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Vagus Nerve Stimulation as a Tool to Induce Plasticity in Pathways Relevant for Extinction Learning
Published on: August 21, 2015
Reduced synaptic activity precedes synaptic stripping in vagal motoneurons after axotomy
Jun Yamada1, Yoshinori Hayashi, Shozo Jinno
1Laboratory of Oral Aging Science, Faculty of Dental Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Abstract:
Activated microglia, which spread on the motor neurons following nerve injury, engage in the displacement of detached afferent synaptic boutons from the surface of regenerating motor neurons. This phenomenon is known as "synaptic stripping." The present study attempted to examine whether changes in the synaptic inputs after motor nerve injury correlated with the microglial attachment to the dorsal motor neurons of the vagus (DMV). DMV neurons in Wistar rats could survive after nerve injury, whereas most of injured DMV neurons in the C57BL/6 mice died. At 2 days after nerve injury, a significant decrease was observed in the frequencies of both spontaneous and miniature EPSCs and IPSCs recorded from DMV neurons in the slice preparation but not from the mechanically dissociated neurons in the Wistar rats. At this stage, no direct apposition of microglia on the injured neurons was observed. High-K(+) stimulation restored their frequencies to control levels. Furthermore, PPADS and DPCPX, antagonists of P2 and adenosine receptors, respectively, also stimulated the recovery of their frequencies. In contrast, no significant change was detected in the spontaneous EPSCs frequency recorded from the severely injured DMV neurons in the slice preparation of the C57BL/6 mice. These observations strongly suggest that presynaptic inhibition through glia-derived ATP and adenosine, thus precedes synaptic stripping in regenerating DMV neurons following nerve injury.
Insights
Following nerve injury, presynaptic inhibition via glia-derived ATP and adenosine precedes synaptic stripping in regenerating vagal motor neurons. This mechanism aids neuron survival in Wistar rats but not in C57BL/6 mice.
Area of Science:
- Neuroscience
- Cell Biology
- Neuroinflammation
Background:
- Nerve injury triggers microglial activation and synaptic stripping.
- The dorsal motor nucleus of the vagus (DMV) contains motor neurons crucial for various physiological functions.
- Differential survival of DMV neurons after injury has been observed between rat and mouse strains.
Purpose of the Study:
- To investigate the correlation between synaptic input changes and microglial attachment to DMV neurons post-nerve injury.
- To elucidate the role of glial-derived mediators in presynaptic function and neuronal survival after vagal nerve injury.
Main Methods:
- Electrophysiological recordings (spontaneous and miniature EPSCs/IPCs) from DMV neurons in Wistar rats and C57BL/6 mice.
- Slice preparation and mechanically dissociated neuron techniques were employed.
- Pharmacological manipulation using high-K+ stimulation and antagonists for P2 and adenosine receptors.
Main Results:
- Wistar rat DMV neurons showed decreased EPSC/IPSC frequencies in slice preparations post-injury, which were restored by high-K+ or receptor antagonists.
- Mechanically dissociated Wistar rat DMV neurons did not exhibit these frequency changes.
- C57BL/6 mice showed no significant changes in spontaneous EPSC frequency in injured DMV neurons.
- Microglial apposition was not observed at the early stage of injury.
Conclusions:
- Presynaptic inhibition mediated by glia-derived ATP and adenosine precedes synaptic stripping in regenerating DMV neurons.
- This presynaptic inhibition mechanism appears to contribute to the survival of DMV neurons in Wistar rats.
- The findings highlight distinct responses to nerve injury between different rodent strains, possibly due to differential glial involvement.
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