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Journal articles on the topic 'Audiogenic seizures'

Author: Grafiati

Published: 25 May 2024

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1

Hrnčić, Dragan, Danijela Vučević, Aleksandra Rašić, Tatjana Radosavljević, Dušan Mladenović, Veselinka Šušić, Dragan Djurić, and 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 (October 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, and 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 (March 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, and Dolores E. López. "Proteomic and Bioinformatic Tools to Identify Potential Hub Proteins in the Audiogenic Seizure-Prone Hamster GASH/Sal." Diagnostics 13, no. 6 (March 9, 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, and Alexey Sarapultsev. "Wireless EEG Recording of Audiogenic Seizure Activity in Freely Moving Krushinsky-Molodkina Rats." Biomedicines 12, no. 5 (April 24, 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, and Inga I. Poletaeva. "Rodent Brain Pathology, Audiogenic Epilepsy." Biomedicines 9, no. 11 (November 8, 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 (December 16, 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, and Yu О. Sokolova. "Etiopathogenetic mechanisms of epilepsy and comparative characteristics of audiogenic epilepsy experimental models." Epilepsy and paroxysmal conditions 15, no. 4 (December 22, 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, and Jikia Gogi. "Hormesis Effect of Radon in Rats of the Krushinsky-Molodkina Line." European Scientific Journal, ESJ 18, no. 14 (April 30, 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, and Andrew Sparkes. "Audiogenic reflex seizures in cats." Veterinary Record 173, no. 19 (November 15, 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, and Laurent Garosi. "Audiogenic reflex seizures in cats." Journal of Feline Medicine and Surgery 18, no. 4 (April 27, 2015): 328–36. http://dx.doi.org/10.1177/1098612x15582080.

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11

Kinboshi, Masato, Saki Shimizu, Tomoji Mashimo, Tadao Serikawa, Hidefumi Ito, Akio Ikeda, Ryosuke Takahashi, and Yukihiro Ohno. "Down-Regulation of Astrocytic Kir4.1 Channels during the Audiogenic Epileptogenesis in Leucine-Rich Glioma-Inactivated 1 (Lgi1) Mutant Rats." International Journal of Molecular Sciences 20, no. 5 (February 26, 2019): 1013. http://dx.doi.org/10.3390/ijms20051013.

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The dysfunction of astrocytic inwardly rectifying potassium (Kir) 4.1 channels, which mediate the spatial potassium-buffering function of astrocytes, is known to be involved in the development of epilepsy. Here, we analyzed the Kir4.1 expressional changes in Leucine-Rich Glioma-Inactivated 1 (Lgi1) mutant rats, which is a model of autosomal dominant lateral temporal lobe epilepsy in humans, to clarify the role of astrocytic Kir4.1 channels in Lgi1-related epileptogenesis. Priming acoustic stimulation (at postnatal day 16) conferred seizure susceptibility on Lgi1 mutant rats, which evoked audiogenic seizures with test stimulation at eight weeks. In the seizure-susceptible Lgi1 mutant rats (before test stimulation), astrocytic Kir4.1 expression was down-regulated region-specifically in the cerebral cortex, hippocampus, and amygdala. In addition, prophylactic treatments of Lgi1 mutant rats with valproic acid (VPA, 30 mg/kg and 200 mg/kg) for two weeks prevented both the development of seizure susceptibility and the down-regulation of Kir4.1 expression in astrocytes. The present study demonstrated for the first time that the astrocytic Kir4.1 expression was reduced in the Lgi1-related seizure model, suggesting that the down-regulation of Kir4.1 channels in astrocytes is involved in audiogenic epileptogenesis caused by Lgi1 mutation. In addition, VPA seemed to have a prophylactic effect on Lgi1-related seizures.

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Stanojlovic, Olivera, Dragana Zivanovic, Slobodan Mirkovic, and Danijela Vucevic. "Behavioral and electroencephalographic effects of delta sleep inducing peptide and its analogue on metaphit-induced audiogenic seizures in rats." Srpski arhiv za celokupno lekarstvo 132, no. 11-12 (2004): 421–26. http://dx.doi.org/10.2298/sarh0412421s.

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INTRODUCTION Delta sleep inducing peptide (DSIP) is well known natural somnogenic peptide that has many other physiological functions. DSIP analogues representing hepta-and octapeptides (also known as long) as well as tetrapeptide (termed short, used in our experiments) were synthesized with a view to evaluate the peptide specificity in sleep. The effects of DSIP and its analogue DSIP1-4 on metaphit 1-[1(3-isothiocyanatophenyl-ciclohexyl)-piperidine] induced audiogenic seizures were evaluated in rats. METHODS Male Wistar albino rats were divided into 4 groups: 1. Saline; 2. Metaphit; 3. Metaphit + DSIP, and 4. Metaphit + DSIP1-4. To examine the blocking effects of DSIP and its analogue on fully developed metaphit seizures, the last two groups were injected after the 8th audiogenic testing. Animals were injected with metaphit (10 mg/kg) intraperitoneally (i.p.) and exposed to sound stimulation (100?3 dB, 60 s) at hourly intervals. The incidence and severity (running, clonus and tonus) of seizures were analyzed. For electroencephalographic (EEG) recordings, three gold-plated electrodes were used. Convulsive behavior was assessed by incidence of motor seizure and by seizure severity grade, determined by descriptive rating scale ranging from 0 to 3:0- no response, 1 -wild running only; 2-wild running followed by clonic seizures of all four limbs with body rollover; 3 - wild running progressing to generalized clonic convulsions followed by tonic extension of fore-and hind legs and tail. Sound onset, seizure events, and sound offset, along with the animal's behavior (convulsive or other) were characterized with EEG changes. RESULTS In most animals, the administration of metaphit resulted in electroencephalographic abnormalities, elicited epileptic-form activity in the form of spikes, polyspikes and spike-wave complexes. Maximum incidence and severity of metaphit convulsions occurred 8 h after the injection (9/12, 75%), then abated gradually and disappeared 30 h later. Both DSIP and DSIP1-4 significantly increased the power spectra of d waves and decreased the incidence of seizures, mean seizure grade and tonic component of metaphit-induced convulsions. DISCUSSION Metaphit has been shown to induce audiogenic seizures after systemic and intracerebroventricular administration and to be truly epileptic in small rodents [8-11], although about 8 h after metaphit administration, the power spectra increased and was more intense in the period of sound onset and seizure events. Taken together, DSIP makes an optimal ratio between inhibitory and excitatory amino acid neurotransmitters and may represent one of the endogenous control systems of the brain, thus exerting the protective effect against the seizures [14,15,19]. The results obtained throughout the present study corroborate and broaden the data on prolonged antiepileptic DSIP effect. CONCLUSION The results of the present study strongly suggest that treatment of adult rats with DSIP and its analogue DSIPM should be considered as potential natural antiepileptics.

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Garcia-Cairasco, N., M. C. Doretto, M. J. Ramalho, J. Antunes-Rodrigues, and K. O. Nonaka. "Audiogenic and audiogenic-like seizures: Locus of induction and seizure severity determine postictal prolactin patterns." Pharmacology Biochemistry and Behavior 53, no. 3 (March 1996): 503–10. http://dx.doi.org/10.1016/0091-3057(95)02040-3.

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Федотова, И. Б., А. В. Поликарпова, О. В. Перепелкина, Г. М. Николаев, О. В. Смирнова, and И. И. Полетаева. "Blood corticosterone in rats with different susceptibility to audiogenic epilepsy." Nauchno-prakticheskii zhurnal «Patogenez», no. 3() (September 29, 2018): 64–67. http://dx.doi.org/10.25557/2310-0435.2018.03.64-67.

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Актуальность. Селектированная на проявление судорог в ответ на сильный звук (аудиогенную эпилепсию, АЭ) линия крыс Крушинского-Молодкиной (КМ) - модель судорожных состояний человека, c быстрым развитием судорожного припадка в ответ на включение звука (100-120 дБ). Однако у крыс с АЭ изменений уровня кортикостерона (КС) в крови в связи с судорогами не определяли, хотя анализ связи АЭ и стресс-реакции - важная практическая задача. Методы. Уровень КС в образцах сыворотки крови определяли с помощью набора у крыс линии КМ, а также у крыс линии «0», селектированных из гибридной популяции КМ х Вистар на отсутствие АЭ, и у крыс популяции Вистар. Результаты. У всех крыс КМ был зарегистрирован аудиогенный припадок, тогда как у крыс линии «0» и Вистар судорог не было. Через 30 мин после действия звука (и судорог) у крыс КМ повышеается уровень КС, тогда как сразу после судорог (через 1-3 мин) данная реакция не обнаруживается. У крыс линии «0» обнаружен достоверно более высокий фоновый уровень КС, по сравнению с КМ и Вистар. Уровень КС у них, как и у крыс Вистар, после действия звука не изменялся. Заключение. Подъем уровня КС в крови после действия звука наблюдали только у крыс КМ через 30 мин после припадка АЭ. Крысы линии «0», у которых нет судорог в ответ на звук, обнаружили более высокий, чем у КМ и Вистар уровень КС в фоне. Aims. The Krushinsky-Molodkina (KM) rat strain, which was selected for a seizure response to a sound (audiogenic epilepsy, AE), is known as a model of human seizure states. Although the association of blood CS with stress reaction is an important practical issue, blood levels of corticosterone (CS) have never been analyzed in rats with AE in relation with seizures. Methods. Serum concentration of CS was measured using IBL International Corticosterone ELISA kits in KM rats, rats of the «0» strain, which was selected (based on F2 KM х Wistar hybrids) for the lack of seizures in response to a sound, and Wistar rats. Results. All KM rats developed AE seizures in response to a sound while no seizures were observed in rats of the «0» strain and Wistar rats. The increase in blood CS was observed only in KM rats at 30 min after AE seizure. At background, the level of CS was significantly higher in rats of the «0» strain, which did not develop seizures in response to a sound, than in KM and Wistar rats. CS levels remained unchanged in both «0» and Wistar rats after the sound exposure. Conclusions. The increase in blood CS occurred in KM rats at 30 min after the seizure episode. At background, the CS level was higher in rats of the «0» strain, which did not respond with seizures to a sound, than in Wistar and KM rats. Therefore, the blood level of CS depends in a complicated way on both AE and the selection history of the «0» rat strain.

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Alekhina, T. A. "EFFECT OF TAURINE ON MANIFESTATION OF AUDIOGENIC EPILEPSY IN RATS WITH PENDULUM MOVEMENTS." Журнал высшей нервной деятельности им. И.П. Павлова 73, no. 1 (January 1, 2023): 88–93. http://dx.doi.org/10.31857/s0044467723010033.

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A decrease of taurine in hippocampus of the line of rats with pendulum movements (PM), predisposed to audiogenic epilepsy, was shown. Taurine (aminoethanesulfonic acid) is known to be an anticonvulsant drug. The aim of the present work was to verify the predictive validity of taurine in rats with pendulum movements (PM). In neonatal period the exogenous taurine administration did not influence a convulsive activity at the age of 1.5 and 3 months in PM rats. The increase in the number of audiogenic seizures after taurine injections was found in adolescent period in 1.5 months and in prolonged point – in 3 months. The number of abortive seizures decreased under acute injection of taurine in adult PM rats, but the level of ictal and postictal indicators restored one month later, at the age of 4 months. Obtained results indicate the absence of effect of taurine administered to rats in the neonatal age, while at the long-term scale, the rats showed the increasing seizure activity under the action of taurine in adolescent period and confirm the predictive validity of this drug in adult PM rats.

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Rebik, Anastasiya, Nadezda Broshevitskaya, Syldys Kuzhuget, Pavel Aleksandrov, Kenul Abbasova, Maria Zaichenko, and Inna Midzyanovskaya. "Audiogenic Seizures and Social Deficits: No Aggravation Found in Krushinsky–Molodkina Rats." Biomedicines 11, no. 9 (September 18, 2023): 2566. http://dx.doi.org/10.3390/biomedicines11092566.

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Epilepsy or epileptic syndromes affect more than 70 million people, often comorbid with autism spectrum disorders (ASD). Seizures are concerned as a factor for social regression in ASD. A stepwise experimental approach to this problem requires an animal model to provoke seizures and monitor subsequent behavior. We used rats of the Krushinsky–Molodkina (KM) strain as a validated inbred genetic model for human temporal lobe epilepsy, with recently described social deficiency and hypolocomotion. Generalized tonic-clonic seizures in KM rats are sound-triggered, thus being controlled events in drug-naïve animals. We studied whether seizure experience would aggravate contact deficits in these animals. Locomotor and contact parameters were registered in “the elevated plus maze”, “socially enriched open field”, and “social novelty/social preference tests” before and after sound-provoked seizures. The triple seizure provocations minimally affected the contact behavior. The lack of social drive in KM rats was not accompanied by a submissive phenotype, as tested in “the tube dominance test”, but featured with a poor contact repertoire. Here, we confirmed our previous findings on social deficits in KM rats. The contact deficiency was dissociated from hypolocomotion and anxiety and did not correlate with seizure experience. It was established that experience of rare, generalized tonic-clonic convulsions did not lead to an impending regress in contact motivation, as seen in an animal model of genetic epilepsy and comorbid social deficiency. One of the oldest animal models for epilepsy has a translational potential to study mechanisms of social behavioral deficits in future neurophysiological and pharmacological research.

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de Azevedo, Belarmino Alves, and Pedro Fontana. "Audiogenic seizures and the pineal gland." Biological Psychiatry 23, no. 7 (April 1988): 734–40. http://dx.doi.org/10.1016/0006-3223(88)90058-3.

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Damasceno, Samara, Nathália Bustamante de Menezes, Cristiane de Souza Rocha, Alexandre Hilário Berenguer de Matos, André Schwambach Vieira, Márcio Flávio Dutra Moraes, Almir Souza Martins, Iscia Lopes-Cendes, and Ana Lúcia Brunialti Godard. "Transcriptome of the Wistar audiogenic rat (WAR) strain following audiogenic seizures." Epilepsy Research 147 (November 2018): 22–31. http://dx.doi.org/10.1016/j.eplepsyres.2018.08.010.

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Wicker, Evan, Veronica C. Beck, Colin Kulick-Soper, Catherine V. Kulick-Soper, Safwan K. Hyder, Carolina Campos-Rodriguez, Tahiyana Khan, Prosper N’Gouemo, and Patrick A. Forcelli. "Descending projections from thesubstantia nigra pars reticulatadifferentially control seizures." Proceedings of the National Academy of Sciences 116, no. 52 (December 16, 2019): 27084–94. http://dx.doi.org/10.1073/pnas.1908176117.

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Three decades of studies have shown that inhibition of thesubstantia nigra pars reticulata(SNpr) attenuates seizures, yet the circuits mediating this effect remain obscure. SNpr projects to the deep and intermediate layers of the superior colliculus (DLSC) and the pedunculopontine nucleus (PPN), but the contributions of these projections are unknown. To address this gap, we optogenetically silenced cell bodies within SNpr, nigrotectal terminals within DLSC, and nigrotegmental terminals within PPN. Inhibition of cell bodies in SNpr suppressed generalized seizures evoked by pentylenetetrazole (PTZ), partial seizures evoked from the forebrain, absence seizures evoked by gamma-butyrolactone (GBL), and audiogenic seizures in genetically epilepsy-prone rats. Strikingly, these effects were fully recapitulated by silencing nigrotectal projections. By contrast, silencing nigrotegmental terminals reduced only absence seizures and exacerbated seizures evoked by PTZ. These data underscore the broad-spectrum anticonvulsant efficacy of this circuit, and demonstrate that specific efferent projection pathways differentially control different seizure types.

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Stanojlovic, Olivera, Dragan Hrncic, Drenka Turjacanin, Dragana Zivanovic, and Veselinka Susic. "Delta sleep-inducing peptide and its analogues alleviate the severity of metaphit-induced audiogenic seizures in rats." Medical review 60, no. 9-10 (2007): 436–40. http://dx.doi.org/10.2298/mpns0710436s.

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Introduction. We investigated the potential of delta sleep-inducing peptide (DSIP) and its analogue DSIP-12 (a nonapeptide with alanine in position 2 of DISP molecule substituted by beta-alanine) and tetrapeptide analogue DSIP1-4, to antagonize metaphit- (1-1(3-isothiocyanatophenyl)-cyclohexyl piperidine) induced generalized reflex audiogenic seizures in adult male Wistar albino rats. Material and Methods. Five groups of adult male Wistar rats were intraperitoneally treated with: 1. saline; 2. metaphit; 3. metaphit + DSIP; 4. metaphit + DSIP1-4 and 5. metaphit + DSIP-12. To examine the blocking effects of DSIP and its analogues on fully developed metaphit seizures, in the last three groups they were administered 8h after metaphit injection. The rats were stimulated using an electric bell (1003 dB, 5-8 kHz, 60 s) one hour after metaphit injection and afterwards at hourly intervals during the experiment. For EEG recordings and power spectra three gold-plated screws were implanted into the skull. Results. In metaphit-treated animals EEGs appeared as polyspikes and spike-wave complexes, while power spectra were increasing. The incidence and severity of metaphit-induced audiogenic seizures reached a peak value at 7-12 h after injection. Both DSIP and DSIP analogues significantly increased power spectra of delta waves and decreased the incidence of seizures, as well as mean seizure grade and tonic component of metaphit-induced convulsions. Conclusion. Taken together, these results suggest that DSIP and its analogues should be considered as potential antiepileptic agents. .

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Osterweil, Emily K. "Seizing control of fragile X syndrome." Science Translational Medicine 12, no. 524 (January 1, 2020): eaba2902. http://dx.doi.org/10.1126/scitranslmed.aba2902.

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Garbuz, David G., Artem A. Davletshin, Svetlana A. Litvinova, Irina B. Fedotova, Natalya M. Surina, and Inga I. Poletaeva. "Rodent Models of Audiogenic Epilepsy: Genetic Aspects, Advantages, Current Problems and Perspectives." Biomedicines 10, no. 11 (November 15, 2022): 2934. http://dx.doi.org/10.3390/biomedicines10112934.

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Animal models of epilepsy are of great importance in epileptology. They are used to study the mechanisms of epileptogenesis, and search for new genes and regulatory pathways involved in the development of epilepsy as well as screening new antiepileptic drugs. Today, many methods of modeling epilepsy in animals are used, including electroconvulsive, pharmacological in intact animals, and genetic, with the predisposition for spontaneous or refractory epileptic seizures. Due to the simplicity of manipulation and universality, genetic models of audiogenic epilepsy in rodents stand out among this diversity. We tried to combine data on the genetics of audiogenic epilepsy in rodents, the relevance of various models of audiogenic epilepsy to certain epileptic syndromes in humans, and the advantages of using of rodent strains predisposed to audiogenic epilepsy in current epileptology.

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Lowrie, Mark, Sarah Thomson, Claire Bessant, Andrew Sparkes, Robert J. Harvey, and Laurent Garosi. "Levetiracetam in the management of feline audiogenic reflex seizures: a randomised, controlled, open-label study." Journal of Feline Medicine and Surgery 19, no. 2 (July 9, 2016): 200–206. http://dx.doi.org/10.1177/1098612x15622806.

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Objectives Currently, there are no published randomised, controlled veterinary trials evaluating the efficacy of antiepileptic medication in the treatment of myoclonic seizures. Myoclonic seizures are a hallmark of feline audiogenic seizures (FARS). Methods This prospective, randomised, open-label trial compared the efficacy and tolerability of levetiracetam (20–25 mg/kg q8h) with phenobarbital (3–5 mg/kg q12h) in cats with suspected FARS that experienced myoclonic seizures. Cats were included that had ⩾12 myoclonic seizure days during a prospective 12 week baseline period. This was followed by a 4 week titration phase (until a therapeutic serum concentration of phenobarbital was achieved) and a 12 week treatment phase. Results Fifty-seven cats completed the study: 28 in the levetiracetam group and 29 in the phenobarbital group. A reduction of ⩾50% in the number of myoclonic seizure days was seen in 100% of patients in the levetiracetam group and in 3% of patients in the phenobarbital group ( P <0.001) during the treatment period. Levetiracetam-treated cats had higher freedom from myoclonic seizures (50.0% vs 0%; P <0.001) during the treatment period. The most common adverse events were lethargy, inappetence and ataxia, with no difference in incidence between levetiracetam and phenobarbital. Adverse events were mild and transient with levetiracetam but persistent with phenobarbital. Conclusions and relevance These results suggest that levetiracetam is an effective and well tolerated treatment for cats with myoclonic seizures and is more effective than phenobarbital. Whether it will prevent the occurrence of generalised tonic–clonic seizures and other forebrain signs if used early in the course of FARS is not yet clear.

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Maurois, Pierre, Nicole Pages, Pierre Bac, Michèle German-Fattal, Geneviève Agnani, Bernadette Delplanque, Jean Durlach, Jacques Poupaert, and Joseph Vamecq. "Threshold to N-methyl-D-aspartate-induced seizures in mice undergoing chronic nutritional magnesium deprivation is lowered in a way partly responsive to acute magnesium and antioxidant administrations." British Journal of Nutrition 101, no. 3 (June 16, 2008): 317–21. http://dx.doi.org/10.1017/s0007114508006752.

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Magnesium deficiency may be induced by a diet impoverished in magnesium. This nutritional deficit promotes chronic inflammatory and oxidative stresses, hyperexcitability and, in mice, susceptibility to audiogenic seizures. Potentiation by low-magnesium concentrations of the opening of N-methyl-d-aspartate (NMDA) receptor/calcium channel in in vitro and ex vivo studies, and responsiveness to magnesium of in vivo brain injury states are now well established. By contrast, little or no specific attention has been, however, paid to the in vivo NMDA receptor function/excitability in magnesium deficiency. The present work reports for the first time that, in mice undergoing chronic nutritional deprivation in magnesium (35 v. 930 parts per million for 27 d in OF1 mice), NMDA-induced seizure threshold is significantly decreased (38 % of normal values). The attenuation in the drop of NMDA seizure threshold (percentage of reversal) was 58 and 20 % upon acute intraperitoneal administrations of magnesium chloride hexahydrate (28 mg magnesium/kg) and the antioxidant ebselen (20 mg/kg), respectively. In nutritionally magnesium-deprived animals, audiogenic seizures are completely prevented by these compound doses. Taken as a whole, our data emphasise that chronic magnesium deprivation in mice is a nutritional in vivo model for a lowered NMDA receptor activation threshold. This nutritional model responds remarkably to acute magnesium supply and moderately to acute antioxidant administration.

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Lyutova, L. V., V. B. Koshelev, and M. A. Karabasova. "HAEMOSTASIS AND FIBRINOLYSIS AFTER EXPERIMENTAL AUDIOGENIC SEIZURES/." Journal of Thrombosis and Haemostasis 5 (July 2007): P—W—628—P—W—628. http://dx.doi.org/10.1111/j.1538-7836.2007.tb03185.x.

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Vergnes, Marguerite, Michèle Kiesmann, Christian Marescaux, Antoine Depaulis, Gabriel Micheletti, and Jean-Marie Warter. "Kindling of Audiogenic Seizures in the Rat." International Journal of Neuroscience 36, no. 3-4 (January 1987): 167–76. http://dx.doi.org/10.3109/00207458709058791.

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Grosso, S., M. A. Farnetani, E. Bernardoni, G. Morgese, and P. Balestri. "Intractable reflex audiogenic seizures in Aicardi syndrome." Brain and Development 29, no. 4 (May 2007): 243–46. http://dx.doi.org/10.1016/j.braindev.2006.09.005.

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Garcia-Cairasco, N., V. C. Terra, and M. C. Doretto. "Midbrain substrates of audiogenic seizures in rats." Behavioural Brain Research 58, no. 1-2 (December 1993): 57–67. http://dx.doi.org/10.1016/0166-4328(93)90090-d.

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Reid, Howard M., and Robert L. Collins. "Monaural and binaural audiogenic seizures in mice." Behavioral and Neural Biology 51, no. 2 (March 1989): 136–44. http://dx.doi.org/10.1016/s0163-1047(89)90767-x.

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Delfino-Pereira, Polianna, Poliana Berti Dutra, Jose Antonio Cortes de Oliveira, Izabel Cristina Casanova Turatti, Artur Fernandes, Norberto Peporine Lopes, and Norberto Garcia-Cairasco. "Are Predator Smell (TMT)-Induced Behavioral Alterations in Rats Able to Inhibit Seizures?" Chemical Senses 45, no. 5 (March 4, 2020): 347–57. http://dx.doi.org/10.1093/chemse/bjaa023.

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Abstract We aimed to evaluate the chemical and behavioral effects of 2,5-dihydro-2,4,5-trimethylthiazoline (TMT) after olfactory exposure and to verify their influence in the expression of acute audiogenic seizures in the Wistar Audiogenic Rat (WAR) strain. PROTOCOL 1: TMT gas chromatography was applied to define odor saturation in a chamber to different concentrations, time required for saturation and desaturation, and if saturation was homogeneous. Also, male Adult Wistar rats were exposed to saline (SAL) or to different TMT concentrations and their behaviors were evaluated (neuroethology). PROTOCOL 2: Male adult WARs were exposed for 15 s to SAL or TMT, followed by sound stimulation for 1 min or until tonic–clonic convulsion. Behavioral analysis included latencies (wild running and tonic–clonic convulsion), seizure severity indexes, and neuroethology. Gas chromatography established a saturation homogeneous to different concentrations of TMT, indicating that saturation and desaturation occurred in 30 min. TMT triggered fear-like or aversion-like reactions associated with reduction in motor activity and in grooming behavior, in the 2 highest concentrations. Pure TMT presented anticonvulsant properties, such as less-severe seizure phenotype, as well as a decrease in tonic–clonic convulsion expression. TMT elicited fear-like or aversion-like behaviors in Wistar and WAR and can be utilized in a quantifiable and controllable way. Our results suggested possible antagonism between “fear-related” or “aversion-related” and “seizure-related” networks.

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Surina, N. M., I. B. Fedotova, G. M. Nikolaev, V. V. Grechenko, L. V. Gankovskaya, A. D. Ogurtsova, and I. I. Poletaeva. "Neuroinflammation in the pathogenesis of the audiogenic epilepsy: altered proinflammatory cytokine levels in Krushinsky-Molodkina seizure-prone rats." Биохимия 88, no. 4 (April 15, 2023): 588–99. http://dx.doi.org/10.31857/s0320972523040048.

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Neuroinflammation plays an important role in epileptogenesis, however, most studies are performed on pharmacological models of epilepsy, while data on non-invasive, including genetic, models are practically absent. In Krushinsky-Molodkina (KM) strain rats with high genetically caused predisposition to AE (intensive audiogenic seizure fit in response to the action of sound) and in the control strain “0” (not predisposed to AE), the levels of a number of pro-inflammatory cytokines were investigated using multiplex immunofluorescence magnetic assay (MILLIPLEX map Kit). Cytokine levels were determined in the dorsal striatum tissue and in the brain stem. Background levels of IL-1β, IL-6 and TNF-α in the dorsal striatum of KM rats were significantly lower than in rats “0” (32.31, 27.84 and 38.87% of decrease, respectively, p < 0.05, 0.05 and 0.01), whereas in the brain stem in the “background” state of interstrain differences in levels of these metabolites were not detected. 4 h after sound exposure, the TNF-α level in the dorsal striatum of KM rats was significantly (38.34%, p < 0.01) lower than in “0” rats. In KM rats, after the action of sound and the subsequent seizure fit, the levels of IL-1β and IL-6 in the dorsal striatum were significantly higher compared to the background (35.29 and 50.21%, of increase, p < 0.05, 0.01, respectively). The IL-2 level in KM rats in the background state was not detected, whereas after audiogenic seizures its level was 14.01 pg/ml (significantly higher, p < 0.01). In the brain stem of KM rats, the levels of IL-1β and TNF-α after audiogenic seizures were significantly lower than in the background (13.23 and 23.44% of decrease, respectively, p < 0.05). In rats of the “0” strain, the levels of cytokines in the dorsal striatum after the action of sound (which did not cause AE seizures) did not differ from those in the background, while the levels of IL-1β in their brain stem were lower than in the background (40.28%, p < 0.01). Thus, the differences between the background levels of cytokines and those after the action of sound were different in rats that differed in their predisposition to AE, which suggests the involvement of these metabolites in the pathophysiology of epilepsy.

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Sills, Graeme J. "Seizures Beget Seizures: A Lack of Experimental Evidence and Clinical Relevance Fails to Dampen Enthusiasm." Epilepsy Currents 7, no. 4 (July 2007): 103–4. http://dx.doi.org/10.1111/j.1535-7511.2007.00189.x.

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Three Brief Epileptic Seizures Reduce Inhibitory Synaptic Currents, GABAACurrents, and GABAA-Receptor Subunits. Evans MS, Cady CJ, Disney KE, Yang L, LaGuardia JJ. Epilepsia 2006;4710):1655–1664. PURPOSE: Cellular mechanisms activated during seizures may exacerbate epilepsy. γ-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in brain, and we hypothesized that brief epileptic seizures may reduce GABA function. METHODS: We used audiogenic seizures (AGSs) in genetically epilepsy-prone rats (GEPRs) to investigate effects of seizures on GABA-mediated inhibition in the presence of epilepsy. GEPRs are uniformly susceptible to AGSs beginning at 21 postnatal days. AGSs are brief convulsions lasting 20 s, and they begin in inferior colliculus (IC). We evoked three seizures in GEPRs and compared the results with those in seizure-naive GEPRs and nonepileptic Sprague-Dawley (SD) rats, the GEPR parent strain. RESULTS: Whole-cell recording in IC slices showed that GABA-mediated monosynaptic inhibitory postsynaptic currents (IPSCs) were reduced 55% by three brief epileptic seizures. Whole-cell recording in IC neuronal cultures showed that currents elicited by GABA were reduced 67% by three seizures. Western blotting for the alpha1 and alpha4 subunits of the GABAA receptor showed no statistically significant effects. In contrast, three brief epileptic seizures reduced gamma2 subunit levels by 80%. CONCLUSIONS: The effects of the very first seizures, in animals known to be epileptic, in an area of brain known to be critical to the seizure network, were studied. The results indicate that even brief epileptic seizures can markedly reduce IPSCs and GABA currents and alter GABAA-receptor subunit protein levels. The cause of the reductions in IPSCs and GABA currents is likely to be altered receptor subunit composition, with reduced gamma2 levels causing reduced GABAA-receptor sensitivity to GABA. Seizure-induced reductions in GABA-mediated inhibition could exacerbate epilepsy.

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Lazarini-Lopes, Willian, Gleice Kelli Silva-Cardoso, Christie Ramos Andrade Leite-Panissi, and Norberto Garcia-Cairasco. "Increased TRPV1 Channels and FosB Protein Expression Are Associated with Chronic Epileptic Seizures and Anxiogenic-like Behaviors in a Preclinical Model of Temporal Lobe Epilepsy." Biomedicines 10, no. 2 (February 10, 2022): 416. http://dx.doi.org/10.3390/biomedicines10020416.

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Epilepsies are neurological disorders characterized by chronic seizures and their related neuropsychiatric comorbidities, such as anxiety. The Transient Receptor Potential Vanilloid type-1 (TRPV1) channel has been implicated in the modulation of seizures and anxiety-like behaviors in preclinical models. Here, we investigated the impact of chronic epileptic seizures in anxiety-like behavior and TRPV1 channels expression in a genetic model of epilepsy, the Wistar Audiogenic Rat (WAR) strain. WARs were submitted to audiogenic kindling (AK), a preclinical model of temporal lobe epilepsy (TLE) and behavioral tests were performed in the open-field (OF), and light-dark box (LDB) tests 24 h after AK. WARs displayed increased anxiety-like behavior and TRPV1R expression in the hippocampal CA1 area and basolateral amygdala nucleus (BLA) when compared to control Wistar rats. Chronic seizures increased anxiety-like behaviors and TRPV1 and FosB expression in limbic and brainstem structures involved with epilepsy and anxiety comorbidity, such as the hippocampus, superior colliculus, and periaqueductal gray matter. Therefore, these results highlight previously unrecognized alterations in TRPV1 expression in brain structures involved with TLE and anxiogenic-like behaviors in a genetic model of epilepsy, the WAR strain, supporting an important role of TRPV1 in the modulation of neurological disorders and associated neuropsychiatric comorbidities.

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Garcia-Cairasco, N., and R. M. E. Sabbatini. "Neuroethological evaluation of audiogenic seizures in hemidetelencephalated rats." Behavioural Brain Research 33, no. 1 (May 1989): 65–77. http://dx.doi.org/10.1016/s0166-4328(89)80019-1.

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Gerrish, K. E., D. J. M. Fuller, E. W. Gerner, and H. L. Gensler. "Inhibition of DFMO-induced audiogenic seizures by chlordiazepoxide." Life Sciences 52, no. 13 (January 1993): 1101–8. http://dx.doi.org/10.1016/0024-3205(93)90431-2.

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Nikolaeva, S. D., A. P. Ivlev, A. A. Naumova, A. A. Kulikov, M. V. Glazova, and E. V. Chernigovskaya. "Dysregulation of GABAergic System in the Inferior Colliculi of Rats during the Development of Audiogenic Epilepsy." Российский физиологический журнал им И М Сеченова 109, no. 7 (July 1, 2023): 890–901. http://dx.doi.org/10.31857/s0869813923070105.

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Epilepsy is tightly associated with dysfunction of inhibitory GABA neurotransmission. In this study, Krushinsky–Molodkina (KM) rats genetically prone to audiogenic seizures (AGS) were used. KM rats are characterized by the development of audiogenic epilepsy during postnatal ontogenesis, with AGS onset at the age of 1.5–2 months and fully developed AGS expression by 3rd month. We analyzed GABAergic system of the inferior colliculi (IC) of KM rats at different stages of postnatal development. Wistar rats were used as a control. In the IC of young KM rats, Na+/K+/Cl– cotransporter 1 (NKCC1) expression was increased, while K+/Cl– cotransporter 2 (KCC2) was unchanged indicating impairment of postsynaptic GABA action at early stages of postnatal development. Moreover, we revealed also an increase in the expression of vesicular GABA transporter (VGAT) in the IC which additionally pointed on the higher activity of GABA release. In adult rats, in opposite, we revealed a decrease in the expression of KCC2 transporter indicating downregulation of GABA inhibition on the target cells. Thus, GABA dysregulation in the IC can mediate the seizure susceptibility in adult KM rats.

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Aleksandrova, E. P., A. P. Ivlev, A. A. Kulikov, L. S. Nikitina, M. V. Glazova, and E. V. Chernigovskaya. "CHRONIC DYSREGULATION OF GLUTAMATERGIC TRANSMISSION IN THE HIPPOCAMPUS OF KRUSHINSKY–MOLODKINA RATS INDUCED BY REPEATED EPILEPTIFORM SEIZURES." Журнал эволюционной биохимии и физиологии 59, no. 5 (September 1, 2023): 427–40. http://dx.doi.org/10.31857/s0044452923050029.

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Temporal lobe epilepsy is characterised by the development of associated neurological and psychiatric disorders. One of the possible causes is obviously a disturbance in the balance of the excitatory and inhibitory neurotransmitter systems of the hippocampus. Chronic abnormalities in the molecular mechanisms of regulation of hippocampal glutamatergic system activity in temporal lobe epilepsy are currently poorly understood. In the present study, we used Krushinsky–Molodkina (KM) rats subjected to repeated audiogenic seizures to simulate temporal lobe epilepsy. Molecular mechanisms of regulation of glutamate production by hippocampal neurons were analysed one week after the end of short-term (14 seizures) and long-term (21 seizures) kindling. In the hippocampus of КM rats, kindling results in activation of ERK1/2 kinases as well as activation of the transcription factor CREB and increased expression of the transcription factor Fra1, glutaminase and the vesicular glutamate transporters VGLUT1 and 2, that is proteins responsible for glutamate production. These data indicate increased activity of glutamatergic hippocampal neurons persisting for a week at rest after the completion of the last audiogenic stimulation. Enhanced expression of mGluR1 glutamate receptors, whose activation is known to result in Ca2+ release and increased excitotoxicity, is also shown. Long-term enhancement of glutamatergic transmission induced by repeated epileptiform seizures is not only responsible for further epileptogenesis, but may also underlie the development of neurodegenerative complications.

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Krivopalov, S. A., B. G. Yushkov, M. Yu Bykova, and K. N. Zabegalov. "Gender differences in the pool of free amino acid neurotransmitters in Krushinsky-Molodkina rats." Biomeditsinskaya Khimiya 66, no. 2 (2020): 124–29. http://dx.doi.org/10.18097/pbmc20206602124.

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The study of the role of neurotransmitter systems in the pathogenesis of epilepsy is one of the priorities of epileptology. New data on the functions of free neurotransmitter-like amino acid in the central nervous system are of the greatest importance and determine the prospects for the development of novel effective anticonvulsants. It is widely believed in clinical medicine that epilepsy has distinct gender characteristics. The aim of this study was to investigate the gender peculiarities in the content of neurotransmitter amino acids in the brain of Krushinsky-Molodkina (KM) rats, which were used as model organisms for the study of genetically induced audiogenic epilepsy. The content of Asp, Glu, GABA, Gly, and Tau of the medulla oblongata, hippocampus and cerebral cortex were determined using high-performance liquid chromatography (HPLC) in intact KM rats, KM rats exposed to a series of epileptiform seizures, and Wistar rats (control group). Both the Wistar and KM rats had gender distinctions in the distribution of free amino acids among the investigated brain parts. The audiogenic epilepsy was characterized by smoothing gender differences as well as differences between the concentrations of free amino acids in the cortex and medulla oblongata, specific for Wistar rats. The changes observed in male rats after the set of seizures included the increase in GABA concentration and a decrease in the Gly level in all investigated brain parts, as well as the decrease of the Tau content in the cortex and hippocampus. At the same time, the Glu content in cortex increased, while the Asp level decreased. After 6 days of audiogenic stimulations the female KM rats demonstrated the increase in the Glu level in all investigated brain parts, the increase in Gly and Asp levels in hippocampus, and no changes in the GABA content. Thus, after the set of epileptiform seizures the KM rats achieved a new steady state of the studied amino acids pool, which differed in males and females. In this case, gender differences significantly changed after the seizures.

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Gonçalves-Sánchez, Jaime, Consuelo Sancho, Dolores E. López, Orlando Castellano, Begoña García-Cenador, Gabriel Servilha-Menezes, Juan M. Corchado, Norberto García-Cairasco, and Jesús M. Gonçalves-Estella. "Effect of Vagus Nerve Stimulation on the GASH/Sal Audiogenic-Seizure-Prone Hamster." International Journal of Molecular Sciences 25, no. 1 (December 20, 2023): 91. http://dx.doi.org/10.3390/ijms25010091.

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Vagus nerve stimulation (VNS) is an adjuvant neuromodulation therapy for the treatment of refractory epilepsy. However, the mechanisms behind its effectiveness are not fully understood. Our aim was to develop a VNS protocol for the Genetic Audiogenic Seizure Hamster from Salamanca (GASH/Sal) in order to evaluate the mechanisms of action of the therapy. The rodents were subject to VNS for 14 days using clinical stimulation parameters by implanting a clinically available neurostimulation device or our own prototype for laboratory animals. The neuroethological assessment of seizures and general behavior were performed before surgery, and after 7, 10, and 14 days of VNS. Moreover, potential side effects were examined. Finally, the expression of 23 inflammatory markers in plasma and the left-brain hemisphere was evaluated. VNS significantly reduced seizure severity in GASH/Sal without side effects. No differences were observed between the neurostimulation devices. GASH/Sal treated with VNS showed statistically significant reduced levels of interleukin IL-1β, monocyte chemoattractant protein MCP-1, matrix metalloproteinases (MMP-2, MMP-3), and tumor necrosis factor TNF-α in the brain. The described experimental design allows for the study of VNS effects and mechanisms of action using an implantable device. This was achieved in a model of convulsive seizures in which VNS is effective and shows an anti-inflammatory effect.

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&NA;. "Dizocilpine: inhibits audiogenic seizures in rats undergoing alochol withdrawal." Inpharma Weekly &NA;, no. 730 (March 1990): 4–5. http://dx.doi.org/10.2165/00128413-199007300-00008.

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Maxson, Stephen C. "A genetic context for the study of audiogenic seizures." Epilepsy & Behavior 71 (June 2017): 154–59. http://dx.doi.org/10.1016/j.yebeh.2015.12.031.

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Damasceno, Denis D., Silvia Q. Savergnini, Enéas R. M. Gomes, Silvia Guatimosim, Anderson J. Ferreira, Maria C. Doretto, and Alvair P. Almeida. "Cardiac dysfunction in rats prone to audiogenic epileptic seizures." Seizure 22, no. 4 (May 2013): 259–66. http://dx.doi.org/10.1016/j.seizure.2013.01.006.

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Garcia-Cairasco, N., J. A. C. Oliveira, H. Wakamatsu, S. T. B. Bueno, and F. S. Guimarães. "Reduced exploratory activity of audiogenic seizures suceptible Wistar rats." Physiology & Behavior 64, no. 5 (July 1998): 671–74. http://dx.doi.org/10.1016/s0031-9384(98)00129-2.

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Niki, Hiroaki, Tsuyoshi Miyakawa, and Takeshi Yagi. "Increased susceptibility of audiogenic seizures in Fyn-deficient mice." Neuroscience Research Supplements 19 (January 1994): S99. http://dx.doi.org/10.1016/0921-8696(94)92542-9.

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Zivanovic, Dragana, Olivera Stanojlovic, Jelena Stojanovic, and Veselinka Susic. "Induction of audiogenic seizures in imipenem/cilastatin-treated rats." Epilepsy & Behavior 5, no. 2 (April 2004): 151–58. http://dx.doi.org/10.1016/j.yebeh.2003.11.022.

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Kawai, Hiromichi, Maria Laura Allende, Ryuichi Wada, Mari Kono, Kazunori Sango, Chuxia Deng, Tsuyoshi Miyakawa, et al. "Mice Expressing Only Monosialoganglioside GM3 Exhibit Lethal Audiogenic Seizures." Journal of Biological Chemistry 276, no. 10 (December 27, 2000): 6885–88. http://dx.doi.org/10.1074/jbc.c000847200.

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Reid, Howard M., and Robert L. Collins. "Monaural Audiogenic Seizures: Evidence for Control by Parallel Processes." Epilepsia 33, no. 5 (September 1992): 785–88. http://dx.doi.org/10.1111/j.1528-1157.1992.tb02182.x.

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Debler, E. A., M. N. Lipovac, A. Lajtha, B. V. Zlokovic, D. S. Dunlop, A. E. Jacobson, K. C. Rice, B. Costa, and M. E. A. Reith. "Metaphit-Induced Audiogenic Seizures in Mice: I. Pharmacologic Characterization." Epilepsia 34, no. 2 (March 1993): 201–10. http://dx.doi.org/10.1111/j.1528-1157.1993.tb02400.x.

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Ross, Karen C., and James R. Coleman. "Audiogenic seizures in the developmentally primed Long-Evans rat." Developmental Psychobiology 34, no. 4 (May 1999): 303–13. http://dx.doi.org/10.1002/(sici)1098-2302(199905)34:2<303::aid-dev6>3.0.co;2-x.

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Zivanovic, Dragana, Olivera Stanojlovic, Slobodan Mirkovic, and Veselinka Susic. "Ontogenetic study of metaphit-induced audiogenic seizures in rats." Developmental Brain Research 155, no. 1 (March 2005): 42–48. http://dx.doi.org/10.1016/j.devbrainres.2004.11.006.

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