Inflammatory markers in the hippocampus after audiogenic kindling

Deus, Júnia L. de; Amorim, Margarete Cristiane de Costa Trindade; Filho, Procópio Cleber Gama de Barcellos; Oliveira, José Antônio Cortes de; Batalhão, Marcelo Eduardo; García-Cairasco, Norberto; Cárnio, Evelin Capellari; Branco, Luiz Guilherme de Siqueira; Cunha, Alexandra Olímpio Siqueira

doi:10.1016/j.neulet.2020.134830

Cited by 7 publications

(4 citation statements)

References 31 publications

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“…Moreover, it is worth noting that AuK induced a decrease in WAR's spatial memory retention in the Morris water maze test, but the chronic acoustic stimulation (no seizures) had no effect on Wistar's performance in the same memory test. Moreover, neurotransmission in the hippocampal Schaffer-collaterals fibers and their excitability were not affected by the chronic exposure to acoustic stimulation in Wistar rats (Cunha et al, 2015) and AuK-dependent limbic recruitment in WARs is not associated with any inflammatory process or oxidative stress, suggesting that this neuroplastic anatomical change is a "network expansion process, " primarily linked to the genetic selection for the epilepsy phenotype in WARs (de Deus et al, 2020). Therefore, except for the small percentage of Wistar susceptible animals (usually discarded), acoustic stimulation does not induce audiogenic seizures in Wistar rats, as well as epileptic-like alterations or epilepsy-related comorbidities.…”

Section: Discussionmentioning

confidence: 93%

Cannabinoid Receptor Type 1 (CB1R) Expression in Limbic Brain Structures After Acute and Chronic Seizures in a Genetic Model of Epilepsy

Lazarini-Lopes

Silva-Júnior

Servilha-Menezes

et al. 2020

Front. Behav. Neurosci.

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The endocannabinoid system (ECS) is related to several physiological processes, associated to the modulation of brain excitability, with impact in the expression of susceptibility and control of epileptic seizures. The cannabinoid receptor type 1 (CB1R) is widely expressed in the brain, especially in forebrain limbic structures. Changes in CB1R expression are associated with epileptic seizures in animal models and humans. The Wistar Audiogenic Rat (WAR) strain is a genetic model of epilepsy capable of mimicking tonic-clonic and limbic seizures in response to intense sound stimulation. The WAR strain presents several behavioral and physiological alterations associated with seizure susceptibility, but the ECS has never been explored in this strain. Therefore, the aim of the present study was to characterize CB1R expression in forebrain limbic structures important to limbic seizure expression in WARs. We used a detailed anatomical analysis to assess the effects of acute and chronic audiogenic seizures on CB1R expression in several layers and regions of hippocampus and amygdala. WARs showed increased CB1R immunostaining in the inner molecular layer of the hippocampus, when compared to control Wistar rats. Acute and chronic audiogenic seizures increased CB1R immunostaining in several regions of the dorsal hippocampus and amygdala of WARs. Also, changes in CB1R expression in the amygdala, but not in the hippocampus, were associated with limbic recruitment and limbic seizure severity in WARs. Our results suggest that endogenous alterations in CB1R immunostaining in WARs could be associated with genetic susceptibility to audiogenic seizures. We also demonstrated CB1R neuroplastic changes associated with acute and chronic seizures in the amygdala and hippocampus. Moreover, the present study brings important information regarding CB1R and seizure susceptibility in a genetic model of seizures and supports the relationship between ECS and epilepsy.

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Section: Discussionmentioning

confidence: 93%

Cannabinoid Receptor Type 1 (CB1R) Expression in Limbic Brain Structures After Acute and Chronic Seizures in a Genetic Model of Epilepsy

Lazarini-Lopes

Silva-Júnior

Servilha-Menezes

et al. 2020

Front. Behav. Neurosci.

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“…In a pentylenetetrazol (PTZ) kindling rat seizure model, suppression of the HMGB1/RAGE/TLR4 inflammatory cascade by administration of pentoxifylline resulted in reduced ROS levels, whilst also improving cognition, memory and hippocampal neuronal survival [ 54 ], suggesting that regulation of neuroinflammatory pathways has a positive downstream effect on OS. However, this concept cannot be expanded to all epilepsies; using a rat model of audiogenic seizures, de Deus and colleagues reported similar levels of IL-6, IL-10, TNF-α and IL-1β between controls and experimental animals, but high correlation between seizure severity and nitrate levels [ 55 ].…”

Section: Role Of Os In Neuroinflammation and Epilepsymentioning

confidence: 99%

The Interconnected Mechanisms of Oxidative Stress and Neuroinflammation in Epilepsy

et al. 2022

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One of the most important characteristics of the brain compared to other organs is its elevated metabolic demand. Consequently, neurons consume high quantities of oxygen, generating significant amounts of reactive oxygen species (ROS) as a by-product. These potentially toxic molecules cause oxidative stress (OS) and are associated with many disorders of the nervous system, where pathological processes such as aberrant protein oxidation can ultimately lead to cellular dysfunction and death. Epilepsy, characterized by a long-term predisposition to epileptic seizures, is one of the most common of the neurological disorders associated with OS. Evidence shows that increased neuronal excitability—the hallmark of epilepsy—is accompanied by neuroinflammation and an excessive production of ROS; together, these factors are likely key features of seizure initiation and propagation. This review discusses the role of OS in epilepsy, its connection to neuroinflammation and the impact on synaptic function. Considering that the pharmacological treatment options for epilepsy are limited by the heterogeneity of these disorders, we also introduce the latest advances in anti-epileptic drugs (AEDs) and how they interact with OS. We conclude that OS is intertwined with numerous physiological and molecular mechanisms in epilepsy, although a causal relationship is yet to be established.

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“…Moreover, it is worth noting that AuK induced a decrease in WAR's spatial memory retention in the Morris water maze test, but the chronic acoustic stimulation (no seizures) had no effect on Wistar's performance in the same memory test. Moreover, neurotransmission in the hippocampal Schaffer-collaterals fibers and their excitability were not affected by the chronic exposure to acoustic stimulation in Wistar rats and AuK-dependent limbic recruitment in WARs is not associated with any inflammatory process or oxidative stress, suggesting that this neuroplastic anatomical change is a "network expansion process, " primarily linked to the genetic selection for the epilepsy phenotype in WARs (de Deus et al, 2020). Therefore, except for the small percentage of Wistar susceptible animals (usually discarded), acoustic stimulation does not induce audiogenic seizures in Wistar rats, as well as epileptic-like alterations or epilepsy-related comorbidities.…”

Section: Discussionmentioning

confidence: 94%

“…De maneira similar, O recrutamento de áreas límbicas e corticais associadas ao desenvolvimento de crises comportamentais clônicas e límbicas são as principais características do KA BERNARDINO et al, 2015). De forma similar, crises límbicas associadas ao recrutamento límbico em WARs também não foram associadas com processos inflamatórios ou com estresse oxidativo (DE DEUS et al, 2020), sugerindo que as alterações neuroplásticas e anatômicas associadas seriam processos de expansão da rede neuronal epileptogênica primariamente relacionados com a seleção genética da linhagem WAR.…”

Section: Discussionunclassified

Efeitos do tratamento com canabidiol (CBD) em modelos genéticos de epilepsias: estudos comportamentais, farmacológicos e eletrofisiológicos

Lopes¹

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Agradeço aos meus pais, Roberto e Cristina, pelo apoio, incentivo e suporte que sempre me deram. Agradeço à Gleice Kelli, minha companheira de vida, pela compreensão, apoio e convivência que tivemos durante todo esse tempo.Agradeço ao professor Dr. Norberto Garcia Cairasco pela oportunidade oferecida ao abrir as portas de seu laboratório, pela excelente mentoria, liberdade criativa e, acima de tudo, pela confiança em meu trabalho. Além de um orientador, tive um amigo ao longo desta trajetória.Agradeço aos meus colegas do Laboratório de Neurofisiologia e Neuroetologia Experimental (LNNE) pelos conhecimentos e ensinamentos compartilhados e pelos momentos alegres e descontraídos que sempre tivemos. Agradeço aos técnicos do LNNE, Flávio e José Antônio, por todo o suporte que me deram e por tudo que me ensinaram. Um agradecimento especial ao José Antônio pelos ensinamentos sobre modelos audiogênicos e análises neuroetológicas.Agradeço aos funcionários do Programa de Pós-Graduação em Neurologia e Neurociências da FMRP-USP, em especial à secretária Luci, pelo auxílio prestado durante meu Doutorado. Este agradecimento também se estende ao Departamento de Fisiologia da FMRP-USP.

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Inflammatory markers in the hippocampus after audiogenic kindling

Cited by 7 publications

References 31 publications

Cannabinoid Receptor Type 1 (CB1R) Expression in Limbic Brain Structures After Acute and Chronic Seizures in a Genetic Model of Epilepsy

Cannabinoid Receptor Type 1 (CB1R) Expression in Limbic Brain Structures After Acute and Chronic Seizures in a Genetic Model of Epilepsy

The Interconnected Mechanisms of Oxidative Stress and Neuroinflammation in Epilepsy

Efeitos do tratamento com canabidiol (CBD) em modelos genéticos de epilepsias: estudos comportamentais, farmacológicos e eletrofisiológicos

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