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

Long-term Potentiation01:25

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 Potentiation01:35

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.
Neuroplasticity01:01

Neuroplasticity

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.
Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

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 specific...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Chemical Synapses01:26

Chemical Synapses

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...

You might also read

Related Articles

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

Sort by
Same author

Toward a Pluralistic Model for the Schizophrenia Spectrum-Dopamine and Beyond.

JAMA psychiatry·2026
Same author

Parvalbumin and anxiety across development in female offspring of the MAM neurodevelopmental model of schizophrenia.

Journal of psychiatric research·2026
Same author

Antipsychotic drug action, novel treatment targets, and the failure of current clinical trial designs in evaluating new target molecules.

Biological psychiatry·2026
Same author

Endothelial KLF4 depletion drives age-related neurovascular dysfunction and neuropsychiatric impairment.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Astrocytic D1 Dopamine-Signaling Regulates Synaptic Remodeling and Cocaine Seeking.

bioRxiv : the preprint server for biology·2026
Same author

Prefrontal Cortex Dysfunction as a Precipitating Factor for Schizophrenia and Depression.

Journal of neurochemistry·2026

Related Experiment Video

Updated: May 12, 2026

Dopamine Release at Individual Presynaptic Terminals Visualized with FFNs
09:37

Dopamine Release at Individual Presynaptic Terminals Visualized with FFNs

Published on: August 31, 2009

Dopamine triggers heterosynaptic plasticity.

Masago Ishikawa1, Mami Otaka, Yanhua H Huang

  • 1Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|April 19, 2013
PubMed
Summary
This summary is machine-generated.

Dopamine release from the brain’s ventral tegmental area triggers synaptic plasticity in the nucleus accumbens core. This dopamine-mediated plasticity is disrupted by cocaine withdrawal, impacting emotional regulation.

More Related Videos

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

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

Presynaptic Dopamine Dynamics in Striatal Brain Slices with Fast-scan Cyclic Voltammetry
08:49

Presynaptic Dopamine Dynamics in Striatal Brain Slices with Fast-scan Cyclic Voltammetry

Published on: January 12, 2012

Related Experiment Videos

Last Updated: May 12, 2026

Dopamine Release at Individual Presynaptic Terminals Visualized with FFNs
09:37

Dopamine Release at Individual Presynaptic Terminals Visualized with FFNs

Published on: August 31, 2009

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

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

Presynaptic Dopamine Dynamics in Striatal Brain Slices with Fast-scan Cyclic Voltammetry
08:49

Presynaptic Dopamine Dynamics in Striatal Brain Slices with Fast-scan Cyclic Voltammetry

Published on: January 12, 2012

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Dopamine Signaling

Background:

  • Dopamine is traditionally viewed as a neuromodulator, influencing but not initiating synaptic plasticity.
  • The ventral tegmental area (VTA) to nucleus accumbens core (NAcCo) pathway is crucial for motivation and emotion.

Purpose of the Study:

  • To investigate the role of action-potential-activated dopamine release in synaptic plasticity.
  • To determine if dopamine triggers or modulates long-term depression (LTD) at GABAergic synapses.
  • To examine the effect of cocaine withdrawal on dopamine-mediated LTD.

Main Methods:

  • Electrophysiological recordings in VTA-NAcCo pathways.
  • Investigating heterosynaptic plasticity.
  • Assessing the impact of cocaine withdrawal on synaptic function.

Main Results:

  • Action-potential-dependent dopamine release heterosynaptically triggers LTD at GABAergic synapses in the NAcCo.
  • This LTD is mediated by presynaptic dopamine D1 receptors and inhibits GABA release.
  • Dopamine-mediated LTD is abolished following withdrawal from cocaine exposure.
  • This contrasts with plasticity induced by volume or pharmacological dopamine release.

Conclusions:

  • Dopamine release can actively trigger synaptic plasticity, specifically LTD, challenging previous assumptions.
  • Disruption of this dopamine-mediated LTD during cocaine withdrawal may underlie rigid emotional states in addiction.
  • This mechanism allows for flexible neuronal output, essential for adaptive behavior.