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Related Concept Videos

Synaptic Signaling01:09

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
Synaptic Signaling01:12

Synaptic Signaling

Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Integration of Synaptic Events01:28

Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
Action Potential01:14

Action Potential

Neurons communicate by firing action potentials—the electrochemical signal that is propagated along the axon. The signal results in the release of neurotransmitters at axon terminals, thereby transmitting information to the nervous system. An action potential is a specific "all-or-none" change in membrane potential that results in a rapid spike in voltage.
Membrane potential in neurons
Neurons typically have a resting membrane potential of about -70 millivolts (mV). When they receive...
Electrical Synapses01:28

Electrical Synapses

Electrical synapses found in all nervous systems play important and unique roles. In these synapses, the presynaptic and postsynaptic membranes are very close together (3.5 nm) and are actually physically connected by channel proteins forming gap junctions.
Gap junctions allow the current to pass directly from one cell to the next. In contrast, in the chemical synapse, the neurotransmitters carry the information through the synaptic cleft from one neuron to the next. They consist of two...

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Related Experiment Video

Updated: May 8, 2026

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology
10:52

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Published on: April 23, 2019

ADAM10 in synaptic physiology and pathology.

Stefano Musardo1, Elena Marcello, Fabrizio Gardoni

  • 1Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.

Neuro-Degenerative Diseases
|September 7, 2013
PubMed
Summary

Activity-dependent plasticity regulates synaptic levels of ADAM10 (a disintegrin and metalloproteinase 10), an enzyme involved in Alzheimer's disease pathogenesis. Long-term potentiation reduces ADAM10 at synapses, while long-term depression increases it.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Amyloid-beta (Aβ) peptide generation initiates the cascade leading to Alzheimer's disease.
  • Amyloid precursor protein (APP) processing by β- and γ-secretases produces Aβ, while α-secretase cleavage prevents deposition.
  • A disintegrin and metalloproteinase 10 (ADAM10) functions as the primary α-secretase in neurons.

Purpose of the Study:

  • Investigate mechanisms controlling synaptic abundance of ADAM10.
  • Understand how synaptic localization of ADAM10 impacts its shedding activity.

Main Methods:

  • Studied the effects of long-term potentiation and long-term depression (LTD) on ADAM10.
  • Examined the role of clathrin adaptor protein 2 (AP2) complex in ADAM10 endocytosis.
  • Investigated the interaction between ADAM10 and synapse-associated protein 97 (SAP97) during LTD.

Main Results:

  • Long-term potentiation decreases synaptic ADAM10 levels and activity via AP2-mediated endocytosis.
  • Long-term depression (LTD) increases synaptic ADAM10 membrane insertion and activity.
  • ADAM10 interaction with SAP97 is crucial for LTD-induced trafficking, maintenance, and spine morphology changes.

Conclusions:

  • Novel mechanism for regulating ADAM10 activity at synapses involves interactions with SAP97 and AP2.
  • Synaptically regulated ADAM10 activity modulates synaptic functioning.
  • Findings offer insights into Alzheimer's disease pathogenesis and potential therapeutic targets.