Metabolic changes in rat striatum following convulsive seizures

Darbin, Olivier; Risso, J.J.; Carré, E.; Lonjon, M.; Naritoku, Dean K.

doi:10.1016/j.brainres.2005.05.030

Cited by 20 publications

(12 citation statements)

References 28 publications

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“…This is in agreement with earlier studies on brain homogenates which also reported several-fold increases in lactate (Duffy et al 1975;Chapman et al 1977). In the past, build-up of lactate in the brain has often been associated with cellular damage, and when accompanied by increased lactate/pyruvate ratios, was interpreted to reflect anaerobic metabolism in some studies on seizure development (Darbin et al 2005;Slais et al 2008). Our data, however, show that glucose levels are increased during seizures, not decreased, as would be expected in ischemia (Kiewert et al 2010).…”

Section: Discussionsupporting

confidence: 92%

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Early metabolic responses to lithium/pilocarpine‐induced status epilepticus in rat brain

Imran

Hillert

Klein

2015

Journal of Neurochemistry

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The lithium-pilocarpine model of status epilepticus is a wellknown animal model of temporal lobe epilepsy. We combined this model with in vivo microdialysis to investigate energy metabolites and acute cellular membrane damage during seizure development. Rats were implanted with dialysis probes and pretreated with lithium chloride (127 mg/kg i.p.). Twenty-four hours later, they received pilocarpine (30 mg/kg s.c.) which initiated seizures within 30 min. In the dialysate from rat hippocampus, we observed a transient increase in glucose and a prominent, five-fold increase in lactate during seizures. Lactate release was because of neuronal activation as it was strongly reduced by infusion of tetrodotoxin, administration of atropine or when seizures were terminated by diazepam or ketamine. In ex vivo assays, mitochondrial function as measured by respirometry was not affected by 90 min of seizures. Extracellular levels of choline, however, increased two-fold and glycerol levels 10-fold, which indicate cellular phospholipid breakdown during seizures. Within 60 min of pilocarpine administration, hydroxylation of salicylate increased two-fold and formation of isoprostanes 20-fold, revealing significant oxidative stress in hippocampal tissue. Increases in lactate, glycerol and isoprostanes were abrogated, and increases in choline were completely prevented, when hippocampal probes were perfused with calcium-free solution. Similarly, administration of pregabalin (100 mg/kg i.p.), a calcium channel ligand, 15 min prior to pilocarpine strongly attenuated parameters of membrane damage and oxidative stress. We conclude that seizure development in a rat model of status epilepticus is accompanied by increases in extracellular lactate, choline and glycerol, and by oxidative stress, while mitochondrial function remains intact for at least 90 min. Membrane damage depends on calcium influx and can be prevented by treatment with pregabalin.

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Section: Discussionsupporting

confidence: 92%

“…In the past, build‐up of lactate in the brain has often been associated with cellular damage, and when accompanied by increased lactate/pyruvate ratios, was interpreted to reflect anaerobic metabolism in some studies on seizure development (Darbin et al . ; Slais et al . ).…”

Section: Discussionmentioning

confidence: 99%

Early metabolic responses to lithium/pilocarpine‐induced status epilepticus in rat brain

Imran

Hillert

Klein

2015

Journal of Neurochemistry

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“…For example, Darbin et al observed no significant change in striatal LPR when generalized convulsive seizures were induced in rats with electroshock. However, a significant increase in subcutaneous tissue LPR was observed [120]. These experimental findings have also been observed in comatose TBI patients.…”

Section: Seizuressupporting

confidence: 75%

Potential Non-Hypoxic/Ischemic Causes of Increased Cerebral Interstitial Fluid Lactate/Pyruvate Ratio: A Review of Available Literature

2011

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Microdialysis, an in vivo technique that permits collection and analysis of small molecular weight substances from the interstitial space, was developed more than 30 years ago and introduced into the clinical neurosciences in the 1990s. Today cerebral microdialysis is an established, commercially available clinical tool that is focused primarily on markers of cerebral energy metabolism (glucose, lactate, and pyruvate) and cell damage (glycerol), and neurotransmitters (glutamate). Although the brain comprises only 2% of body weight, it consumes 20% of total body energy. Consequently, the ability to monitor cerebral metabolism can provide significant insights during clinical care. Measurements of lactate, pyruvate, and glucose give information about the comparative contributions of aerobic and anaerobic metabolisms to brain energy. The lactate/pyruvate ratio reflects cytoplasmic redox state and thus provides information about tissue oxygenation. An elevated lactate pyruvate ratio (>40) frequently is interpreted as a sign of cerebral hypoxia or ischemia. However, several other factors may contribute to an elevated LPR. This article reviews potential non-hypoxic/ischemic causes of an increased LPR.

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“…Miller and Medina (1986) evidenced a very rapid (detectable 6 min postchallenge) and important (2-to 5-fold the control values) increase of lactate during at least the first two hours following the injection of 0.9 LD 50 of soman in rats. In other models of electrically or chemically induced seizures (kainate, pilocarpine, lithium-pilocarpine, bicuculine), an increase of lactate was also generally observed in the first hours, either total lactate by in vivo NMR (Meric et al, 1994;Najm et al, 1998;Van Eijsden et al, 2004) or extracellular lactate (Patel et al, 2005;Darbin et al, 2005;Slais et al, 2008). Finally, an increase of cerebral lactate has also been observed clinically during spontaneous seizures (During et al, 1994).…”

Section: Metabolitesmentioning

confidence: 91%

Changes in mouse brain metabolism following a convulsive dose of soman: A proton HRMAS NMR study

Fauvelle¹,

Dorandeu²,

Carpentier³

et al. 2010

Toxicology

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Metabolic changes in rat striatum following convulsive seizures

Cited by 20 publications

References 28 publications

Early metabolic responses to lithium/pilocarpine‐induced status epilepticus in rat brain

Early metabolic responses to lithium/pilocarpine‐induced status epilepticus in rat brain

Potential Non-Hypoxic/Ischemic Causes of Increased Cerebral Interstitial Fluid Lactate/Pyruvate Ratio: A Review of Available Literature

Changes in mouse brain metabolism following a convulsive dose of soman: A proton HRMAS NMR study

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