Classification of Current Experimental Models of Epilepsy.

Introduction: This article provides an overview of several experimental models, including in vivo, genetics, chemical, knock-in, knock-out, electrical, in vitro, and optogenetics models, that have been employed to investigate epileptogenesis. The present review introduces a novel categorization of these models, taking into account the fact that the most recent classification that gained widespread acceptance was established by Fisher in 1989. A significant number of such models have become virtually outdated.

Unraveling the ozone impact and oxidative stress on the nervous system.

Ozone (O₃), a potent oxidant, can penetrate the body through breathing, generating reactive oxygen species (ROS) and triggering inflammatory processes. Oxidative stress, an imbalance between the production of ROS and the body's antioxidant capacity, plays a crucial role in the pathophysiology of various neurodegenerative diseases. This phenomenon can negatively impact the Central Nervous System (CNS), inducing structural and functional alterations that contribute to the development of neurological pathologies.

Tilianin obtained from Agastache mexicana inhibits monoamine oxidase and modifies depressive behavior in rats.

Background: Agastache mexicana is used in traditional medicine to treat anxiety, insomnia, pain, among others. In a previous study, the methanolic extract exerted anxiolytic and sedative effects, as observed behaviorally, associated with one of its major components, tilianin.

Objective: To assess the effect produced by the extracts and tilianin obtained from Agastache mexicana on depressive-induced behavior model and on the activity of monoamine oxidases (MAOs).

Exposure to Ozone Downregulates Bcl-2 and Increases Executing Caspases-3 and -8 in the Hippocampus, Frontal Cortex, and Cerebellum of Rats.

Introduction Ozone (O3) is one of the most prevalent atmospheric pollutants, arising from a photochemical reaction between volatile organic compounds (VOC), nitrogen oxides (NOx), and sunlight. O3 triggers oxidative stress, resulting in lipid oxidation, inflammation, alterations in metabolic and cellular signaling, and potentially initiating cell death in vulnerable brain regions. Inflammation and oxidative stress are recognized for their ability to induce cell death, primarily through the apoptosis pathway, involving various proteins that participate in this process via two pathways: intrinsic and extrinsic.

Rats in Epilepsy Research: A Bibliometric Analysis of Citations Between 1969 and 2020 on Experimental Models in Epilepsy.

Epilepsy stands as a prominent neurological disorder, affecting a substantial number of individuals who, unfortunately, do not respond to conventional antiepileptic medications. To unravel the intricate mechanisms underlying epileptic seizures and explore potential therapeutic avenues, researchers have turned to animal models. Among these models, rats have emerged as one of the cornerstones of epilepsy research.

The Role of the Vagus Nerve in the Microbiome and Digestive System in Relation to Epilepsy.

The Enteric Nervous System (ENS) is described as a division of the Peripheral Nervous System (PNS), located within the gut wall and it is formed by two main plexuses: the myenteric plexus (Auerbach's) and the submucosal plexus (Meissner's). The contribution of the ENS to the pathophysiology of various neurological diseases such as Parkinson's or Alzheimer's disease has been described in the literature, while some other studies have found a connection between epilepsy and the gastrointestinal tract. The above could be explained by cholinergic neurons and neurotransmission systems in the myenteric and submucosal plexuses, regulating the vagal excitability effect.

Repurposing Simvastatin in Parkinson's Disease Model: Protection Is throughout Modulation of the Neuro-Inflammatory Response in the .

Parkinson's disease is a neurodegenerative disorder characterized by oxidative stress and immune activation in the nigro-striatal pathway. Simvastatin regulates cholesterol metabolism and protects from atherosclerosis disease. Simvastatin-tween 80 was administered 7 days before sterotaxic intrastriatal administration of MPP (1-methyl-4-phenylpyridine) in rats.

The Participation of Ca Channels in Epilepsy: A Bibliometric Analysis of the Scientific Literature in Latin America.

Background: Bibliometric analysis allows us to quantify and evaluate scientific activity, and it has become increasingly important in all areas of scientific literature. Thanks to these analyses, we can infer where science should put greater efforts into elucidating the underlying mechanisms of diseases that have yet to be fully described or investigated.

Objective: This paper delves into published articles related to the involvement of calcium (Ca) channels in epilepsy, which is a condition with a high prevalence in Latin America.

Molecular and Genetic Mechanisms of Neurotoxicity During Anti-seizure Medications Use.

Epilepsy is a multifactorial pathology that has allowed the development of various drugs aiming to combat it. This effort was formally initiated in the 1940s when phenytoin began to be used. It eventually turned out to be a drug with great anticonvulsant efficacy.

Caloric restriction: Anti-inflammatory and antioxidant mechanisms against epileptic seizures.

Caloric restriction (CR) possesses different cellular mechanisms. Though there are still gaps in the literature regarding its plausible beneficial effects, the suggestion that this alternative therapy can improve the inflammatory and antioxidant response to control epileptic seizures is explored throughout this study. Epilepsy is the second most prevalent neurodegenerative disease in the world.

Clothianidin and Thiacloprid Mixture Administration Induces Degenerative Damage in the Dentate Gyrus and Alteration in Short-Term Memory in Rats.

Neonicotinoids are pesticides that act as agonists of nicotinic receptors for acetylcholine in insects' central nervous system (CNS). Chronic exposure to neonicotinoids in humans is related to autism, memory loss, and finger tremor. In this article, we evaluate the effect of subchronic oral administration of two neonicotinoids in the same mixture: clothianidin and thiacloprid.

The short form of the SUR1 and its functional implications in the damaged brain.

Sulfonylurea receptor (SUR) belongs to the adenosine 5'-triphosphate (ATP)-binding cassette (ABC) transporter family; however, SUR is associated with ion channels and acts as a regulatory subunit determining the opening or closing of the pore. Abcc8 and Abcc9 genes code for the proteins SUR1 and SUR2, respectively. The SUR1 transcript encodes a protein of 1582 amino acids with a mass around 140-177 kDa expressed in the pancreas, brain, heart, and other tissues.

Serotonin and noradrenaline content and release in the dorsal hippocampus during learning and spatial memory in prenatally stressed rats.

Prenatal stress causes learning and spatial memory deficits in adulthood by modifying hippocampal function. The dorsal hippocampus contains serotonergic and noradrenergic neuron terminals, which are related to cognitive processes. It is currently unknown whether prenatal stress modifies serotonin (5-HT) and noradrenaline (NA) content and their release in the hippocampus during cognitive performance.

Decreased serotonin content and release in the ventral hippocampus of prenatally stressed male rats in response to forced swim test.

Prenatal stress modifies the serotonergic system by altering the synthesis, metabolism, receptors and serotonin content in the hippocampus. However, it is currently unknown whether serotonin release in the ventral hippocampus of prenatally stressed rats is altered. In this study, serotonin (5-HT) and its metabolite, 5‑hydroxyindoleacetic acid (5-HIAA) levels were analysed in dialysates (in vivo) and in homogenates (in vitro) of the ventral hippocampus.

Caloric Restriction and Ketogenic Diet Therapy for Epilepsy: A Molecular Approach Involving Pathway and K Channels.

Epilepsy is a neurological disorder in which, in many cases, there is poor pharmacological control of seizures. Nevertheless, it may respond beneficially to alternative treatments such as dietary therapy, like the ketogenic diet or caloric restriction. One of the mechanisms of these diets is to produce a hyperpolarization mediated by the adenosine triphosphate (ATP)-sensitive potassium (K) channels (K channels).

Anticonvulsant mechanisms of the ketogenic diet and caloric restriction.

Many treatments have been proposed to control epileptic seizures, such as the ketogenic diet and caloric restriction. However, seizure control has not yet been improved completely in all patients. Probably, due to the lack of understanding regarding this neurological disorder pathogenesis or pathophysiology, including its molecular approach.

Characterization of the antiapoptotic effect of copper sulfate on striatal and midbrain damage induced by MPP in rats.

1-Methyl-4-phenylpyridinium ion (MPP)-induced neurotoxicity produces cellular damage resembling that encountered in Parkinson's disease. The mechanisms of cellular death after MPP include the participation of oxidative stress in the loss of dopaminergic neurons. Among the mechanisms of defense against oxidative stress, several copper-dependent proteins have been implicated: Cu/Zn-SOD, ceruloplasmin, and metallothionein.

Antiepileptogenic Effect of Retinoic Acid.

Retinoic acid, a metabolite of vitamin A, acts through either genomic or nongenomic actions. The genomic action of retinoids exerts effects on gene transcription through interaction with retinoid receptors such as retinoic acid receptors (RARα, β, and γ) and retinoid X receptors (RXRα, β, and γ) that are primarily concentrated in the amygdala, pre-frontal cortex, and hippocampal areas in the brain. In response to retinoid binding, RAR/RXR heterodimers undergo major conformational changes and orchestrate the transcription of specific gene networks.

Hydroxytyrosol inhibits MAO isoforms and prevents neurotoxicity inducible by MPP+ invivo.

Parkinson's disease is considered to be due to an increase in the catabolism of dopamine by the action of monoamine oxidase (MAO) enzymes which leads to an increase in reactive oxygen species (ROS) and loss of dopaminergic neurons. Here, in a model of neurotoxicity inducible by 1-methyl-4-phenylpyridinium (MPP+), we tested the effect of hydroxytyrosol (HTy), a potent antioxidant, on generation of ROS. Five minutes after a single intravenous administration of 1.

Activation of the Extrinsic and Intrinsic Apoptotic Pathways in Cerebellum of Kindled Rats.

The purpose of this study is to determine the activation of the extrinsic and intrinsic apoptotic pathways in the cerebellum of rats exposed to amygdaloid electrical kindling. Western blot analyses were carried out for caspase-8 and caspase-9, Bid, Bax, and Bcl-2 in the cerebellum and immunohistochemistry of Bid, Bax, cytochrome C, and VDAC (voltage-dependent anion channels) in the cerebellar cortex of Wistar male rats with 0, 15, and 45 kindling stimulations. In the experimental group of 45 stimuli, we observed an increase in protein activation of caspase-9 and truncated Bid and Bax, in addition to a decrease in expression of pro-caspase-8 and the anti-apoptotic protein Bcl-2, determined by Western blot.

Epicatechin Reduces Spatial Memory Deficit Caused by Amyloid-β25⁻35 Toxicity Modifying the Heat Shock Proteins in the CA1 Region in the Hippocampus of Rats.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by dementia and the aggregation of the amyloid beta peptide (Aβ). Aβ is the most neurotoxic sequence, whose mechanism is associated with the neuronal death in the Cornu Ammonis 1 (CA1) region of the hippocampus (Hp) and cognitive damage. Likewise, there are mechanisms of neuronal survival regulated by heat shock proteins (HSPs).

Neurorehabilitation of saccadic ocular movement in a patient with a homonymous hemianopia postgeniculate caused by an arteriovenous malformation: A Case Report.

Rationale: Visual therapy, which includes a restorative and compensatory approach, seems to be a viable treatment option for homonymous defects of the visual field in patients with postgeniculate injury of the visual pathway, due to occipital arteriovenous malformation (AVM). Until now, the Mexican population suffering from homonymous hemianopia did not have health services that provided any type of visual therapy for their condition.

Patient Concerns: A 31-year-old patient, who underwent a surgical procedure for resection of the AVM, was referred with posterior low vision on the left side.

Copper sulfate pretreatment prevents mitochondrial electron transport chain damage and apoptosis against MPP-induced neurotoxicity.

Intrastriatal injection of 1-methyl-4-phenylpyridinium (MPP) is considered a model to reproduce some biochemical alterations observed in Parkinson's disease (PD) patients. Among those alterations, inhibition of mitochondrial complex I activity, increased free radical production and reduced antioxidant responses have been reported. Copper (Cu) plays an important role in the metabolism and antioxidative responses through its participation as a cofactor in the cytochrome c oxidase enzyme (COX), Cu/Zn-superoxide dismutase (Cu/Zn-SOD), and metallothioneins.

Increase Signaling of Wnt/β-Catenin Pathway and Presence of Apoptosis in Cerebellum of Kindled Rats.

Background: Epilepsy is one of the most common neurological disorders in humans, and the role of the cerebellum in its physiopathology remains the subject of study. The Purkinje cells (PC), whose axons target the dentate and interpositus nuclei, form the main cerebellar output to forebrain structures involved in epilepsy. Cerebellar atrophy related to loss of PC has been reported in chronic epilepsy although its mechanism remains unclear.

Decreased Expression of Sox-1 in Cerebellum of Rat with Generalized Seizures Induced by Kindling Model.

The single feature of all malformations in cortical development is the clinical association with epilepsy. It has been proven that Sox-1 expression is essential during neurodevelopment and it is reported that Sox-1 knockout mice present spontaneous generalized seizures. Particularly in cerebellum, Sox-1 plays a key role in the Bergmann´s glia (BG) function, which allows the correct function of the Purkinje cells (PC).