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Related Concept Videos

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

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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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Long-term Potentiation

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Related Experiment Video

Updated: Jun 17, 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

Senescent synapses and hippocampal circuit dynamics.

Sara N Burke1, Carol A Barnes

  • 1Evelyn F. McKnight Brain Institute, University of Arizona, Tucson, AZ 85724, USA.

Trends in Neurosciences
|January 15, 2010
PubMed
Summary
This summary is machine-generated.

Aging impairs excitatory synaptic transmission in the hippocampus, affecting plasticity and potentially contributing to cognitive decline. Changes in calcium (Ca2+) homeostasis may underlie these age-related synaptic alterations.

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Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
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Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice
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Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice

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Related Experiment Videos

Last Updated: Jun 17, 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

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

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Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice
08:58

Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice

Published on: July 2, 2020

Area of Science:

  • Neuroscience
  • Aging Research
  • Synaptic Plasticity

Background:

  • Excitatory synaptic transmission is crucial for hippocampal function.
  • Aging is associated with cognitive decline, partly due to hippocampal alterations.
  • Synaptic plasticity in the hippocampus is vital for learning and memory.

Purpose of the Study:

  • To review age-associated changes in hippocampal synaptic function.
  • To explore the contribution of these changes to cognitive decline.
  • To discuss whether altered hippocampal circuits are detrimental or compensatory.

Main Methods:

  • Review of existing literature on aging, synaptic transmission, and hippocampal plasticity.
  • Analysis of studies investigating changes in hippocampal subregions (granule, CA3, CA1 cells).
  • Examination of the role of calcium (Ca2+) homeostasis in age-related synaptic modifications.

Main Results:

  • Aging alters excitatory synaptic transmission in hippocampal granule and pyramidal cells (CA3, CA1).
  • Functional changes contribute to impaired synaptic plasticity in aged hippocampi.
  • Deficits in plasticity are observed in both artificially and behaviorally induced forms, potentially linked to Ca2+ homeostasis changes.

Conclusions:

  • Age-related synaptic alterations in the hippocampus contribute to cognitive impairments.
  • The role of altered intracellular Ca2+ levels in aging is complex, with both detrimental and potentially beneficial effects.
  • Understanding these changes is key to differentiating detrimental effects from compensatory processes in the aging brain.