Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Long-term Depression

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...

Long-term Depression

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.

You might also read

Related Articles

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

Sort by

Same author

A dahlia flower extract has antidiabetic properties by improving insulin function in the brain.

Life metabolism·2025

Same author

Calcium-induced calcium release activates spontaneous miniature outward currents in newt medullary reticular formation neurons.

Journal of neurophysiology·2018

Same author

Inhibition of hippocampal excitability by citalopram.

Epilepsia·2012

Same author

The antidepressant drug fluoxetine inhibits persistent sodium currents and seizure-like events.

Epilepsy research·2012

Same author

Low-magnesium medium induces epileptiform activity in mouse olfactory bulb slices.

Journal of neurophysiology·2011

Same author

SAP97 directs NMDA receptor spine targeting and synaptic plasticity.

The Journal of physiology·2011

Search research articles

Related Experiment Video

Updated: Jun 10, 2026

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays

Published on: May 15, 2018

Lithium modulates cortical excitability in vitro.

Charlotte Butler-Munro¹, Emma J Coddington, Cristina H Shirley

¹Department of Physiology, University of Otago, Dunedin, New Zealand.

|July 20, 2010

Summary

Lithium and antiepileptic drugs may treat bipolar disorder by targeting coupled sodium and potassium channels. These channels control neuron excitability, offering a new understanding of mood stabilization.

More Related Videos

Simultaneous Electroencephalography, Real-time Measurement of Lactate Concentration and Optogenetic Manipulation of Neuronal Activity in the Rodent Cerebral Cortex

Simultaneous Electroencephalography, Real-time Measurement of Lactate Concentration and Optogenetic Manipulation of Neuronal Activity in the Rodent Cerebral Cortex

Published on: December 19, 2012

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Published on: March 31, 2016

Related Experiment Videos

Last Updated: Jun 10, 2026

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays

Published on: May 15, 2018

Simultaneous Electroencephalography, Real-time Measurement of Lactate Concentration and Optogenetic Manipulation of Neuronal Activity in the Rodent Cerebral Cortex

Simultaneous Electroencephalography, Real-time Measurement of Lactate Concentration and Optogenetic Manipulation of Neuronal Activity in the Rodent Cerebral Cortex

Published on: December 19, 2012

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Induction of an Isoelectric Brain State to Investigate the Impact of Endogenous Synaptic Activity on Neuronal Excitability In Vivo

Published on: March 31, 2016

Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

Bipolar disorder involves mood swings, potentially linked to abnormal brain neuron excitability and ion channel function.
Effective treatments include antiepileptic drugs and lithium, but their precise neuronal mechanisms remain unclear.
A paradox exists: antiepileptic drugs reduce sodium (Na+) influx, while lithium enters neurons through these channels.

Purpose of the Study:

To investigate the effects of lithium on neuronal excitability in brain slices.
To explore the potential shared mechanism of action between lithium and antiepileptic drugs in regulating neuron function.

Main Methods:

Electrophysiological recordings were performed on mouse olfactory bulb neurons in vitro.
Neurons were treated with varying concentrations of lithium (1-10mM).
Changes in membrane potential, action potential, and synaptic responses were analyzed.

Main Results:

Lithium treatment depolarized mitral cells and blocked action potential hyperpolarization.
Lithium modulated neuronal responses to synaptic input.
These effects suggest lithium alters the excitability of olfactory bulb neurons.

Conclusions:

Lithium's action may involve reducing the activation of potassium (K+) channels by Na+ influx at therapeutic concentrations.
Both lithium and effective antiepileptic drugs might target a shared membrane complex of coupled Na+ and K+ channels.
This shared target could be crucial for controlling brain neuron excitability and stabilizing mood in bipolar disorder.