Jove
Visualize
Contáctanos
JoVE
x logofacebook logolinkedin logoyoutube logo
ACERCA DE JoVE
Visión GeneralLiderazgoBlogCentro de Ayuda JoVE
AUTORES
Proceso de PublicaciónConsejo EditorialAlcance y PolíticasRevisión por ParesPreguntas FrecuentesEnviar
BIBLIOTECARIOS
TestimoniosSuscripcionesAccesoRecursosConsejo Asesor de BibliotecasPreguntas Frecuentes
INVESTIGACIÓN
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchivo
EDUCACIÓN
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualCentro de Recursos para ProfesoresSitio de Profesores
Términos y Condiciones de Uso
Política de Privacidad
Políticas

Videos de Conceptos Relacionados

Epilepsy and Seizures: Overview01:24

Epilepsy and Seizures: Overview

243
Epilepsy is a chronic neurological disease marked by recurrent, unpredictable seizures. These seizures are caused by abnormal electrical discharges in the brain, leading to behavior, sensation, or consciousness alterations. They can also cause transient impairment of awareness, interfering with daily activities.
Various factors can trigger epilepsy, including genetic factors, brain damage, metabolic causes, and unknown etiology. Diagnosis of epilepsy involves electroencephalography (EEG), which...
243
Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

Antiepileptic Drugs: GABAergic Pathway Potentiators

525
γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
The key GABA pathway potentiators used in epilepsy management are as follows.
Benzodiazepines are a well-known class of drugs used for...
525
Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

477
Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...
477
Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

244
Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
244
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

406
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
406
Gene Therapy00:59

Gene Therapy

25.7K
Gene therapy is a technique where a gene is inserted into a person’s cells to prevent or treat a serious disease. The added gene may be a healthy version of the gene that is mutated in the patient, or it could be a different gene that inactivates or compensates for the patient’s disease-causing gene. For example, in patients with severe combined immunodeficiency (SCID) due to a mutation in the gene for the enzyme adenosine deaminase, a functioning version of the gene can be...
25.7K

También podría leer

Artículos Relacionados

Artículos vinculados a este trabajo por autores compartidos, revista y gráfico de citas.

Ordenar por
Same author

WONOEP XVII appraisal: The role of the extracellular matrix in epilepsy.

Epilepsia·2026
Same author

Individualized and stereotypical seizure semiology in a porcine model of post-traumatic epilepsy.

bioRxiv : the preprint server for biology·2026
Same author

Ongoing loss of viable neurons for weeks after mild perinatal hypoxia-ischemia.

bioRxiv : the preprint server for biology·2025
Same author

WONOEP appraisal: Targeted therapy development for early onset epilepsies.

Epilepsia·2024
Same author

Neuronal Death: Now You See It, Now You Don't.

The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry·2024
Same author

Brief apnea with hypoventilation reduces seizure duration and shifts seizure location for several hours in a model of severe traumatic brain injury.

Epilepsia·2024

Video Experimental Relacionado

Updated: Aug 21, 2025

Electrophoretic Delivery of γ-aminobutyric Acid GABA into Epileptic Focus Prevents Seizures in Mice
07:01

Electrophoretic Delivery of γ-aminobutyric Acid GABA into Epileptic Focus Prevents Seizures in Mice

Published on: May 16, 2019

9.1K

Terapia génica para la epilepsia

Kevin Staley1

  • 1Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

Science (New York, N.Y.)
|November 15, 2022
PubMed
Resumen
Este resumen es generado por máquina.

La inhibición dirigida de la actividad de las células cerebrales bajo demanda redujo efectivamente las convulsiones en modelos de ratón. Este hallazgo ofrece nuevas estrategias potenciales para controlar trastornos neurológicos como la epilepsia.

Más Videos Relacionados

Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy
09:29

Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy

Published on: August 17, 2021

2.5K
Using a Bipolar Electrode to Create a Temporal Lobe Epilepsy Mouse Model by Electrical Kindling of the Amygdala
09:49

Using a Bipolar Electrode to Create a Temporal Lobe Epilepsy Mouse Model by Electrical Kindling of the Amygdala

Published on: June 29, 2022

2.6K

Videos de Experimentos Relacionados

Last Updated: Aug 21, 2025

Electrophoretic Delivery of γ-aminobutyric Acid GABA into Epileptic Focus Prevents Seizures in Mice
07:01

Electrophoretic Delivery of γ-aminobutyric Acid GABA into Epileptic Focus Prevents Seizures in Mice

Published on: May 16, 2019

9.1K
Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy
09:29

Preparation and Implantation of Electrodes for Electrically Kindling VGAT-Cre Mice to Generate a Model for Temporal Lobe Epilepsy

Published on: August 17, 2021

2.5K
Using a Bipolar Electrode to Create a Temporal Lobe Epilepsy Mouse Model by Electrical Kindling of the Amygdala
09:49

Using a Bipolar Electrode to Create a Temporal Lobe Epilepsy Mouse Model by Electrical Kindling of the Amygdala

Published on: June 29, 2022

2.6K

Área de la Ciencia:

  • La neurociencia
  • Investigación de la epilepsia

Sus antecedentes:

  • La epilepsia es un trastorno neurológico caracterizado por convulsiones recurrentes.
  • Los tratamientos actuales para la epilepsia tienen limitaciones y efectos secundarios.
  • Comprender la generación de convulsiones es crucial para desarrollar nuevas terapias.

Objetivo del estudio:

  • Investigar la eficacia de la inhibición neuronal bajo demanda para reducir la frecuencia de las convulsiones.
  • Para explorar una posible estrategia terapéutica para el control de las convulsiones.

Principales métodos:

  • Utilizó técnicas optogenéticas para el control preciso de la actividad neuronal en ratones.
  • Se indujeron y monitorearon convulsiones espontáneas en un modelo de ratón.
  • Inhibición bajo demanda de poblaciones neuronales específicas.

Principales resultados:

  • La inhibición de la actividad neuronal bajo demanda disminuyó significativamente la aparición de convulsiones espontáneas.
  • La intervención fue bien tolerada en el modelo animal.
  • Se identificaron objetivos neuronales específicos para una supresión eficaz de las convulsiones.

Conclusiones:

  • La inhibición específica de la actividad neuronal es un enfoque viable para reducir la frecuencia de las convulsiones.
  • Este método es prometedor como una futura estrategia terapéutica para la epilepsia.
  • Se necesitan más investigaciones para trasladar estos hallazgos al tratamiento de la epilepsia humana.