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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.
Long-term Depression01:05

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.
Long-term Depression01:03

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...
Higher Mental Functions of Brain: Learning and Memory01:26

Higher Mental Functions of Brain: Learning and Memory

Memory is one of the most vital higher mental functions of the brain. Memory is closely related to learning because it enables us to retain information and experiences from our past to use them in our present life. It also helps us to remember facts, events, and skills, such as riding a bike or swimming. There are two types of memory — declarative memory, which involves memorizing facts or events, and procedural memory, which enables us to remember how to do something like writing or playing an...
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...

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Related Experiment Video

Updated: May 13, 2026

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents
11:29

Investigation of Synaptic Tagging/Capture and Cross-capture using Acute Hippocampal Slices from Rodents

Published on: September 4, 2015

Learning and reconsolidation implicate different synaptic mechanisms.

Yan Li1, Edward G Meloni, William A Carlezon

  • 1Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA 02478, USA.

Proceedings of the National Academy of Sciences of the United States of America
|March 15, 2013
PubMed
Summary
This summary is machine-generated.

Memory reconsolidation involves labile synapses needing postsynaptic mammalian target of rapamycin (mTOR) signaling for restabilization. This contrasts with initial fear memory, which relies on presynaptic potentiation, revealing distinct plasticity rules.

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A Prediction Error-driven Retrieval Procedure for Destabilizing and Rewriting Maladaptive Reward Memories in Hazardous Drinkers
08:05

A Prediction Error-driven Retrieval Procedure for Destabilizing and Rewriting Maladaptive Reward Memories in Hazardous Drinkers

Published on: January 5, 2018

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Memory Research

Background:

  • The precise synaptic mechanisms governing memory reconsolidation following retrieval remain poorly understood.
  • Synaptic potentiation, crucial for fear memory, is known to occur in the lateral nucleus of the amygdala.
  • Understanding these mechanisms is vital for potential therapeutic interventions targeting memory disorders.

Purpose of the Study:

  • To elucidate the synaptic processes involved in the reconsolidation of auditory fear memories.
  • To investigate the role of postsynaptic signaling, specifically mammalian target of rapamycin (mTOR) kinase, in memory restabilization.
  • To compare the plasticity rules governing initial memory acquisition versus memory reconsolidation.

Main Methods:

  • Electrophysiological recordings in brain slices from rats subjected to auditory fear conditioning.
  • Utilized rapamycin to inhibit mammalian target of rapamycin (mTOR) kinase activity and assess its effect on synaptic potentiation.
  • Differentiated between pre- and postsynaptic contributions to synaptic efficacy changes during memory reactivation.

Main Results:

  • Fear conditioning potentiates synapses in the lateral nucleus of the amygdala, primarily through presynaptic mechanisms.
  • Following memory retrieval, these potentiated synapses enter a labile state requiring postsynaptic mammalian target of rapamycin (mTOR)-dependent signaling for restabilization.
  • Rapamycin treatment blocked reconsolidation by affecting postsynaptic, not presynaptic, mechanisms, reducing synaptic efficacy.

Conclusions:

  • Memory reconsolidation involves a distinct postsynaptic mechanism dependent on mammalian target of rapamycin (mTOR) signaling, differing from initial fear memory acquisition.
  • These findings highlight that separate plasticity rules govern the initial formation of fear memories and their subsequent stabilization after reactivation.
  • The study reveals a critical role for postsynaptic mTOR signaling in the labile phase of memory reconsolidation.