Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A single episode of status epilepticus (SE) induced in rodents by the convulsant pilocarpine, produces, after a latent period of > or = 2 weeks, a chronic epileptic condition. During the latent period of epileptogenesis, most CA1 pyramidal cells that normally fire in a regular pattern, acquire low-threshold bursting behaviour, generating high-frequency clusters of 3-5 spikes as their minimal response to depolarizing stimuli. Recruitment of a Ni(2+)- and amiloride-sensitive T-type Ca(2+) current (I(CaT)), shown to be up-regulated after SE, plays a critical role in burst generation in most cases. Several lines of evidence suggest that I(CaT) driving bursting is located in the apical dendrites. Thus, bursting was suppressed by focally applying Ni(2+) to the apical dendrites, but not to the soma. It was also suppressed by applying either tetrodotoxin or the K(V)7/M-type K(+) channel agonist retigabine to the apical dendrites. Severing the distal apical dendrites approximately 150 microm from the pyramidal layer also abolished this activity. Intradendritic recordings indicated that evoked bursts are associated with local Ni(2+)-sensitive slow spikes. Blocking persistent Na(+) current did not modify bursting in most cases. We conclude that SE-induced increase in I(CaT) density in the apical dendrites facilitates their depolarization by the backpropagating somatic spike. The I(CaT)-driven dendritic depolarization, in turn, spreads towards the soma, initiating another backpropagating spike, and so forth, thereby creating a spike burst. The early appearance and predominance of I(CaT)-driven low-threshold bursting in CA1 pyramidal cells that experienced SE most probably contribute to the emergence of abnormal network discharges and may also play a role in the circuitry reorganization associated with epileptogenesis.
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PMID:Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis. 1799 77

Activation of inflammatory and immune pathways may contribute to the development of epilepsy. Dendritic cells (DCs), a heterogeneous group of professional antigen presenting cells, can be detected in the brain under several inflammatory conditions. However, the spatiotemporal distribution and origin of seizure-induced DCs accumulation in the brain have not been explored yet. In the present study, we demonstrate the presence of CD11c-positive DCs in the hippocampus, thalamus and temporal cortex following Li-pilocarpine induced status epilepticus (SE) in rats. Recruitment of DCs occurs as early as 1 day following the induction of SE, reaching peak time at day 3, and still evident until day 5. The recruitment of DCs in the brain following lithium chloride administration was not detected. The observed DCs cannot be double-labeled with Iba-1 (an activated microglia marker) and whole-body radiation prevents seizure-induced DCs accumulation in brain parenchyma. Our data suggest that the recruitment of DCs in the epileptic brain may be derived from peripheral circulation and this population of immune cells may be involved in the immune processes after SE.
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PMID:Brain recruitment of dendritic cells following Li-pilocarpine induced status epilepticus in adult rats. 2319 67

Mapping the circuits underlying the generation and propagation of seizures is critically important for understanding their pathophysiology. We review evidence to suggest that circuits engaged in secondarily generalized seizures are likely to be more complex than those currently proposed. Focal seizures have been proposed to engage canonical thalamocortical circuits that mediate primarily generalized absence seizures, leading to secondarily generalized tonic-clonic seizures. In addition to traveling through the canonical thalamocortical circuits, secondarily generalized seizures could also travel through the striatum, globus pallidus, substantia nigra reticulata, and corpus callosum to the contralateral hemisphere. Recruitment of principal neurons in superficial layers 2/3 of the cortex can play a critical role in corticocortical seizure spread. Understanding the neuronal structures engaged in generating secondarily generalized seizures could provide novel targets for neuromodulation for the treatment of seizures. Furthermore, these sites may be loci of neuronal plasticity facilitating epileptogenesis. This article is part of the Special Issue "Proceedings of the 7th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures".
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PMID:Circuits generating secondarily generalized seizures. 3143