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Updated: Jul 9, 2026
11:02
Presynaptically Silent Synapses Studied with Light Microscopy
Published on: January 4, 2010
Inactivity produces increases in neurotransmitter release and synapse size
V N Murthy1, T Schikorski, C F Stevens
1Department of Molecular and Cellular Biology, Harvard University, 16 Divinity Avenue, Cambridge, MA 02138, USA.
Neuron
|November 24, 2001
Summary
Pharmacologically silencing hippocampal synapses for days increases their strength and size. This involves larger synaptic components and an increased readily releasable pool (RRP) of vesicles, enhancing neurotransmission.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Cell Biology
Background:
- Synaptic strength is crucial for learning and memory.
- Understanding structural and functional changes in synapses is key to deciphering neural circuit function.
Purpose of the Study:
- To investigate the structural and functional adaptations of hippocampal synapses when subjected to prolonged pharmacological silencing.
- To determine the relationship between synaptic size, vesicle dynamics, and neurotransmitter release.
Main Methods:
- Hippocampal neurons in culture were pharmacologically silenced for several days.
- Synaptic strength was measured physiologically.
- Synapse size and vesicle number were analyzed using electron microscopy.
- The readily releasable pool (RRP) and release probability were quantified.
Main Results:
- Prolonged silencing led to a significant increase in synaptic strength.
- Synapse size, including the active zone, postsynaptic density, and bouton, increased.
- The number of docked vesicles and total vesicles per synapse increased, while docked vesicles per active zone area remained constant.
- The readily releasable pool (RRP) size and release probability were elevated.
Conclusions:
- Pharmacological silencing induces structural hypertrophy of hippocampal synapses.
- Increased synapse size correlates with an expanded readily releasable pool and enhanced release probability.
- These findings suggest a compensatory mechanism for maintaining synaptic function during prolonged inactivity.
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