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Related Concept Videos

Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Integration of Synaptic Events01:28

Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses01:26

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Postsynaptic Potential (PSP)01:32

Postsynaptic Potential (PSP)

Postsynaptic potential (PSP) refers to a change in the electrical potential of a neuron when neurotransmitters released by presynaptic neurons bind to postsynaptic receptors. This potential can either be excitatory, leading to depolarization and ultimately action potential generation, or inhibitory, leading to hyperpolarization and suppression of the postsynaptic neuron.
There are two types of receptors: ionotropic and metabotropic.
The ionotropic receptor is the membrane protein that has an...

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Related Experiment Video

Updated: Jul 4, 2026

Preparing Undercut Model of Posttraumatic Epileptogenesis in Rodents
07:58

Preparing Undercut Model of Posttraumatic Epileptogenesis in Rodents

Published on: September 15, 2011

Synaptic strength modulation after cortical trauma: a role in epileptogenesis.

Sinziana Avramescu1, Igor Timofeev

  • 1Centre de Recherche Université Laval Robert-Giffard, Québec, Canada.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|July 4, 2008
PubMed
Summary

Traumatic brain injuries can cause abnormal brain cell activity, leading to seizures. This study reveals that after injury, cortical neurons become more connected and excitable, potentially driving seizure generation.

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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Published on: August 15, 2017

Direct-current Stimulation and Multi-electrode Array Recording of Seizure-like Activity in Mice Brain Slice Preparation
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Direct-current Stimulation and Multi-electrode Array Recording of Seizure-like Activity in Mice Brain Slice Preparation

Published on: June 7, 2016

Related Experiment Videos

Last Updated: Jul 4, 2026

Preparing Undercut Model of Posttraumatic Epileptogenesis in Rodents
07:58

Preparing Undercut Model of Posttraumatic Epileptogenesis in Rodents

Published on: September 15, 2011

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
09:07

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Published on: August 15, 2017

Direct-current Stimulation and Multi-electrode Array Recording of Seizure-like Activity in Mice Brain Slice Preparation
09:39

Direct-current Stimulation and Multi-electrode Array Recording of Seizure-like Activity in Mice Brain Slice Preparation

Published on: June 7, 2016

Area of Science:

  • Neuroscience
  • Neurophysiology
  • Traumatic Brain Injury Research

Background:

  • Traumatic brain injuries (TBIs) often result in abnormal neuronal hyperexcitability, contributing to seizures and epilepsy.
  • While neuronal rewiring after lesions is known, the functional impact on synaptic connectivity due to chronic deafferentation post-cortical trauma remains unclear.

Purpose of the Study:

  • To investigate the functional consequences of anatomical changes after cortical trauma.
  • To understand synaptic connectivity adaptation in response to decreased input from chronic deafferentation.

Main Methods:

  • Simultaneous intracellular (IC) and extracellular (EC) recordings in cat cortex under acute and chronic conditions (2, 4, 6 weeks post-trauma).
  • Induction of cortical trauma via white matter transection beneath the suprasylvian gyrus.
  • Analysis of spike-triggered averages of IC membrane potential using EC spikes.

Main Results:

  • Increased connection probability and synaptic efficacy between cortical neurons were observed weeks after trauma.
  • No significant changes in inhibitory interactions were found in the traumatized cortex.
  • Enhanced neuronal input resistance, intrinsic excitability, and increased silent network periods accompanied the heightened synaptic efficacy.

Conclusions:

  • Electrophysiological data confirm functional consequences of previously documented anatomical changes in injured cortex.
  • Homeostatic synaptic plasticity, compensating for reduced activity in deafferented areas, may lead to uncontrollable cortical hyperexcitability.
  • This hyperexcitability is a proposed mechanism for seizure generation following TBI.