were arterioles, and in one ischemic animal, the only permeable vessels were arterioles. Pinocytotic activity was determined in capillaries and arterioles and expressed as the number of horseradish peroxidase-containing pinocytotic vesicles per square millimeter of endothelial cytoplasmic area +/- standard error. The pinocytotic activity in capillaries and arterioles, respectively, was 12.2 +/- 5.4 and 6.7 +/- 3.0 in normal rats, 86.7 +/- 22.1 and 267 +/- 46.1 after seizures, and 52.7 +/- 10.6 and 91.2 +/- 33.2 following cerebral ischemia. These results indicate the importance of the arterioles in maintaining and altering the blood-brain barrier and suggest that abnormal blood-brain barrier permeability occurs first within the arteriole.
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PMID:The importance of cerebral arterioles in alterations of the blood-brain barrier. 740 36

Activation of the dorsal midbrain has a powerful anticonvulsant effect in the maximal electroshock model of epilepsy. The suppression of tonic seizures can be obtained most reliably from an area centred on the intercollicular nucleus overlapping into the deep layers of the superior colliculus and adjacent mesencephalic reticular formation. As part of a series of investigations to identify neural mechanisms responsible for mediating the anticonvulsant properties of the dorsal midbrain, the present study provides an anatomical description of the efferent projections of this region. Small amounts of wheatgerm agglutinin-horseradish peroxidase (10-30 nl of a 1% solution) were injected into the intercollicular nucleus and surrounding tissue. The resulting anterograde transport of the tracer was plotted on a set of standard atlas sections. Four major output pathways were identified: (i) an ipsilateral descending projection which had terminations in the microcellular tegmental nucleus, lateral and ventral pontine reticular nucleus pars oralis, ventrolateral tegmental nucleus, ventral and caudal pontine reticular nucleus pars caudalis, raphe magnus nucleus and the gigantocellular nucleus; (ii) a contralateral descending projection which for the most part targeted the same brainstem structures but with weaker terminal labelling; (iii) a projection to the contralateral dorsal midbrain with comparatively weak terminal label in the contralateral superior colliculus, intercollicular nucleus, periaqueductal gray, mesencephalic reticular formation and cuneiform area; (iv) ipsilateral ascending pathway with terminations in the red nucleus, zona incerta, peripeduncular area, parafascicular nucleus, lateral hypothalamus, parts of the pretectum and caudal thalamus. At a general level the dorsal midbrain anticonvulsant zone shares its major output projections and efferent targets with at least one of its near neighbours, including the superior colliculus, periaqueductal gray, the cuneiform nucleus and pedunculopontine nucleus. The possibility that anticonvulsant properties of the intercollicular area can simply be attributed to a unique set of efferent projections is therefore not supported by the anatomy.
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PMID:The dorsal midbrain anticonvulsant zone--II. Efferent connections revealed by the anterograde transport of wheatgerm agglutinin-horseradish peroxidase from injections centred on the intercollicular area in the rat. 754 3

Wheatgerm agglutinin-horseradish peroxidase (WGA-HRP) histochemistry was combined with post-embedding immunogold cytochemistry in order to establish whether the subthalamic nucleus (STN) gives origin to glutamate (Glu)-enriched nerve terminals in substantia nigra, pars reticulata (SNr). Two adult cats served as normal controls and in two other animals crystalline WGA-HRP had been implanted bilaterally in STN. In all four animals ultrathin sections from SN were subjected to an immunogold procedure using antiserum raised against either Glu or gamma-aminobutyric acid (GABA). In some experiments the sections were subjected to consecutive incubations with both GABA and Glu antisera. These two antisera label two morphologically distinct types of boutons in SNr. The GABA antiserum labels boutons with pleomorphic vesicles, and they establish symmetrical synaptic contacts, mainly with dendritic shafts and spines, and occasionally with cell bodies. The Glu antiserum labels boutons with vesicles which are smaller and more uniform with regard to size and shape than those seen in the GABA-labelled boutons. The Glu-labelled boutons are engaged in asymmetrical synaptic contacts mainly with dendritic shafts and more rarely with cell bodies. The number of GABA-labelled boutons in SNr greatly exceeds the number of Glu-labelled ones. In the experimental material a considerable number of boutons in SNr are labelled with WGA-HRP reaction product. Several of these boutons are enriched in Glu-like immunoreactivity (Glu-LI), but not in GABA-LI. It is concluded that the subthalamonigral projection in the cat is likely to use Glu as a transmitter. The findings are briefly discussed with respect to the role played by STN in movement disorders and the involvement of excitatory amino acids in SN for the propagation of epileptic seizures and development of neurotoxicity.
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PMID:Terminals of subthalamonigral fibres are enriched with glutamate-like immunoreactivity: an electron microscopic, immunogold analysis in the cat. 767 8


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