Changes in Extracellular Amino Acids During Soman‐and Kainic Acid‐Induced Seizures

Wade, John V.; Samson, Frederick E.; Nelson, Stanley R.; Pazdernik, Thomas L.

doi:10.1111/j.1471-4159.1987.tb02912.x

Cited by 134 publications

(41 citation statements)

References 22 publications

(16 reference statements)

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“…In this approach, we observed a transient disappearance of myelinated fibers in the affected regions. Experimentally induced excessive neuronal activity (electroconvulsion, kainic acid, pilocarpine, pentylenetetrazole) is known to lead to glial activation and increased glutamate levels [24,70,71]. These events also affect and destroy myelin-forming oligodendrocytes through excitatory cell stress, a phenomenon which might be mirrored by the decrease in Black Gold staining [25 -27].…”

Section: Myelination In the Hippocampus Following Lesion And Seizurementioning

confidence: 99%

Myelination in the hippocampus during development and following lesion

Meier

Bräuer

Heimrich

et al. 2004

Cellular and Molecular Life Sciences (CMLS)

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Myelin is crucial for the stabilization of axonal projections in the developing and adult mammalian brain. However, myelin components also act as a non-permissive and repellent substrate for outgrowing axons. Therefore, one major factor which accounts for the lack of axonal regeneration in the mature brain is myelin. Here we report on the appearance of mature, fully myelinated axons during hippocampal development and following entorhinal lesion with the myelin-specific marker Black Gold. Although entorhinal axons enter the hippocampal formation at embryonic day 17, light and ultrastructural analysis revealed that mature myelinated fibers in the hippocampus occur in the second postnatal week. During postnatal development, increasing numbers of myelinated fibers appear and the distribution of myelinated fibers at postnatal day 25 was similar to that found in the adult. After entorhinal cortex lesion, a specific anterograde denervation in the hippocampus takes place, accompanied by a long-lasting loss of myelin. Quantitative analysis of myelin and myelin breakdown products at different time points after lesion revealed a temporally close correlation to the degeneration and reorganization pha-ses in the hippocampus. In contrast, electroconvulsive seizures resulted in brief demyelination and a faster recovery time course. In conclusion, we could show that the appearance of mature axons in the hippocampus is temporally regulated during development. In the adult hippocampus, demyelination was found after anterograde degeneration and also following seizures, suggesting that independent types of insult lead to demyelination. Reappearing mature axons were found in the hippocampus following axonal sprouting. Therefore, our quantitative analysis of mature axons and myelination effectively reflects the readjusted axonal density and possible electrophysiological balance following lesion.

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Section: Myelination In the Hippocampus Following Lesion And Seizurementioning

confidence: 99%

Myelination in the hippocampus during development and following lesion

Meier

Bräuer

Heimrich

et al. 2004

Cellular and Molecular Life Sciences (CMLS)

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“…It has been observed that KA-induced seizures and neurotoxicity are reduced in the immature nervous system, a developmental stage when TAU levels are high (Stafstrom et al, 1992). KA has been shown to increase extracellular TAU in the piriform cortex 2-5 fold 60-90 minutes after systemic administration (Wade et al, 1987). Extracellular TAU also increases 5-6 fold in hippocampus 30-60 minutes after KA administration as determined by microdialysis (Menendez et al, 1989).…”

Section: Introductionmentioning

confidence: 97%

Kainic acid (KA)-induced seizures in Sprague-Dawley rats and the effect of dietary taurine (TAU) supplementation or deficiency

et al. 1999

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Male Sprague-Dawley rats received TAU supplementation (1.5% in drinking water) or TAU deficient diets for 4 weeks to test for a possible neuroprotective role of TAU in KA-induced (10 mg/kg s.c.) seizures. TAU supplementation significantly increased serum and hippocampal TAU levels, but not TAU content in temporal cortex or striatum. TAU deficient diets did not attenuate serum or tissue TAU levels. Dietary TAU supplementation failed to decrease the number or latency of partial or clonic-tonic seizures or wet dog shakes, whereas a TAU deficient diet decreased the number of clonictonic and partial seizures. This study does not support previous observations of an anticonvulsant effect of TAU against KA-induced seizures. KA-treatment decreased alpha 2-adrenergic receptor binding sites and TAU content in the temporal cortex across all dietary treatment groups, supporting previous evidence of severe KA-induced damage and neuronal loss in this brain region.

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“…Cholinergic seizures originate in striatal-nigral pathways (initiation sites) and with fast-acting agents (soman) rapidly spread to limbic related areas and finally culminate in full-blown status epilepticus (Pazdernik et al, 2001). Activation of muscarinic receptors initiates a cascade of biochemical events that culminate in a glutamate-driven limbic status epilepticus (Wade et al, 1987;Lallement et al, 1991;Shih and McDonough, 1997;Solberg and Belkin, 1997).…”

Section: Introductionmentioning

confidence: 99%

Alterations in brain glutathione homeostasis induced by the nerve gas soman

et al. 2003

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Public awareness of the dangers of chemical and biological warfare has been heightened in recent times. In particular, chemical nerve agents such as soman and its analogs have been developed and used in war as well as recent incidents, such as in Iraq and Japan. Soman, a rapid acting acetylcholinesterase inhibitor, produces a status epilepticus that leads to extensive neuropathology in vulnerable brain regions (eg, piriform cortex and hippocampus). This study was undertaken to determine whether oxidative mechanisms are involved in brain pathology during soman toxicity. Intracellular thiols such as glutathione (GSH) and protein sulfhydryls (PrSH) are among the most critical antioxidants used to combat oxidative stress. Here we report that during the seizure phase (1 h post soman exposure), PrSH levels in piriform cortex and hippocampus were decreased without changes in glutathione (GSH) levels. However, by 24 h post soman exposure (pathology phase), GSH levels were decreased by nearly 50% in the piriform cortex with a corresponding decrease in PrSH groups. The shift to a more oxidized thiol status indicates that oxygen free radicals likely participate in the neuropathology associated with soman-induced seizures.

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Changes in Extracellular Amino Acids During Soman‐and Kainic Acid‐Induced Seizures

Cited by 134 publications

References 22 publications

Myelination in the hippocampus during development and following lesion

Myelination in the hippocampus during development and following lesion

Kainic acid (KA)-induced seizures in Sprague-Dawley rats and the effect of dietary taurine (TAU) supplementation or deficiency

Alterations in brain glutathione homeostasis induced by the nerve gas soman

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