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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 Depression01:03

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.
Neuroplasticity01:01

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

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Related Experiment Video

Updated: Jul 7, 2026

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording
14:27

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

Published on: August 11, 2019

Target-cell-specific bidirectional synaptic plasticity at hippocampal output synapses.

Pawel Fidzinski1, Oded Shor, Joachim Behr

  • 1Department of Psychiatry and Psychotherapy, Charité Universitätsmedizin Berlin, Chariteplatz 1, 10117 Berlin, Germany. pawel.fidzinski@charite.de

The European Journal of Neuroscience
|March 4, 2008
PubMed
Summary
This summary is machine-generated.

Hippocampal-subiculum synapses exhibit distinct plasticity based on cell type. Burst-spiking cells show NMDAR-dependent long-term depression (LTD), while regular-spiking cells display mGluR-dependent long-term potentiation (LTP).

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Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System
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Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

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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

Related Experiment Videos

Last Updated: Jul 7, 2026

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording
14:27

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

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Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System
09:51

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

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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

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Memory Formation

Background:

  • The hippocampus is crucial for explicit memory.
  • The subiculum relays hippocampal information.
  • Subicular pyramidal cells have distinct firing properties (burst-spiking vs. regular-spiking).

Purpose of the Study:

  • To investigate low-frequency-induced synaptic plasticity in rat subicular burst-spiking and regular-spiking cells.
  • To determine the molecular mechanisms underlying synaptic plasticity in these cell types.
  • To explore how cell-specific plasticity influences hippocampal output.

Main Methods:

  • Electrophysiological recordings in rat subiculum.
  • Low-frequency stimulation (0.5-5 Hz) protocols.
  • Pharmacological manipulation targeting N-methyl-D-aspartate receptors (NMDAR) and metabotropic glutamate receptors (mGluR).
  • Postsynaptic calcium signaling (Ca2+) inhibition using BAPTA.

Main Results:

  • Burst-spiking cells: Low-frequency stimulation induces frequency-dependent LTD (max at 1 Hz), dependent on NMDAR and masking mGluR-dependent LTP.
  • Regular-spiking cells: Low-frequency stimulation induces mGluR-dependent LTP, masking NMDAR-dependent LTD.
  • Both plasticity forms depend on postsynaptic Ca2+ signaling.
  • LTP and LTD coexist at CA1-subiculum synapses, with the dominant form depending on the postsynaptic cell type.

Conclusions:

  • Synaptic plasticity at CA1-subiculum synapses is cell-type specific.
  • A novel sliding-threshold model is proposed, driven by relative NMDAR and mGluR activation.
  • Discharge properties of postsynaptic cells dictate synaptic plasticity direction, enabling target-specific information processing.