scholarly journals Correlation between Hypermetabolism and Neuronal Damage during Status Epilepticus Induced by Lithium and Pilocarpine in Immature and Adult Rats

1999 ◽  
Vol 19 (2) ◽  
pp. 195-209 ◽  
Author(s):  
Maria José da Silva Fernandes ◽  
Céline Dubé ◽  
Sylvette Boyet ◽  
Christian Marescaux ◽  
Astrid Nehlig
Keyword(s):  
Status Epilepticus ◽  
Substantia Nigra ◽  
Present Model ◽  
Neuronal Damage ◽  
Cresyl Violet ◽  
Adult Rats ◽  
Cresyl Violet Staining ◽  
Variable Extent ◽  
Extent Of Damage ◽  
Deoxyglucose Method

The correlation between seizure-induced hypermetabolism and subsequent neuronal damage was studied in 10-day-old (P10), 21-day-old (P21), and adult rats subjected to lithium-pilocarpine status epilepticus (SE). Local CMRglc (LCMRglc) values were measured by the [14C]2-deoxyglucose method for a duration of 45 minutes starting at 60 minutes after the onset of SE, and neuronal damage was assessed by cresyl violet staining at 6 days after SE. In P21 and adult rats, LCMRglc values were increased by 275 to 875% in all thalamic, cortical, forebrain, and hypothalamic regions plus the substantia nigra. In addition, at P21 there were also large increases in LCMRglc in brainstem regions. In P10 rats, metabolic increases were mostly located in cortical and forebrain regions plus the substantia nigra but did not affect hypothalamic, thalamic, or brainstem areas. In adult rats, there was an anatomical correlation between hypermetabolism and neuronal damage. At P21, although hypermetabolism occurred in regions with damage, the extent of damage varied considerably with the animals and ranged from an almost negligible to a very extended degree. Finally, in P10 rats, although quite pronounced hypermetabolism occurred, there was no neuronal damage induced by the seizures. Thus, in the present model of epilepsy, the correlation between marked hypermetabolism and neuronal damage can be shown in adult rats. Conversely, immature rats can sustain major metabolic activations that lead either to a variable extent of damage, as seen at P21, or no damage, as recorded at P10.

scholarly journals Local Cerebral Blood Flow during Lithium–Pilocarpine Seizures in the Developing and Adult Rat: Role of Coupling between Blood Flow and Metabolism in the Genesis of Neuronal Damage

2002 ◽  
Vol 22 (2) ◽  
pp. 196-205 ◽  
Author(s):  
Anne Pereira de Vasconcelos ◽  
Arielle Ferrandon ◽  
Astrid Nehlig
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Status Epilepticus ◽  
Metabolic Rate ◽  
Neuronal Damage ◽  
Adult Brain ◽  
Local Cerebral Blood Flow ◽  
Adult Rats ◽  
Flow Rates ◽  
Cerebral Metabolic Rate

Coupling between local cerebral blood flow and local cerebral metabolic rate for glucose is involved in the pathogenesis of epilepsy-related neuronal damage in the adult brain; however, its role in the immature brain is unknown. Lithium–pilocarpine–induced status epilepticus is associated with extended damage in adult rats, mostly in the forebrain limbic areas and thalamus, whereas damage was moderate in 21-day-old rats (P21) or absent in P10 rats. The quantitative autoradiographic [14C]iodoantipyrine technique was applied to measure the consequences of lithium-pilocarpine status epilepticus on local cerebral blood flow. In adult and P21 rats, local cerebral blood flow rates increased by 50% to 400%; the highest increases were recorded in regions showing damage in adults. At P10, local cerebral blood flow rates decreased by 40% to 60% in most areas, except in some forebrain regions showing no change during status epilepticus. In areas injured when status epilepticus was induced in adults, a strong hypermetabolism ( Fernandes et al., 1999 ) not matched by comparable local cerebral blood flow increases was present in rats of all ages, whereas in damage-resistant areas, local cerebral metabolic rate for glucose and local cerebral blood flow remained coupled in the three age groups. Thus, the level of coupling between blood flow supply and metabolism is not involved in seizure-related brain damage in the developing brain, which appears to be resistant to the consequences of such a mismatch.

scholarly journals Utility of manual fractional anisotropy measurements in the management of patients with Parkinson disease: a feasibility study with a 1.5-T magnetic resonance imaging system

2021 ◽  
Vol 10 (2) ◽  
pp. 205846012199347
Author(s):  
Romulo V de Oliveira ◽  
João S Pereira
Keyword(s):  
Diffusion Tensor Imaging ◽  
Substantia Nigra ◽  
Parkinson Disease ◽  
Fractional Anisotropy ◽  
Diffusion Tensor ◽  
Neuronal Damage ◽  
Magnetic Resonance Imaging System ◽  
Healthy Controls ◽  
Clinical Variables ◽  
Severity Scores

Background Diffusion tensor imaging has emerged as a promising tool for quantitative analysis of neuronal damage in Parkinson disease, with potential value for diagnostic and prognostic evaluation. Purpose The aim of this study was to examine Parkinson disease-associated alterations in specific brain regions revealed by diffusion tensor imaging and how such alterations correlate with clinical variables. Material and Methods Diffusion tensor imaging was performed on 42 Parkinson disease patients and 20 healthy controls with a 1.5-T scanner. Manual fractional anisotropy measurements were performed for the ventral, intermediate, and dorsal portions of the substantia nigra, as well as for the cerebral peduncles, putamen, thalamus, and supplementary motor area. The correlation analysis between these measurements and the clinical variables was performed using χ2 variance and multiple linear regression. Results Compared to healthy controls, Parkinson disease patients had significantly reduced fractional anisotropy values in the substantia nigra ( P < .05). Some fractional anisotropy measurements in the substantia nigra correlated inversely with duration of Parkinson disease and Parkinson disease severity scores. Reduced fractional anisotropy values in the substantia nigra were also correlated inversely with age variable. fractional anisotropy values obtained for the right and left putamen varied significantly between males and females in both groups. Conclusion Manual fractional anisotropy measurements in the substantia nigra were confirmed to be feasible with a 1.5-T scanner. Diffusion tensor imaging data can be used as a reliable biomarker of Parkinson disease that can be used to support diagnosis, prognosis, and progression/treatment monitoring.

scholarly journals Comparison of age‐dependent alterations in thioredoxin 2 and thioredoxin reductase 2 expressions in hippocampi between mice and rats

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Yeon Ho Yoo ◽  
Dae Won Kim ◽  
Bai Hui Chen ◽  
Hyejin Sim ◽  
Bora Kim ◽  
...  
Keyword(s):  
Thioredoxin Reductase ◽  
Pyramidal Cells ◽  
Brain Regions ◽  
Young Age ◽  
Cresyl Violet ◽  
Western Blots ◽  
Protein Levels ◽  
Cresyl Violet Staining ◽  
Age Dependent ◽  
The Brain

Abstract Background Aging is one of major causes triggering neurophysiological changes in many brain substructures, including the hippocampus, which has a major role in learning and memory. Thioredoxin (Trx) is a class of small redox proteins. Among the Trx family, Trx2 plays an important role in the regulation of mitochondrial membrane potential and is controlled by TrxR2. Hitherto, age-dependent alterations in Trx2 and TrxR2 in aged hippocampi have been poorly investigated. Therefore, the aim of this study was to examine changes in Trx2 and TrxR2 in mouse and rat hippocampi by age and to compare their differences between mice and rats. Results Trx2 and TrxR2 levels using Western blots in mice were the highest at young age and gradually reduced with time, showing that no significant differences in the levels were found between the two subfields. In rats, however, their expression levels were the lowest at young age and gradually increased with time. Nevertheless, there were no differences in cellular distribution and morphology in their hippocampi when it was observed by cresyl violet staining. In addition, both Trx2 and TrxR2 immunoreactivities in the CA1-3 fields were mainly shown in pyramidal cells (principal cells), showing that their immunoreactivities were altered like changes in their protein levels. Conclusions Our current findings suggest that Trx2 and TrxR2 expressions in the brain may be different according to brain regions, age and species. Therefore, further studies are needed to examine the reasons of the differences of Trx2 and TrxR2 expressions in the hippocampus between mice and rats.

Prophylactic treatment with melatonin after status epilepticus: Effects on epileptogenesis, neuronal damage, and behavioral changes in a kainate model of temporal lobe epilepsy

2013 ◽  
Vol 27 (1) ◽  
pp. 174-187 ◽  
Author(s):  
Jana Tchekalarova ◽  
Zlatina Petkova ◽  
Daniela Pechlivanova ◽  
Slavianka Moyanova ◽  
Lidia Kortenska ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Prophylactic Treatment ◽  
Neuronal Damage ◽  
Behavioral Changes

scholarly journals Optimal concentration of necrostatin-1 for protecting against hippocampal neuronal damage in mice with status epilepticus

2020 ◽  
Vol 15 (5) ◽  
pp. 936 ◽  
Author(s):  
Ri-Sheng Liang ◽  
Dong-Qi Lin ◽  
Xin-Ying Cai ◽  
Chun-Hua Wang ◽  
Bin Yang
Keyword(s):  
Status Epilepticus ◽  
Neuronal Damage ◽  
Optimal Concentration

Histamine 1 receptor knock out mice show age-dependent susceptibility to status epilepticus and consequent neuronal damage

2012 ◽  
Vol 100 (1-2) ◽  
pp. 80-92 ◽  
Author(s):  
Tiina-Kaisa Kukko-Lukjanov ◽  
Maria Grönman ◽  
Minnamaija Lintunen ◽  
Hanna B. Laurén ◽  
Kimmo A. Michelsen ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Neuronal Damage ◽  
Knock Out ◽  
Age Dependent ◽  
Knock Out Mice

scholarly journals The Differentially Expressed Circular RNAs in the Substantia Nigra and Corpus Striatum of Nrf2-Knockout Mice

2018 ◽  
Vol 50 (3) ◽  
pp. 936-951 ◽  
Author(s):  
Jun-Hui Yang ◽  
Run-Jiao Zhang ◽  
Jia-Jie Lin ◽  
Ming-Chao Cao ◽  
Qie Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Substantia Nigra ◽  
Microarray Analysis ◽  
Corpus Striatum ◽  
Neuronal Damage ◽  
Interaction Network ◽  
Differentially Expressed ◽  
Circular Rnas ◽  
Related Factor ◽  
Qrt Pcr

Background/Aims: The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway plays a protective role in both acute neuronal damage and chronic neurodegeneration-related oxidative stress. Circular RNAs (circRNAs) are involved with various diseases in the central nervous system (CNS). This study aimed to identify the key circRNAs involved in Nrf2-neuroprotection against oxidative stress. Methods: The differentially expressed circRNAs (DEcircRNAs) in the substantia nigra and corpus striatum between Nrf2 (-/-) and Nrf2 (+/+) mice were identified by microarray analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was then used to validate the expression of selected DEcircRNAs in the substantia nigra and corpus striatum between Nrf2 (-/-) and Nrf2 (+/+) mice. Based on our previous microarray analysis of the differentially expressed mRNAs (DEmRNAs) in the substantia nigra and corpus striatum between Nrf2 (-/-) and Nrf2 (+/+) mice, the DEcircRNA-miRNA-DEmRNA interaction network was constructed. Functional annotation of DEmRNAs that shared the same binding miRNAs with DEcircRNAs was performed using gene ontology (GO) and pathway analyses. Results: A total of 65 and 150 significant DEcircRNAs were obtained in the substantia nigra and corpus striatum of Nrf2 (-/-) mice, respectively, and seventeen shared DEcircRNAs were found in both these two tissues. The qRT-PCR results were generally consistent with the microarray results. The DEcircRNA-miRNA-DEmRNA interaction network and pathway analysis indicated that mmu_circRNA_34132, mmu_circRNA_017077 and mmu-circRNA-015216 might be involved with Nrf2-mediated neuroprotection against oxidative stress. Mmu_circRNA_015216 and mmu_circRNA_017077 might play roles in the Nrf2-related transcriptional misregulation and Nrf2-mediated processes of rheumatoid arthritis, respectively. In addition to these two processes, mmu_circRNA_34132 may be a potential regulator of Nrf2-mediated protection for diabetes mellitus and Nrf2-mediated defence against ROS in hearts. Conclusion: In conclusion, our study identified the key DEcircRNAs in the substantia nigra and corpus striatum of Nrf2 (-/-) mice, which might provide new clues for further exploring the mechanism of Nrf2-mediated neuroprotection against oxidative stress and other Nrf2-mediated processes.

scholarly journals Decreased Cerebrospinal Fluid Orexin-A (Hypocretin-1) Concentrations in Patients after Generalized Convulsive Status Epilepticus

2020 ◽  
Vol 9 (10) ◽  
pp. 3354
Author(s):  
Mojdeh Samzadeh ◽  
Ewa Papuć ◽  
Marzena Furtak-Niczyporuk ◽  
Konrad Rejdak
Keyword(s):  
Cerebrospinal Fluid ◽  
Status Epilepticus ◽  
Neuronal Damage ◽  
Study Groups ◽  
Convulsive Status Epilepticus ◽  
Orexin A ◽  
Diagnostic Lumbar Puncture ◽  
Turn Over ◽  
Hypocretin 1

The effects of status epilepticus on the orexin/hypocretin system have yet to be investigated. The present study aimed to assay orexin-A/hypocretin-1 in the cerebrospinal fluid (CSF) of patients after generalized convulsive status epilepticus (GCSE). The study groups included 20 GCSE patients, 24 patients diagnosed with epilepsy but remaining in remission (ER), and 25 normal controls (CTR). Diagnostic lumbar puncture was performed in GCSE patients within 3–10 days of seizure cessation, as well as in the ER and to CTR subjects. Among all GCSE patients, the outcome was graded according to the modified Rankin Scale (mRS) at 1-month follow-up. Orexin-A levels were measured in unextracted CSF samples, using a commercial radioimmunoassay. There was a significant overall difference in median CSF orexin-A concentrations between GCSE, RE, and CTR patients (p < 0.001). The lowest concentrations were noted in the GCSE group compared to ER (p < 0.001) or CTR (p < 0.001). CSF orexin-A levels in GCSE patients inversely correlated with clinical outcome as assessed on the mRS at 1-month follow-up (r = −0.55; p = 0.1). In conclusion, CSF orexin-A levels may serve as a biomarker of increased turn-over of the peptide or post-SE neuronal damage, and implicates the orexin system in the pathogenesis of SE.

scholarly journals Resveratrol Promotes Mitochondrial Biogenesis and Protects against Seizure-Induced Neuronal Cell Damage in the Hippocampus Following Status Epilepticus by Activation of the PGC-1α Signaling Pathway

2019 ◽  
Vol 20 (4) ◽  
pp. 998 ◽  
Author(s):  
Yao-Chung Chuang ◽  
Shang-Der Chen ◽  
Chung-Yao Hsu ◽  
Shu-Fang Chen ◽  
Nai-Ching Chen ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Signaling Pathway ◽  
Mitochondrial Biogenesis ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Protective Mechanism ◽  
Protective Effects ◽  
Prolonged Seizure

Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is known to regulate mitochondrial biogenesis. Resveratrol is present in a variety of plants, including the skin of grapes, blueberries, raspberries, mulberries, and peanuts. It has been shown to offer protective effects against a number of cardiovascular and neurodegenerative diseases, stroke, and epilepsy. This study examined the neuroprotective effect of resveratrol on mitochondrial biogenesis in the hippocampus following experimental status epilepticus. Kainic acid was microinjected into left hippocampal CA3 in Sprague Dawley rats to induce bilateral prolonged seizure activity. PGC-1α expression and related mitochondrial biogenesis were investigated. Amounts of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (Tfam), cytochrome c oxidase 1 (COX1), and mitochondrial DNA (mtDNA) were measured to evaluate the extent of mitochondrial biogenesis. Increased PGC-1α and mitochondrial biogenesis machinery after prolonged seizure were found in CA3. Resveratrol increased expression of PGC-1α, NRF1, and Tfam, NRF1 binding activity, COX1 level, and mtDNA amount. In addition, resveratrol reduced activated caspase-3 activity and attenuated neuronal cell damage in the hippocampus following status epilepticus. These results suggest that resveratrol plays a pivotal role in the mitochondrial biogenesis machinery that may provide a protective mechanism counteracting seizure-induced neuronal damage by activation of the PGC-1α signaling pathway.

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