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Related Concept Videos

Epilepsy and Seizures: Overview01:24

Epilepsy and Seizures: Overview

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...
Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

Antiepileptic Drugs: GABAergic Pathway Potentiators

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 their...
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

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...
Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

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...
Antiepileptic Drugs: Calcium Channel Blockers01:17

Antiepileptic Drugs: Calcium Channel Blockers

Calcium channel blockers, a class of antiepileptic drugs, regulate the flow of calcium ions within neurons.
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...
Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

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...

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Related Experiment Video

Updated: May 29, 2026

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

Decreased CREB levels suppress epilepsy.

Xinjian Zhu1, Xiao Han, Julie A Blendy

  • 1The Children's Hospital of Philadelphia, Division of Neurology, USA.

Neurobiology of Disease
|August 27, 2011
PubMed
Summary

Reducing cAMP response element binding protein (CREB) levels significantly decreased seizures in a mouse epilepsy model. This suggests targeting CREB activity may offer a new therapeutic strategy for preventing epilepsy development.

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Behavioral And Physiological Analysis In A Zebrafish Model Of Epilepsy
08:26

Behavioral And Physiological Analysis In A Zebrafish Model Of Epilepsy

Published on: October 19, 2021

Related Experiment Videos

Last Updated: May 29, 2026

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

Behavioral And Physiological Analysis In A Zebrafish Model Of Epilepsy
08:26

Behavioral And Physiological Analysis In A Zebrafish Model Of Epilepsy

Published on: October 19, 2021

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Epilepsy Research

Background:

  • Epilepsy is a common neurological disorder with no preventative treatments.
  • Genes with cAMP response elements (CREs) are implicated in epileptogenesis.
  • Phosphorylated cAMP response element binding protein (CREB) regulates transcription from CREs and is elevated in epilepsy models and human epilepsy.

Purpose of the Study:

  • To investigate the role of CREB in epileptogenesis.
  • To determine if reducing CREB levels impacts seizure severity and development.
  • To explore molecular changes associated with altered CREB activity following a neurological insult.

Main Methods:

  • Utilized CREB(α∆) mutant mice with reduced CREB levels.
  • Induced status epilepticus (SE) using pilocarpine.
  • Assessed seizure frequency and electrical kindling thresholds.
  • Quantified mRNA levels of brain-derived neurotrophic factor (BDNF), inducible cAMP early repressor (ICER), and KCC2 in the hippocampus and cortex.

Main Results:

  • CREB(α∆) mutant mice exhibited a ~50% reduction in spontaneous seizures post-SE and required more stimulation for kindling.
  • Following SE, BDNF and ICER mRNAs were differentially upregulated in CREB(α∆) mutants compared to wild-type mice.
  • No difference in KCC2 mRNA levels was observed between genotypes after SE.
  • Increased cAMP response element modulator (CREM) mRNA transcripts were found in CREB(α∆) mutants, potentially explaining differential BDNF and ICER regulation.

Conclusions:

  • Decreased CREB levels confer significant protection against seizures and epileptogenesis.
  • Differential regulation of BDNF and ICER by CREM may underlie the reduced seizure susceptibility in CREB(α∆) mutants.
  • Modulating CREB activity presents a potential therapeutic avenue for preventing epilepsy following neurological insults.