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Long-term Depression

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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Long-term Depression

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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.

Long-term Potentiation

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 Potentiation

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.

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...

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Related Experiment Video

Updated: Jul 18, 2026

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

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

Published on: March 23, 2011

Ageing, hippocampal synaptic activity and magnesium.

¹Neurobiologie de la Croissance et de la Sénescence, UMR 549 INSERM, Faculté de Médecine, Université Paris-Descartes, IFR Broca-Sainte Anne, 2 ter rue d'Alésia, 75014 Paris, France. billard@broca.inserm.fr

Magnesium Research

|December 19, 2006

Summary

Ageing impairs memory by altering hippocampal function, with magnesium playing a key role in synaptic transmission and neuronal excitability deficits observed in the elderly.

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Last Updated: Jul 18, 2026

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

Minimizing Hypoxia in Hippocampal Slices from Adult and Aging Mice

Published on: July 2, 2020

Area of Science:

Neuroscience
Aging Research
Cognitive Science

Background:

Ageing is linked to cognitive decline, particularly memory loss, with the hippocampus being a key affected area.
Hippocampal neuronal networks show altered excitability and decreased synaptic transmission with age.
While calcium's role is studied, magnesium's impact on brain ageing and memory is less understood.

Purpose of the Study:

To investigate the role of magnesium in age-associated cognitive impairments, specifically in hippocampal function.
To explore how magnesium influences neuronal excitability, synaptic transmission, and plasticity in the ageing brain.

Main Methods:

Review of existing clinical reports and experimental data on ageing and hippocampal function.
Analysis of the known functions of magnesium in synaptic transmission and neuronal plasticity.
Examination of studies investigating magnesium's role in age-related changes in the hippocampus.

Main Results:

Ageing alters hippocampal neuronal excitability and synaptic transmission, affecting both glutamatergic and cholinergic pathways.
Magnesium is crucial for regulating neurotransmitter release and N-methyl-D-aspartate receptor activity.
Emerging data suggest magnesium deficits contribute to age-related impairments in transmitter release, neuronal excitability, and synaptic plasticity.

Conclusions:

Magnesium dysregulation is a likely contributor to age-related cognitive decline and memory deficits.
Further research is needed to fully understand magnesium's role in hippocampal function during ageing.
Targeting magnesium levels may offer new strategies to mitigate age-related memory loss.