Evidence suggesting secondary epileptogenic lesion after kainic acid: pre treatment with diazepam reduces distant but not local brain damage.
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Experimental models of chronic focal epilepsy: a critical review of four models.Substantia nigra pars reticulata units in 6-hydroxydopamine-lesioned rats: responses to striatal D2 dopamine receptor stimulation and subthalamic lesions.Sequel of spontaneous seizures after kainic acid-induced status epilepticus and associated neuropathological changes in the subiculum and entorhinal cortexStatus epilepticus. Clinical features, pathophysiology, and treatment.In vivo contributions of BH3-only proteins to neuronal death following seizures, ischemia, and traumatic brain injury.Kainic acid: The neurotoxic breakthrough.Seizure-Induced Axonal Sprouting: Assessing Connections Between Injury, Local Circuits, and Epileptogenesis.Effects of kainic acid on high-energy metabolites in the mouse striatum.Mediation of the neuroprotective action of R-phenylisopropyl-adenosine through a centrally located adenosine A1 receptor.Autoradiographic analysis of [3H]kainic acid binding in primate brain.Effects of some antiepileptic drugs in pentetrazol-induced convulsions in mice lesioned with kainic acid.Status epilepticus in well-oxygenated rats causes neuronal necrosis.Changes in cholinergic but not in GABAergic markers in amygdala, piriform cortex, and nucleus basalis of the rat brain following systemic administration of kainic acid.Choline acetyltransferase activity in the rat brain cortex homogenate, synaptosomes, and capillaries after lesioning the nucleus basalis magnocellularis.In vitro and in vivo protection against kainate-induced excitotoxicity by melatonin.Endogenous descending modulation: spatiotemporal effect of dynamic imbalance between descending facilitation and inhibition of nociception.GluR2(B) knockdown accelerates CA3 injury after kainate seizures.Lesion of the amygdala on the right and left side suppresses testosterone secretion but only left-sided intervention decreases serum luteinizing hormone level.Choline acetyltransferase, glutamic acid decarboxylase and somatostatin in the kainic acid model for chronic temporal lobe epilepsy.Chronic epileptogenesis requires development of a network of pathologically interconnected neuron clusters: a hypothesis.Selective reduction of GluR2 protein in adult hippocampal CA3 neurons following status epilepticus but prior to cell loss.Increased cerebrovascular permeability to protein during systemic kainic acid seizures.In vivo binding to peripheral benzodiazepine binding sites in lesioned rat brain: comparison between [3H]PK11195 and [18F]PK14105 as markers for neuronal damage.Choline acetyltransferase depletion in the rat retina after intraocular injection of neurotoxins.
P2860
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P2860
Evidence suggesting secondary epileptogenic lesion after kainic acid: pre treatment with diazepam reduces distant but not local brain damage.
description
1979 nî lūn-bûn
@nan
1979年の論文
@ja
1979年論文
@yue
1979年論文
@zh-hant
1979年論文
@zh-hk
1979年論文
@zh-mo
1979年論文
@zh-tw
1979年论文
@wuu
1979年论文
@zh
1979年论文
@zh-cn
name
Evidence suggesting secondary ...... nt but not local brain damage.
@en
type
label
Evidence suggesting secondary ...... nt but not local brain damage.
@en
prefLabel
Evidence suggesting secondary ...... nt but not local brain damage.
@en
P2093
P1433
P1476
Evidence suggesting secondary ...... nt but not local brain damage.
@en
P2093
E Tremblay
O P Ottersen
P304
P356
10.1016/0006-8993(79)90571-7
P577
1979-04-01T00:00:00Z