Metabolic Disturbances: Hypo- and Hyperglycemic Seizures In Vivo and In Vitro a

Carlen, Peter L.; Zhang, Liang

doi:10.1016/b978-0-12-804066-9.00064-x

Cited by 2 publications

(2 citation statements)

References 100 publications

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“…Our present observations are in line with a recent study demonstrating the mouse CA3 circuitry in generation of seizure-like events following hypoglycemic episodes ex vivo (Florez et al, 2015 ). Together these data indicate a high prevalence of CA3 hyperexcitability under conditions of metabolic disturbances (Carlen and Zhang, 2017 ).…”

Section: Discussionmentioning

confidence: 80%

Contributions of the Hippocampal CA3 Circuitry to Acute Seizures and Hyperexcitability Responses in Mouse Models of Brain Ischemia

Song

Mylvaganam

Wang

et al. 2018

Front. Cell. Neurosci.

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The hippocampal circuitry is widely recognized as susceptible to ischemic injury and seizure generation. However, hippocampal contribution to acute non-convulsive seizures (NCS) in models involving middle cerebral artery occlusion (MCAO) remains to be determined. To address this, we occluded the middle cerebral artery in adult C57 black mice and monitored electroencephalographic (EEG) discharges from hippocampal and neocortical areas. Electrographic discharges in the absence of convulsive motor behaviors were observed within 90 min following occlusion of the middle cerebral artery. Hippocampal discharges were more robust than corresponding cortical discharges in all seizure events examined, and hippocampal discharges alone or with minimal cortical involvement were also observed in some seizure events. Seizure development was associated with ipsilateral hippocampal injuries as determined by subsequent histological examinations. We also introduced hypoxia-hypoglycemia episodes in mouse brain slices and examined regional hyperexcitable responses ex vivo. Extracellular recordings showed that the hippocampal CA3 region had a greater propensity for exhibiting single/multiunit activities or epileptiform field potentials following hypoxic-hypoglycemic (HH) episodes compared to the CA1, dentate gyrus, entorhinal cortical (EC) or neocortical regions. Whole-cell recordings revealed that CA3 pyramidal neurons exhibited excessive excitatory postsynaptic currents, attenuated inhibitory postsynaptic currents and intermittent or repetitive spikes in response to HH challenge. Together, these observations suggest that hippocampal discharges, possibly as a result of CA3 circuitry hyperexcitability, are a major component of acute NCS in a mouse model of MCAO.

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Section: Discussionmentioning

confidence: 80%

Contributions of the Hippocampal CA3 Circuitry to Acute Seizures and Hyperexcitability Responses in Mouse Models of Brain Ischemia

Song

Mylvaganam

Wang

et al. 2018

Front. Cell. Neurosci.

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“…A number of models, both in vitro and in vivo, that mimic the hypoglycemic condition are studied in different animals (Table ) . Results of one of the studies that evaluated insulin‐induced hypoglycemia in rats indicate that neuronal damage is triggered when EEG becomes isoelectric EEG, regardless of the glucose level .…”

Section: Metabolic Errors In Organic Moleculesmentioning

confidence: 99%

Metabolic etiologies in West syndrome

2018

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SummaryWest syndrome (WS) is an early life epileptic encephalopathy associated with infantile spasms, interictal electroencephalography (EEG) abnormalities including high amplitude, disorganized background with multifocal epileptic spikes (hypsarrhythmia), and often neurodevelopmental impairments. Approximately 64% of the patients have structural, metabolic, genetic, or infectious etiologies and, in the rest, the etiology is unknown. Here we review the contribution of etiologies due to various metabolic disorders in the pathology of WS. These may include metabolic errors in organic molecules involved in amino acid and glucose metabolism, fatty acid oxidation, metal metabolism, pyridoxine deficiency or dependency, or acidurias in organelles such as mitochondria and lysosomes. We discuss the biochemical, clinical, and EEG features of these disorders as well as the evidence of how they may be implicated in the pathogenesis and treatment of WS. The early recognition of these etiologies in some cases may permit early interventions that may improve the course of the disease.

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Metabolic Disturbances: Hypo- and Hyperglycemic Seizures In Vivo and In Vitro a

Cited by 2 publications

References 100 publications

Contributions of the Hippocampal CA3 Circuitry to Acute Seizures and Hyperexcitability Responses in Mouse Models of Brain Ischemia

Contributions of the Hippocampal CA3 Circuitry to Acute Seizures and Hyperexcitability Responses in Mouse Models of Brain Ischemia

Metabolic etiologies in West syndrome

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