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Updated: Jun 4, 2026

In-Vivo Calcium Imaging of Sensory Neurons in the Rat Trigeminal Ganglion
Published on: February 9, 2024
Peripheral nerve damage does not alter release properties of developing central trigeminal afferents.
1Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Neonatal damage to the infraorbital nerve (ION) disrupts whisker patterns. This study found that changes in presynaptic release probability (Pr) do not cause functional synapses to become silent after ION damage.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Sensory Systems
Background:
- The infraorbital nerve (ION) is crucial for whisker-related neural patterning (barrelettes) in the trigeminal nerve's principal nucleus (PrV).
- Neonatal ION damage abolishes barrelettes and converts functional synapses to silent ones in the PrV.
Purpose of the Study:
- To investigate the presynaptic release probability (Pr) of ION afferent terminals in the PrV.
- To determine if changes in Pr underlie the conversion of functional synapses to silent synapses after neonatal ION damage.
Main Methods:
- Whole-cell recordings with paired-pulse stimulation.
- MK-801 blocking rate experiments to estimate presynaptic release probability (Pr).
- Investigation across postnatal development and following neonatal ION transection.
Main Results:
- Paired-pulse ratios (PPR) were highly variable, indicating diverse release probabilities.
- PPR distribution peaked around 100% and was not developmentally regulated or target-cell specific.
- Neonatal ION transection did not alter the PPR distribution in central terminals.
Conclusions:
- The conversion of functional synapses to silent synapses following peripheral denervation is not caused by alterations in presynaptic release probability (Pr).
- Synaptic silencing in the PrV after ION damage likely involves postsynaptic mechanisms or other presynaptic factors not assessed here.
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