Bibliographies thématiques / Audiogenic seizures

Littérature scientifique sur le sujet « Audiogenic seizures »

Auteur : Grafiati
Publié le 25 mai 2024

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Articles de revues sur le sujet "Audiogenic seizures"

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Hrnčić, Dragan, Danijela Vučević, Aleksandra Rašić, Tatjana Radosavljević, Dušan Mladenović, Veselinka Šušić, Dragan Djurić et Olivera Stanojlović. « Moderate body hypothermia alleviates behavioral and EEG manifestations of audiogenic seizures in metaphit-treated rats ». Canadian Journal of Physiology and Pharmacology 85, no 10 (octobre 2007) : 1032–37. http://dx.doi.org/10.1139/y07-094.

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We investigated the effects of hypothermia on the incidence and EEG signs of audiogenic seizures in rats treated with metaphit (1-[1(3isothiocyanatophenyl)-cyclohexyl] piperidine), an experimental model of generalized reflex epilepsy. After i.p. injection with metaphit (10 mg/kg) Wistar rats were exposed to audiogenic stimulation at hourly intervals during the time course of the experiment. After intermittent use of an ice pack 8 h after the metaphit treatment, when seizure was fully developed, the body temperature was reduced to 30 ± 0.5 °C in one half of the rats, and maintained at 37 ± 0.5 °C in the other half. Saline-injected rats served as a control group. In the hypothermia group, the incidence of audiogenic seizures induced by metaphit was completely suppressed during the 3 consecutive testing times, while no signs of epileptiform activity were noted in EEG tracings. The termination of hypothermic treatment resulted in the recovery of seizure susceptibility, and during audiogenic stimulation, bursts of spiking activity were recorded in the EEGs of metaphit-treated rats. These findings indicate that moderate body hypothermia is an effective anticonvulsant treatment for audiogenic seizures in metaphit-treated rats.
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Nehlig, Astrid, Marguerite Vergnes, Edouard Hirsch, Sylvette Boyet, Violette Koziel et Christian Marescaux. « Mapping of Cerebral Blood Flow Changes during Audiogenic Seizures in Wistar Rats : Effect of Kindling ». Journal of Cerebral Blood Flow & ; Metabolism 15, no 2 (mars 1995) : 259–69. http://dx.doi.org/10.1038/jcbfm.1995.32.

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The quantitative autoradiographic [14C]iodoantipyrine technique was applied to the measurement of rates of local cerebral blood flow (LCBF) during audiogenic seizures in Wistar AS rats belonging to a genetic strain selected at the Centre de Neurochimie (Strasbourg, France) for their sensitivity to sound. Seizures were elicited in naive rats never exposed to sound (single audiogenic seizures) or in rats previously exposed to 10–40 seizure-inducing sound stimulations until generalization of the seizure to forebrain areas (referred to as “kindled animals”). During single audiogenic seizures, rates of LCBF increased over control values in all areas but the genu of the corpus callosum. The highest increases in LCBF (180–388%) were recorded in the inferior and superior colliculus, reticular formation, monoaminergic cell groupings, especially the substantia nigra, posterior vegetative nuclei, and many thalamic and hypothalamic regions. The lowest increases were seen in forebrain limbic regions and cortical areas. In kindled animals, LCBF rates increased over control levels in 67 areas of the 75 studied. LCBF increases were generally of a lower amplitude in kindled than in naive rats. Differences between the two groups of seizing rats were located mostly in brain-stem regions, mainly the inferior colliculus, reticular formation, substantia nigra, and posterior vegetative nuclei. Conversely, rates of LCBF were similar in forebrain areas of naive and kindled animals. In conclusion, the present data show that there is a good correlation between the structures known to be involved in the expression of audiogenic seizures (inferior colliculus, reticular formation, substantia nigra mainly) and the large increase in LCBF during single audiogenic seizures, while rates of LCBF increase to a lesser extent in forebrain areas not involved in this type of seizures. The circulatory adaptation to kindled seizures is rather a decreased response in brain-stem regions and no change in the forebrain, although the kindling process induces a generalization of the seizure from brain-stem to anterior regions.
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García-Peral, Carlos, Martín M. Ledesma, M. Javier Herrero-Turrión, Ricardo Gómez-Nieto, Orlando Castellano et Dolores E. López. « Proteomic and Bioinformatic Tools to Identify Potential Hub Proteins in the Audiogenic Seizure-Prone Hamster GASH/Sal ». Diagnostics 13, no 6 (9 mars 2023) : 1048. http://dx.doi.org/10.3390/diagnostics13061048.

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The GASH/Sal (Genetic Audiogenic Seizure Hamster, Salamanca) is a model of audiogenic seizures with the epileptogenic focus localized in the inferior colliculus (IC). The sound-induced seizures exhibit a short latency (7–9 s), which implies innate protein disturbances in the IC as a basis for seizure susceptibility and generation. Here, we aim to study the protein profile in the GASH/Sal IC in comparison to controls. Protein samples from the IC were processed for enzymatic digestion and then analyzed by mass spectrometry in Data-Independent Acquisition mode. After identifying the proteins using the UniProt database, we selected those with differential expression and performed ontological analyses, as well as gene-protein interaction studies using bioinformatics tools. We identified 5254 proteins; among them, 184 were differentially expressed proteins (DEPs), with 126 upregulated and 58 downregulated proteins, and 10 of the DEPs directly related to epilepsy. Moreover, 12 and 7 proteins were uniquely found in the GASH/Sal or the control. The results indicated a protein profile alteration in the epileptogenic nucleus that might underlie the inborn occurring audiogenic seizures in the GASH/Sal model. In summary, this study supports the use of bioinformatics methods in proteomics to delve into the relationship between molecular-level protein mechanisms and the pathobiology of rodent models of audiogenic seizures.
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Krivopalov, Sergey, Boris Yushkov et Alexey Sarapultsev. « Wireless EEG Recording of Audiogenic Seizure Activity in Freely Moving Krushinsky-Molodkina Rats ». Biomedicines 12, no 5 (24 avril 2024) : 946. http://dx.doi.org/10.3390/biomedicines12050946.

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This study investigates audiogenic epilepsy in Krushinsky-Molodkina (KM) rats, questioning the efficacy of conventional EEG techniques in capturing seizures during animal restraint. Using a wireless EEG system that allows unrestricted movement, our aim was to gather ecologically valid data. Nine male KM rats, prone to audiogenic seizures, received implants of wireless EEG transmitters that target specific seizure-related brain regions. These regions included the inferior colliculus (IC), pontine reticular nucleus, oral part (PnO), ventrolateral periaqueductal gray (VLPAG), dorsal area of the secondary auditory cortex (AuD), and motor cortex (M1), facilitating seizure observation without movement constraints. Our findings indicate that targeted neural intervention via electrode implantation significantly reduced convulsive seizures in approximately half of the subjects, suggesting therapeutic potential. Furthermore, the amplitude of brain activity in the IC, PnO, and AuD upon audiogenic stimulus onset significantly influenced seizure severity and nature, highlighting these areas as pivotal for epileptic propagation. Severe cases exhibited dual waves of seizure generalization, indicative of intricate neural network interactions. Distinctive interplay between specific brain regions, disrupted during convulsive activity, suggests neural circuit reconfiguration in response to escalating seizure intensity. These discoveries challenge conventional methodologies, opening avenues for novel approaches in epilepsy research and therapeutic interventions.
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Fedotova, Irina B., Natalia M. Surina, Georgy M. Nikolaev, Alexandre V. Revishchin et Inga I. Poletaeva. « Rodent Brain Pathology, Audiogenic Epilepsy ». Biomedicines 9, no 11 (8 novembre 2021) : 1641. http://dx.doi.org/10.3390/biomedicines9111641.

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The review presents data which provides evidence for the internal relationship between the stages of rodent audiogenic seizures and post-ictal catalepsy with the general pattern of animal reaction to the dangerous stimuli and/or situation. The wild run stage of audiogenic seizure fit could be regarded as an intense panic reaction, and this view found support in numerous experimental data. The phenomenon of audiogenic epilepsy probably attracted the attention of physiologists as rodents are extremely sensitive to dangerous sound stimuli. The seizure proneness in this group shares common physiological characteristics and depends on animal genotype. This concept could be the new platform for the study of epileptogenesis mechanisms.
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Vinogradova, Lyudmila V. « Comparative potency of sensory-induced brainstem activation to trigger spreading depression and seizures in the cortex of awake rats : Implications for the pathophysiology of migraine aura ». Cephalalgia 35, no 11 (16 décembre 2014) : 979–86. http://dx.doi.org/10.1177/0333102414565672.

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Background Migraine and epilepsy are highly co-morbid neurological disorders associated with episodic dysfunction of both cortical and subcortical networks. The study examined the interrelation between cortical spreading depression, the electrophysiological correlate of migraine aura and seizures triggered at cortical and brainstem levels by repeated sound stimulation in rats with acoustic hypersensitivity (reflex audiogenic epilepsy). Method In awake, freely moving rats with innate audiogenic epilepsy, 25 episodes of running seizure (brainstem seizures) were induced by repeated sound stimulation. Spreading depression and seizures were recorded using implanted cortical electrodes. Results The first sound-induced brainstem seizures evoked neither spreading depression nor seizures in the cortex. With repetition, brainstem seizures began to be followed by a single cortical spreading depression wave and an epileptiform discharge. Spreading depression was more frequent an early cortical event than seizures: spreading depression appeared after 8.4 ± 1.0 repeated stimulations in 100% rats ( n = 24) while cortical seizures were recorded after 12.9 ± 1.2 tests in 46% rats. Brainstem seizure triggered unilateral long-latency spreading depression. Bilateral short-latency cortical spreading depression was recorded only after intense cortical seizures. Conclusion These data show that episodic brainstem activation is a potent trigger of unilateral cortical spreading depression. Development of intense seizures in the cortex leads to initiation of spreading depression in multiple cortical sites of both hemispheres.
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Bazhanova, Е. D., А. А. Kozlov et Yu О. Sokolova. « Etiopathogenetic mechanisms of epilepsy and comparative characteristics of audiogenic epilepsy experimental models ». Epilepsy and paroxysmal conditions 15, no 4 (22 décembre 2023) : 372–83. http://dx.doi.org/10.17749/2077-8333/epi.par.con.2023.161.

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Epilepsy is a widespread neurological chronic disease characterized by recurrent seizures, manifested as short-term partial or generalized convulsions and accompanied by loss of consciousness. To correctly select a treatment method for epilepsy, it is necessary to investigate the cues resulting in its development, but it is not always possible to identify a cause of the disease and chose proper treatment. Drug resistance remains one of the major issues in treatment of epilepsy, despite a great body of studies describing its nature. In this regard, it is necessary to select a model for examining epileptic seizures and underlying mechanisms, searching for genes involved in regulation of epilepsy as well as assessing effectiveness and safety of new antiepileptic drugs. It was noted that rodents, especially Krushinsky–Molodkina rat strain represent a suitable genetic model for audiogenic epilepsy to dissect the mechanisms of epileptogenesis, genetic basis of seizure susceptibility, development of drug resistance, and testing new antiepileptic drugs. Despite that the audiogenic form of reflex epilepsy is quite rare in humans, it was revealed that the same underlying genes, molecular mechanisms and signaling pathways are responsible for enabling audiogenic seizures in rodents and human epilepsy, additionally coupled to developing similar neuroanatomical anomalies.
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Marine, Nikolaishvili, Nanobashvili Zakharia, Mitagvaria Nodar, Chkadua Gvantsa, Bilanishvili Irina, Nozadze Ekaterine, Rtveladze T, Museliani Tea, Dondoladze Khatuna et Jikia Gogi. « Hormesis Effect of Radon in Rats of the Krushinsky-Molodkina Line ». European Scientific Journal, ESJ 18, no 14 (30 avril 2022) : 1. http://dx.doi.org/10.19044/esj.2022.v18n14p1.

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According to this research, the use of radon inhalation in experimental animals, particularly in genetically determined rats with epileptic seizures, altered all parameters of the epileptic seizure development picture, namely the hidden period and the first and second wild jog duration after the audiogenic signal. On the third day, no response to the audiogenic signal was observed at all, and there was not even a single episode of tonic-clonic seizures. All what was mentioned suggests that radon inhalation can be used to treat epilepsy. This study is the first precedent of attempting R-Ho through inhalation for treatment of epileptic seizures in animal models with further translation to clinical study in humans through pilot phase II study. More profound and scientifically systematized approach is needed to determine the uniqueness of Tskhaltubo water springs, investigating the mechanisms of radon effects on the excitatory and inhibitory functioning of CNS, and the use of further clinical studies to establish its effectiveness on humans.
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Lowrie, Mark, Laurent Garosi, Robert J. Harvey, Claire Bessant et Andrew Sparkes. « Audiogenic reflex seizures in cats ». Veterinary Record 173, no 19 (15 novembre 2013) : 482.1–482. http://dx.doi.org/10.1136/vr.f6820.

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Lowrie, Mark, Claire Bessant, Robert J. Harvey, Andrew Sparkes et Laurent Garosi. « Audiogenic reflex seizures in cats ». Journal of Feline Medicine and Surgery 18, no 4 (27 avril 2015) : 328–36. http://dx.doi.org/10.1177/1098612x15582080.

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Thèses sur le sujet "Audiogenic seizures"

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Gagliardini, Mathilde. « Les crises audiogènes réflexes : une voie d’entrée dans la compréhension des mécanismes de développement et de fonctionnement des voies rétro-cochléaires ». Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS122.pdf.

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L’approche génétique des formes héréditaires de surdité a été efficace pour révéler la physiologie moléculaire de la cochlée. En revanche, elle a fourni jusqu’à présent peu d'informations sur le système auditif central. L’hypothèse de mon laboratoire est qu’une partie des atteintes auditives centrales dans les formes génétiques de surdité seraient passées inaperçues en raison de l’atteinte cochléaire, qui prive le cerveau auditif de tout ou partie des informations acoustiques qu’il reçoit normalement. Mon objectif est de caractériser ces déficits centraux et périphériques masqués dans plusieurs formes génétiques de surdité par la caractérisation du rôle cérébral d’un gène pour lequel des mutations entraînent une surdité périphérique et une susceptibilité aux crises audiogènes chez la souris. Dans la cochlée, Otogéline-like (Otogl) est impliquée dans la cohésion de la touffe ciliaire et dans la membrane tectoriale. Mes résultats ont montré une expression d’Otogl dans les fibres auditives du noyau cochléaire et dans d’autres structures de la cochlée, révélant de nouveaux rôles joués par Otogl dans la cochlée et les voies rétro-cochléaires. Des défauts fonctionnels dans le traitement du son ont été également observés chez les souris hétérozygotes qui n’ont pas de défauts d’audition. Otogl a donc un rôle dans les voies rétrocochléaires en plus de son rôle cochléaire. Mes résultats montrent qu’Otogl est essentiel au fonctionnement de fibres auditives particulières, dites à haut seuil. Les souris mutantes Otogl sont un nouveau modèle d’étude de ces fibres et de leur rôle dans la survenue des crises audiogènes chez la souris
The genetic approach of inherited forms of deafness has been particularly effective for deciphering the molecular physiology of the cochlea. In contrast, this genetic dissection has so far provided little information about the central auditory system. The hypothesis of my laboratory is that part of the central hearing defects in genetic forms of deafness would be concealed due to cochlear damages, which deprive the auditory brain of all or part of the acoustic information it receives. The objective of my thesis was to characterize these masked central and peripheric deficits in a new mutant mouse model for Otogl, a genetic form of deafness. Mutations in Otogl cause peripheral deafness but are also associated to a susceptibility to audiogenic seizures, reflex seizures induced by a loud sound. In the cochlea, otogl is involved in the cohesion of the hair bundle, the mechanical antenna to the sound of sensory cells and in the tectorial membrane. My results showed that Otogl is expressed in the fibers of the primary auditory nerve and in additional structures of the cochlea, unveiling new roles for Otogl in the cochlea and the central auditory pathways. I also uncovered functional deficits in sound processing in heterozygous Otogl+/- mice that did not have peripheral hearing loss. Otogl therefore has a retrocochlear role in addition to its role in the cochlea. These results involve a particular category of auditory nerve fibers, the high-threshold fibers. Otogl mutant mice are a new model for studying high-threshold fibers and their role in the occurrence of audiogenic seizures in mice
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Chaistitwanich, Rachaneeporn. « The Effect of Dietary Calcium and Phosphorus Levels on Audiogenic Seizure Susceptibility and Brain Neurotransmitters in Magnasium Deficient Rats ». DigitalCommons@USU, 1986. https://digitalcommons.usu.edu/etd/5330.

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The effects of dietary calcium and phosphorus levels on audiogenic seizure susceptibility and brain neurotransmitter were investigated in magnesium deficient rats. For 17 days, male weanling rats were fed magnesium deficient diets which also contained deficient (-), adequate (=}, and excess (+) amounts of calcium and/or phosphorus. Reduction of seizure incidence was seen in low calcium and/or low phosphorus diets. High calcium, and high calcium in combination with high phosphorus increased the severity of seizures. High calcium and low phosphorus, and high phosphorus and low calcium diets prevented seizuring. Most magnesium deficient diets resulted in elevation of serum phosphorus, calcium, and sodium concentrations. Within diet treatments, animals that seized had higher serum mineral concentrations than animals that failed to seize. Magnesium deficiency increased serotonin in cerebral cortex, cerebellum, and medulla oblongata and pons, and 5-hydroxyindoleacetic acid concentrations in cerebral cortex. There were no significant diet effects in brain neurotransmitter concentrations in the midbrain. Calcium seemed to play an important role in increasing both audiogenic seizure susceptibility and brain neurotransmitters. However, brain neurotransmitter levels were not related to seizure susceptibility. Calcium increased serum potassium and sodium concentrations and it increased brain serotonin concentration overall. Increasing dietary phosphorus levels increased serum phosphorus decreased serum calcium concentrations, but did not affect brain neurotransmitters.
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Livres sur le sujet "Audiogenic seizures"

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Audiogenic seizures and genomic imprinting. 1996.

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Chapitres de livres sur le sujet "Audiogenic seizures"

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Henry, Kenneth R. « Audiogenic Seizures in Relation to Genetically and Experimentally Produced Cochlear Pathology ». Dans Perspectives in Behavior Genetics, 57–93. London : Routledge, 2021. http://dx.doi.org/10.4324/9781003156239-3.

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Lipovac, Milo N., E. A. Debler, A. Lajtha, B. V. Zloković, A. E. Jacobson, K. C. Rice, A. N. Popović, S. Popadić et M. E. A. Reith. « Anticonvulsant Effects of Phencyclidine and PCP-like Drugs on Audiogenic Seizures Induced by Metaphit in Mice ». Dans Barriers and Fluids of the Eye and Brain, 198–202. London : Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-12306-3_17.

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Faingold, Carl L., Marcus E. Randall et Catherine A. Copley. « Blockade of audiogenic seizures by a GABA-uptake inhibitor, NO-328, in the genetically epilepsy-prone rat ». Dans Amino Acids, 263–68. Dordrecht : Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_29.

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Lipovac, Milo N., V. Susić, B. V. Zloković, A. E. Jacobson, K. C. Rice, A. N. Popović, S. Popadić et M. E. A. Reith. « Epileptogenic Activity of Metaphitinduced Audiogenic Seizure in Small Rodents ». Dans Barriers and Fluids of the Eye and Brain, 192–97. London : Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-12306-3_16.

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Reigel, Charles. « Audiogenic Seizures in Mice and Rats ». Dans Neuropharmacology Methods in Epilepsy Research. CRC Press, 1998. http://dx.doi.org/10.1201/9781420048889.ch6.

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Reigel, Charles. « Audiogenic Seizures in Mice and Rats ». Dans Neuropharmacology Methods in Epilepsy Research. CRC Press, 1998. http://dx.doi.org/10.1201/9780849333620.ch6.

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Reigel, Charles E. « Audiogenic Seizures in Mice and Rats ». Dans Neuropharmacology Methods in Epilepsy Research, 127–54. CRC Press, 2019. http://dx.doi.org/10.1201/9780429186851-6.

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« D ». Dans Genetic variants and strains of the Laboratory mouse, sous la direction de Mary F. Lyon, Sohaila Rastan et S. D. M. Brown, 183–201. Oxford University PressOxford, 1996. http://dx.doi.org/10.1093/oso/9780198548690.003.0006.

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Abstract See also Emv3 locus. Mutations at this locus alter coat color; some alleles are lethal and cause a severe neuromuscular disorder. There is conflicting evidence on whether they affect incidence of audiogenic seizures and phenylalanine hydroxylase activity (15). Spontaneous and radiation-induced mutations from + to J and spontaneous mutations from d to + have been reported repeatedly.
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I., Inga, Irina B., Natalia M. et Zoya A. « Audiogenic Seizures - Biological Phenomenon and Experimental Model of Human Epilepsies ». Dans Clinical and Genetic Aspects of Epilepsy. Intech, 2011. http://dx.doi.org/10.5772/17229.

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Lazarini-Lopes, Willian, Gabriel Servilha-Menezes, Rui Milton Patrício da Silva-Júnior, Ricardo Gómez-Nieto, Dolores E. López et Norberto Garcia-Cairasco. « Genetic models of audiogenic seizures : What they are and how cannabinoids and Cannabis-derived compounds can be used to alleviate their symptoms—An updated narrative ». Dans Medicinal Usage of Cannabis and Cannabinoids, 245–63. Elsevier, 2023. http://dx.doi.org/10.1016/b978-0-323-90036-2.00032-6.

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