Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The asymmetrical breakdown of the blood-brain barrier (BBB) was studied in female rats. Paw preference was assessed by a food reaching test. Adrenaline-induced hypertension was used to destroy the BBB, which was evaluated using triphenyltetrazolium (TTC) staining of the brain slices just after giving adrenaline for 30 s. In normal rats, the whole brain sections exhibited complete staining with TTC. After adrenaline infusion for 30 s, there were large unstained areas in the left brain in right-pawed animals, and vice versa in left-pawed animals. Similar results were obtained in seizure-induced breakdown of BBB. These results were explained by an asymmetric cerebral blood flow depending upon the paw preference in rats. It was suggested that this new method and the results are consistent with contralateral motor control that may be important in determining the dominant cerebral hemisphere in animals.
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PMID:Blood brain barrier in right- and left-pawed female rats assessed by a new staining method. 1248 93

The "dormant basket cell" hypothesis suggests that postinjury hippocampal network hyperexcitability results from the loss of vulnerable neurons that normally excite insult-resistant inhibitory basket cells. We have reexamined the experimental basis of this hypothesis in light of reports that excitatory hilar mossy cells are not consistently vulnerable and inhibitory basket cells are not consistently seizure resistant. Prolonged afferent stimulation that reliably evoked granule cell discharges always produced extensive hilar neuron degeneration and immediate granule cell disinhibition. Conversely, kainic acid-induced status epilepticus in chronically implanted animals produced similarly extensive hilar cell loss and immediate granule cell disinhibition, but only when granule cells discharged continuously during status epilepticus. In both preparations, electron microscopy revealed degeneration of presynaptic terminals forming asymmetrical synapses in the mossy cell target zone, including some terminating on gamma-aminobutyric acid-immunoreactive elements, but no evidence of axosomatic or axoaxonic degeneration in the adjacent granule cell layer. Although parvalbumin immunocytochemistry and in situ hybridization revealed decreased staining, this apparently was due to altered parvalbumin expression rather than basket cell death, because substance P receptor-positive interneurons, some of which contained residual parvalbumin immunoreactivity, survived. These results confirm the inherent vulnerability of dendritically projecting hilar mossy cells and interneurons and the relative resistance of dentate inhibitory basket and chandelier cells that target granule cell somata. The variability of hippocampal cell loss after status epilepticus suggests that altered hippocampal structure and function cannot be assumed to cause the spontaneous seizures that develop in these animals and highlights the importance of confirming hippocampal pathology and pathophysiology in vivo in each case.
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PMID:"Dormant basket cell" hypothesis revisited: relative vulnerabilities of dentate gyrus mossy cells and inhibitory interneurons after hippocampal status epilepticus in the rat. 1262 66

The anatomy of the claustrum (CLA) has been well characterized, but its functional role remains uncertain. The results of recent research suggest that the CLA may be part of a network of structures involved in seizure generalization, and we set out to test this idea. To test persistence, seizures were kindled in the anterior CLA. Following a 14-day suspension of kindling, all rats required only one stimulation to evoke a stage 5 seizure. In another experiment, groups of rats received bilateral lesions of the anterior CLA before and after amygdaloid kindling. We found that small lesions of the anterior CLA retard amygdaloid kindling, but do not block the expression of generalized seizures. Lesions produced after amygdaloid kindling resulted in a shorter seizure duration, but had no marked effect on seizure expression. Another group of rats was tested for transfer of kindling between the anterior CLA and contralateral amygdala. We found an asymmetrical transfer of kindling to the CLA from the amygdala wherein amygdaloid kindling facilitated subsequent kindling of the CLA but kindling of the anterior CLA failed to facilitate kindling of the amygdala. The results add support to the notion that the CLA contributes to the development of generalized limbic seizures.
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PMID:Further evidence for a role of the anterior claustrum in epileptogenesis. 1505 Nov 45

A group of alkyl, cycloalkyl and aryl ester analogs of nifedipine, in which the o-nitrophenyl group at position 4 is replaced by a 2-phenyl-4(5)-imidazolyl substituent, were synthesized and evaluated as calcium channel antagonist using the high K+ contraction of guinea-pig ileal longitudinal smooth muscle, and the activity of 5a-d, 8b and 8f against pentylenetetrazole (PTZ)-induced seizure was assessed. The results for symmetrical esters showed that lengthening of the methylene chain in C3 and C5 ester substituents increased activity. When increasing of the length is accompanied by increasing the hindrance, the activity decreased. In contrast to symmetrical derivatives, comparison of the activities of asymmetrical esters showed that increasing the length of the methylene chain was accompanied by a decrease in their activity. The results demonstrate that 8a was more active, and 5c and 8f were similar in effect to that of the reference drug nifedipine. The time-course of anticonvulsant effect on PTZ-induced seizure threshold of said compounds was assessed and showed that increasing the lipophilicity decreases the time needed for maximum effect. Mice treated with intraperitoneal injection of 25 mg/kg of these derivatives all exhibited increase seizure threshold as compared with control.
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PMID:Lipophilic 4-imidazoly-1,4-dihydropyridines: synthesis, calcium channel antagonist activity and protection against pentylenetetrazole-induced seizure. 1508 43

Although there are many types of epilepsy of both genetic and acquired forms, temporal lobe epilepsy (TLE) with hippocampal sclerosis is probably the single most common human epilepsy, and the one most intensely studied. Despite a wealth of descriptive data obtained from patient histories, imaging techniques, electroencephalographic recording, and histological studies, the epileptogenic process remains poorly understood. Progress toward understanding the etiology of an acquired neurological disorder is largely dependent on the degree to which experimental animal models reflect the human condition. Recent observations suggest that significant disparities exist between the features of human TLE with hippocampal sclerosis and those of animal models that involve prolonged status epilepticus to initiate the epileptogenic process. TLE most commonly involves patients with focal seizures who exhibit limited and often asymmetrical brain damage, did not experience status epilepticus prior to the onset of epilepsy, and who appear relatively normal on neurological examination. Conversely, animals subjected to prolonged status epilepticus exhibit severe brain damage, behavioral abnormalities, and frequent generalized seizures. In addition, although many TLE patients exhibit an atrophic hippocampus that may, or may not, be a source of spontaneous seizures, hippocampal damage in animals subjected to status epilepticus is an inconsistent and often minor part of a much greater constellation of damage to other brain structures. Furthermore, many patients exhibit developmental structural abnormalities that presumably play a role in the clinical etiology, whereas most animal models involve severe insults in initially normal laboratory rats. Although much has been learned using the current animal models, the available data suggest the need for a critical reappraisal of the assumptions underlying their use, and the need to develop experimental preparations that may more closely model the human epileptic state.
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PMID:The neurobiology of temporal lobe epilepsy: too much information, not enough knowledge. 1577 Oct

We have mapped the macaque amygdala for the distribution of synaptic zinc (Zn), a co-factor of glutamate implicated in plasticity, as well as in several excitotoxic and other pathophysiological conditions. In brief, we found that the amygdala is Zn enriched in all nuclear groups (i.e., basolateral and cortical groups, as well as central and medial nuclei) but with marked differences in density. By comparing parallel tissue series histologically reacted for Zn and parvalbumin (PV), we further found that regions high in Zn are typically low in PV neuropil. In the basolateral group, there is a particularly distinct dorsoventral gradation such that Zn levels are most dense ventrally, i.e., in the paralaminar nucleus, the ventral division of the lateral nucleus, and the parvicellular divisions of both the basal nucleus and the accessory basal nucleus. PV levels are least dense in these same regions. For the central and medial nuclei, there is a slight mediolateral gradient, with Zn levels being higher medially. PV is low overall in these nuclei. Electron microscopic results confirmed that Zn is contained in synaptic boutons. These form asymmetrical, presumably excitatory, synapses, and the postsynaptic targets are mainly spines of projection neurons. The inhomogeneous distribution of Zn in the monkey amygdala may be related to different types or degrees of plasticity among the amygdaloid subnuclei. The complementary distribution with PV parallels that of several other substances and is interesting in the context of subnuclear vulnerability for human neuronal disease, such as seizure and Alzheimer's disease.
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PMID:Distribution of synaptic zinc in the macaque monkey amygdala. 1598 2

Early myoclonic encephalopathy (EME) is a rare malignant epileptic syndrome. The erratic myoclonus with or without focal motor seizures, time of onset before 3 months of age, and suppression-burst (SB) pattern in EEG are accepted as the diagnostic criteria for EME. We report a 40-day-old infant with the diagnosis of non-ketotic hyperglycinemia (NKHG). The infant developed myoclonic and focal tonic seizures on the first day of life. His first sleep EEG recorded after onset of seizure was normal. Because of the diagnosis of NKHG and early developed myoclonic seizure, we thought the infant might be EME, and repeated sleep EEG on admission in which asymmetrical SB pattern was seen. We concluded that the absence of SB pattern in the first EEG recording does not exclude the diagnosis of EME, but repetition of EEG is necessary to demonstrate the presence of SB pattern to meet the diagnostic criteria for EME.
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PMID:Repetitive EEG recordings are necessary for the diagnosis of early myoclonic encephalopathy. 1601 70

Overexcitation of neuronal networks in some forebrain structures and pathological synchronization of neuronal activity play crucial role in epileptic seizures. Seizure activity can be elicited experimentally by different convulsants. Because of various distribution of excitatory and inhibitory connections in the neocortex there might be laminar differences in seizure sensitivity. Current source density (CSD) analysis or immunocytochemical c-Fos localization offer suitable tools to localize increased activation of neurons during seizure. In the present experiments, interictal epileptiform activity elicited by 4-aminopiridine, bicuculline or Mg(2+)-free solution was recorded with a 16-channel multielectrode assembly in different layers of the somatosensory cortex, and CSDs were calculated. Parallel c-Fos immunocytochemistry was applied. Each convulsant elicited characteristic activation pattern. 4-aminopiridine induced relatively short discharges, which were associated with a huge sink in layer V, the sink and source pattern was relatively simple. Mg(2+)-free solution elicited the longest discharges, sinks appeared typically in the supragranular layers II and III than quickly distributed toward layers V and VI. Bicuculline induced rather similar seizure pattern as Mg(2+)-free solution, but the amplitudes of field potentials were larger, while the durations shorter. The peak of c-Fos activation, however, was not parallel with the largest electrical activation. Larger amount of stained cells appeared in layers II and III in 4-aminopiridine and bicuculline, respectively. In Mg(2+)-free solution the highest c-Fos activity was detected in upper layer VI. Long-lasting cellular effects do not always correspond to the largest electrical responses, which are primarily determined by the activation of asymmetrical pyramidal neurons. Interneurons, which possess more symmetric process arborisation, play less important role in the generation of field potentials, although they may be intensively activated during seizure.
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PMID:Laminar analysis of initiation and spread of epileptiform discharges in three in vitro models. 1653 65

Paroxysmal motor phenomena and arousals during sleep are frequent. The differential diagnoses between benign hypnic transient events, epileptic and non-epileptic seizures represent a common clinical problem. Video-EEG monitoring during sleep, recording several episodes in the same patient, is essential in order to characterize these phenomena. It offers the possibility to compare electro-clinical data, to demonstrate the eventual stereotyped pattern of motor phenomena and their progression in time, and to study EEG-polygraphic correlates. The recently described double split-screen synchronized display (DSSSD) technique represents a useful tool for comparing particular clinical patterns of epileptic seizures when dealing with complex, hypermotor phenomena observed in frontal lobe epilepsy. We reviewed the data of 24 patients admitted during a two-year period (2002-2003) to our epilepsy sleep unit for isolated paroxysmal sleep motor events. Four patients presented with very brief paroxysmal arousals without daytime fits. Three of our patients presented isolated paroxysmal arousals, whereas in one, the events were associated with hypermotor seizures. We present a simplified variant of the DSSSD method (modified DSSSD) that can be used to study episodes of paroxysmal arousals in order to confirm their stereotyped motor pattern. The clinical aspects and the EEG-polygraphy patterns were informative, with the absence of asymmetrical tonic or dystonic posturing of the limbs. Scalp EEG alone does not usually provide much information in patients with isolated paroxysmal arousals. Coupled to the modified DSSSD technique, it may allow confirmation of the diagnosis of frontal epilepsy, as was the case in our four patients. [Published with video sequences].
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PMID:Isolated paroxysmal arousals as focal epilepsy. 1656 25

We studied a patient with refractory focal epilepsy using continuous EEG-correlated fMRI. Seizures were characterized by head turning to the left and clonic jerking of the left arm, suggesting a right frontal epileptogenic region. Interictal EEG showed occasional runs of independent nonlateralized slow activity in the delta band with right frontocentral dominance and had no lateralizing value. Ictal scalp EEG had no lateralizing value. Ictal scalp EEG suggested right-sided central slow activity preceding some seizures. Structural 3-T MRI showed no abnormality. There was no clear epileptiform abnormality during simultaneous EEG-fMRI. We therefore modeled asymmetrical EEG delta activity at 1-3 Hz near frontocentral electrode positions. Significant blood oxygen level-dependent (BOLD) signal changes in the right superior frontal gyrus correlated with right frontal oscillations at 1-3 Hz but not at 4-7 Hz and with neither of the two frequency bands when derived from contralateral or posterior electrode positions, which served as controls. Motor fMRI activations with a finger-tapping paradigm were asymmetrical: they were more anterior for the left hand compared with the right and were near the aforementioned EEG-correlated signal changes. A right frontocentral perirolandic seizure onset was identified with a subdural grid recording, and electric stimulation of the adjacent contact produced motor responses in the left arm and after discharges. The fMRI localization of the left hand motor and the detected BOLD activation associated with modeled slow activity suggest a role for localization of the epileptogenic region with EEG-fMRI even in the absence of clear interictal discharges.
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PMID:EEG-fMRI mapping of asymmetrical delta activity in a patient with refractory epilepsy is concordant with the epileptogenic region determined by intracranial EEG. 1667 42


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