Related Experiment Video
Updated: Jul 18, 2026
11:02
Presynaptically Silent Synapses Studied with Light Microscopy
Published on: January 4, 2010
Minimizing synaptic depression by control of release probability.
1Neuroscience Training Program, University of Wisconsin, Madison, Wisconsin 53706, USA. breowit@ohsu.edu
Summary
Activation of GABA(B) receptors enhances auditory synapse strength by reducing postsynaptic AMPA receptor desensitization. This modulation is crucial for maintaining synaptic function during high-frequency neural activity.
Area of Science:
- Neuroscience
- Synaptic Transmission
- Auditory System
Background:
- The avian nucleus magnocellularis synapse exhibits high release probability and synaptic depression.
- Presynaptic GABA(B) receptor activation minimizes depression and enhances synaptic strength during high-frequency activity.
Purpose of the Study:
- To investigate the synaptic mechanisms underlying GABA(B) receptor-mediated enhancement of synaptic strength.
- To determine the roles of presynaptic and postsynaptic factors in synaptic depression and modulation.
Main Methods:
- Electrophysiological recordings of excitatory postsynaptic currents (EPSCs).
- Pharmacological manipulation using Cd(2+) and baclofen to alter release probability.
- Application of aniracetam to modulate AMPA receptor desensitization.
- Analysis of EPSC amplitudes during high-frequency stimulation trains.
Main Results:
- Reducing release probability with Cd(2+) or baclofen increased EPSC amplitudes, an effect not explained by transmitter depletion models alone.
- Aniracetam reduced synaptic depression by decreasing AMPA receptor desensitization, but this effect was abolished when release probability was lowered.
- Direct measurements confirmed AMPA receptor desensitization as a significant postsynaptic depression source.
Conclusions:
- Presynaptic GABA(B) receptor modulation regulates AMPA receptor desensitization at the auditory synapse.
- This regulation controls synaptic strength and modulates information flow during high-frequency activity.
Related Concept Videos
01:05Long-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.
01:03Long-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.
Calcium Ion Concentration Mechanism
If over time, all...
Calcium Ion Concentration Mechanism
If over time, all...
01:26Chemical 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...
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...
01:26Neurochemical Transmission: Sites of Drug Action
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...
01:21Drugs Affecting Neurotransmitter Release or Uptake
Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
01:26Chemical 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...
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...