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Related Concept Videos

Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is critical for...
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 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 Memory01:18

Long-Term Memory

Long-term memory is a relatively permanent type of memory, capable of storing vast amounts of information over extended periods. Its storage capacity is generally considered unlimited.
Long-term memory can be categorized into two primary types: explicit and implicit memory. Explicit memory, also known as declarative memory, involves the conscious recollection of information that we deliberately try to remember, recall, and articulate. This type of memory encompasses specific facts, events, and...
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...
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.

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Related Experiment Video

Updated: Jun 20, 2026

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
09:39

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Published on: June 26, 2013

Dopamine controls persistence of long-term memory storage.

Janine I Rossato1, Lia R M Bevilaqua, Iván Izquierdo

  • 1Centro de Memória, Instituto do Cérebro, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Brazil.

Science (New York, N.Y.)
|August 22, 2009
PubMed
Summary

Long-term memory persistence relies on specific dopamine D1 receptor activity in the hippocampus. Manipulating this system at critical times after learning can control memory duration.

More Related Videos

Combined In Vivo Anatomical and Functional Tracing of Ventral Tegmental Area Glutamate Terminals in the Hippocampus
09:36

Combined In Vivo Anatomical and Functional Tracing of Ventral Tegmental Area Glutamate Terminals in the Hippocampus

Published on: September 9, 2020

Related Experiment Videos

Last Updated: Jun 20, 2026

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
09:39

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

Published on: June 26, 2013

Combined In Vivo Anatomical and Functional Tracing of Ventral Tegmental Area Glutamate Terminals in the Hippocampus
09:36

Combined In Vivo Anatomical and Functional Tracing of Ventral Tegmental Area Glutamate Terminals in the Hippocampus

Published on: September 9, 2020

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Behavioral Science

Background:

  • Long-term memory (LTM) persistence is a key feature, yet the underlying mechanisms remain unclear.
  • Understanding factors influencing LTM duration is crucial for memory research.

Purpose of the Study:

  • To investigate the role of dopamine D1 receptors in the hippocampus in regulating the persistence of long-term fear memory.
  • To identify critical time windows and molecular pathways involved in LTM consolidation and decay.

Main Methods:

  • Rats were trained on a fear conditioning task.
  • Dopamine D1 receptor antagonist (SCH23390) or agonist (SK38393) was administered into the dorsal hippocampus at different post-training time points.
  • Brain-derived neurotrophic factor (BDNF) levels and ventral tegmental area (VTA) regulation were assessed.

Main Results:

  • Administration of SCH23390 12 hours post-training, but not immediately or 9 hours after, caused rapid decay of fear LTM.
  • SK38393 administration at the critical 12-hour time point converted a transient fear memory into a persistent one.
  • These effects were mediated by BDNF and regulated by the VTA.

Conclusions:

  • The persistence of long-term fear memory is dependent on the activation of VTA/hippocampus dopaminergic connections.
  • Specific manipulation of this dopaminergic system at defined post-learning intervals can modulate LTM duration.