Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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: 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...
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: 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...
Seizures l: Introduction01:20

Seizures l: Introduction

Understanding seizures and epilepsy relies on key definitions that help in recognizing, classifying, and managing these disorders. These definitions provide a framework for recognizing, classifying, and managing seizure disorders.DefinitionsA seizure is a sudden, abnormal burst of electrical activity in the brain that can cause changes in awareness, movement, sensation, or behavior, depending on the area involved. Epilepsy is a chronic condition characterized by recurrent, unprovoked seizures,...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Molecular pathways linking traumatic brain injury to cardiovascular dysfunction: therapeutic potential of physical exercise.

Metabolic brain disease·2026
Same author

Effect of Physical Exercise on Acute Post-traumatic Hyperexcitability: The Role of Thrombin/PAR1 Signaling.

Molecular neurobiology·2026
Same author

Effect of culture medium composition, incubation time, and temperature on the biofilm-forming ability of Aspergillus westerdijkiae.

Food research international (Ottawa, Ont.)·2026
Same author

Adolescent swimming exercise induces systemic adaptations and molecular changes in the rat cerebral cortex.

Physiology & behavior·2025
Same author

Neuroinflammation in long COVID: the role of the Val16Ala polymorphism of SOD2 and cognitive impairment.

Neuroscience·2025
Same author

Recurrent spaced concussions in adolescent rats disrupt cortical dopaminergic markers and induce behavioral hyperactivity and impaired object location memory.

Neuroscience·2025

Related Experiment Video

Updated: May 12, 2026

Behavioral Characterization of Pentylenetetrazole-induced Seizures: Moving Beyond the Racine Scale
07:35

Behavioral Characterization of Pentylenetetrazole-induced Seizures: Moving Beyond the Racine Scale

Published on: July 8, 2025

Pentylenetetrazol-induced seizures are associated with Na⁺,K⁺-ATPase activity decrease and alpha subunit

Bárbara P Marquezan1, Vinícius R Funck, Clarissa V Oliveira

  • 1Federal University of Santa Maria, Pharmacology Graduate Program, Department of Physiology and Pharmacology, Santa Maria 97105-900, Brazil.

Epilepsy Research
|April 23, 2013
PubMed
Summary

Pentylenetetrazol (PTZ)-induced seizures reduced Na(+),K(+)-ATPase activity and increased its Ser943 phosphorylation in mice. This suggests targeting Na(+),K(+)-ATPase may offer new treatments for seizure disorders.

Keywords:
ConvulsionEpilepsyPhosphorylationSodium pump

More Related Videos

Pentylenetetrazole-Induced Kindling Mouse Model
07:06

Pentylenetetrazole-Induced Kindling Mouse Model

Published on: June 12, 2018

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
08:47

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats

Published on: November 8, 2018

Related Experiment Videos

Last Updated: May 12, 2026

Behavioral Characterization of Pentylenetetrazole-induced Seizures: Moving Beyond the Racine Scale
07:35

Behavioral Characterization of Pentylenetetrazole-induced Seizures: Moving Beyond the Racine Scale

Published on: July 8, 2025

Pentylenetetrazole-Induced Kindling Mouse Model
07:06

Pentylenetetrazole-Induced Kindling Mouse Model

Published on: June 12, 2018

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
08:47

Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats

Published on: November 8, 2018

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Na(+),K(+)-ATPase is crucial for maintaining neuronal excitability.
  • Pentylenetetrazol (PTZ) is a known inducer of seizures.
  • Alterations in enzyme activity and phosphorylation can impact neurological function.

Purpose of the Study:

  • To investigate the effect of PTZ-induced seizures on Na(+),K(+)-ATPase activity.
  • To examine the phosphorylation state of the Na(+),K(+)-ATPase α subunit following PTZ administration.
  • To explore the correlation between Na(+),K(+)-ATPase function and seizure susceptibility.

Main Methods:

  • Adult male Swiss mice were administered varying doses of PTZ (30, 45, 60 mg/kg).
  • Na(+),K(+)-ATPase activity and α subunit phosphorylation (Ser943) were measured in the cerebral cortex 15 minutes post-administration.
  • Correlations between enzyme activity, phosphorylation, and seizure latency were analyzed.

Main Results:

  • PTZ-induced seizures significantly decreased Na(+),K(+)-ATPase activity at 60 mg/kg.
  • Increased immunoreactivity of phosphorylated Ser943 at the α subunit was observed post-seizure.
  • A positive correlation was found between Na(+),K(+)-ATPase activity and seizure latency.
  • A negative correlation was detected between Ser943 phosphorylation and seizure latency.

Conclusions:

  • PTZ-induced seizures alter Na(+),K(+)-ATPase activity and phosphorylation.
  • Ser943 phosphorylation of the Na(+),K(+)-ATPase α subunit is linked to seizure susceptibility.
  • Targeting Na(+),K(+)-ATPase, specifically Ser943 phosphorylation, may offer a novel therapeutic strategy for seizure disorders.