Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Neuroplasticity01:01

Neuroplasticity

909
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.
909
Chemical Synapses01:26

Chemical Synapses

3.4K
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...
3.4K
Long-term Depression01:03

Long-term Depression

2.7K
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...
2.7K
Long-term Potentiation01:25

Long-term Potentiation

2.9K
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...
2.9K
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

2.9K
Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
2.9K
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

11.2K
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...
11.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Presynaptic quantal size enhancement counteracts post-tetanic release depression.

The Journal of physiology·2024
Same author

Trampolining Accidents in an Adult Emergency Department: Analysis of Trampolining Evolution Regarding Severity and Occurrence of Injuries.

International journal of environmental research and public health·2022
Same author

Antithrombotic Therapy in Spinal Surgery Does Not Impact Patient Safety-A Single Center Cohort Study.

Frontiers in surgery·2022
Same author

Fluid Overload Phenotypes in Critical Illness-A Machine Learning Approach.

Journal of clinical medicine·2022
Same author

The human cognition-enhancing CORD7 mutation increases active zone number and synaptic release.

Brain : a journal of neurology·2022
Same author

Early Reconstitution of Antibody Secreting Cells after Allogeneic Stem Cell Transplantation.

Journal of clinical medicine·2022

Related Experiment Video

Updated: Oct 10, 2025

3D Modeling of Dendritic Spines with Synaptic Plasticity
07:13

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

7.0K

Distinct molecular pathways govern presynaptic homeostatic plasticity.

Anu G Nair1, Paola Muttathukunnel2, Martin Müller2

  • 1Department of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland; Department of Neuroscience, Karolinska Institute, 17177 Stockholm, Sweden.

Cell Reports
|December 15, 2021
PubMed
Summary

Presynaptic homeostatic plasticity (PHP) normally stabilizes synapses. However, this study shows different glutamate receptor inhibitors trigger distinct PHP pathways, revealing diverse homeostatic mechanisms in Drosophila.

Keywords:
Drosophila neuromuscular junctionProtein Kinase Dglutamate receptorshomeostatic plasticityneurotransmitter releasesynaptic transmission

More Related Videos

Presynaptically Silent Synapses Studied with Light Microscopy
11:02

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

11.6K
An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
09:33

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

Published on: June 26, 2018

7.6K

Related Experiment Videos

Last Updated: Oct 10, 2025

3D Modeling of Dendritic Spines with Synaptic Plasticity
07:13

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

7.0K
Presynaptically Silent Synapses Studied with Light Microscopy
11:02

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

11.6K
An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
09:33

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

Published on: June 26, 2018

7.6K

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Biology

Background:

  • Presynaptic homeostatic plasticity (PHP) is a key mechanism that stabilizes synaptic transmission.
  • PHP is generally understood to be triggered by impaired neurotransmitter receptor function and to involve a conserved signaling pathway.
  • Understanding the precise triggers and pathways of PHP is crucial for comprehending neural circuit stability.

Purpose of the Study:

  • To investigate whether different perturbations of glutamate receptors (GluRs) elicit similar or distinct presynaptic homeostatic plasticity (PHP) responses.
  • To elucidate the specific signaling pathways involved in PHP triggered by different GluR inhibitors.
  • To explore the diversity of homeostatic signaling mechanisms at the Drosophila neuromuscular junction.

Main Methods:

  • Utilized the Drosophila neuromuscular junction as a model system.
  • Applied specific glutamate receptor (GluR) antagonists: γ-D-glutamylglycine (γDGG), Philanthotoxin-433 (PhTx), and Gyki-53655 (Gyki).
  • Assessed neurotransmitter release potentiation and analyzed signaling pathways, including Bruchpilot modulation and protein kinase D involvement.

Main Results:

  • Inhibition of GluRs by γDGG did not induce compensatory PHP.
  • PhTx and Gyki induced compensatory PHP, but via separable signaling pathways.
  • PHP induced by Gyki involved presynaptic protein kinase D and distinct molecular players compared to PhTx-induced PHP.

Conclusions:

  • Synapses exhibit differential responses to functionally similar impairments in receptor activity.
  • Homeostatic compensation is achieved through diverse and distinct molecular mechanisms, challenging the notion of a single stereotypic PHP pathway.
  • This highlights significant diversity in synaptic homeostatic signaling.