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Related Concept Videos

Long-term Depression01:03

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.
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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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Overview of Synapses01:25

Overview of Synapses

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A synapse is a specialized structure where two neurons connect, allowing them to pass an electrical or chemical signal to another neuron. It is the point of communication between neurons. The term "synapse" is derived from the Greek word "synapsis," which means "conjunction." The entire process of neural communication revolves around the synapse. When activated, a neuron releases chemicals known as neurotransmitters into the synapse. These neurotransmitters cross the synapse and bind to...
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Chemical Synapses01:26

Chemical Synapses

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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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Chemical Synapses01:26

Chemical Synapses

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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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Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
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Related Experiment Video

Updated: Mar 25, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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Physiological and Pathophysiological Implications of Synaptic Tau.

Philip Regan1, Daniel J Whitcomb1,2, Kwangwook Cho1,2

  • 11 Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (HW-LINE), Bristol, UK.

The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry
|February 25, 2016
PubMed
Summary

Synaptic tau plays a critical role in regulating synapse function, particularly long-term depression. Understanding this novel tau function is key to developing new therapies for tauopathies and related neurodegenerative diseases.

Keywords:
Alzheimer’s diseaseGSK-3βdementiaglutamate receptorslong-term depressionneurodegenerationphosphorylationsynapsesynaptic plasticitytautauopathy

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Neurodegenerative Diseases

Background:

  • Tauopathies are neurodegenerative diseases characterized by neuronal death and cognitive decline.
  • Current understanding of tau's role in dementia pathogenesis is limited, hindering therapeutic development.
  • There is a need to explore tau's physiological functions to understand its pathological contributions.

Purpose of the Study:

  • To review recent evidence on the novel function of tau localized at the synapse.
  • To elucidate the critical role of synaptic tau in regulating synapse physiology.
  • To explore how tau regulation of synapses informs tauopathy and comorbid disease understanding.

Main Methods:

  • Review of recent scientific literature on tau protein localization and function.
  • Analysis of evidence supporting a role for synaptic tau in synaptic plasticity.
  • Discussion of tau phosphorylation pathways, including GSK-3β activation.

Main Results:

  • Multiple lines of evidence indicate tau is present and functional at the synapse.
  • Synaptic tau is critical for the regulation of synapse physiology, including long-term depression (LTD).
  • Tau phosphorylation, regulated by GSK-3β, is integral to its synaptic signaling role.

Conclusions:

  • Synaptic tau has a previously uncharacterized role in regulating synaptic function.
  • Understanding synaptic tau physiology and its regulation is crucial for advancing tauopathy research.
  • This knowledge provides a foundation for designing novel therapeutics for tauopathies.