Enhanced Release of Neurotransmitters in Mice with Chronic Pain
Author Information
Author(s): Toyoda Hiroki, Zhao Ming-Gao, Zhuo Min
Primary Institution: University of Toronto
Hypothesis
The study aims to examine the source of increased excitatory synaptic transmission in the anterior cingulate cortex (ACC) of mice with chronic pain.
Conclusion
Chronic inflammatory pain increases both the probability of neurotransmitter release and the number of available vesicles, while neuropathic pain only increases the probability of neurotransmitter release in ACC synapses.
Supporting Evidence
- The study found that the rate of miniature excitatory postsynaptic currents (mEPSCs) was significantly larger in mice with chronic pain compared to control mice.
- Increased probability of neurotransmitter release was observed in both inflammatory and neuropathic pain models.
- The number of available vesicles was significantly increased in the inflammatory pain model compared to control.
Takeaway
When mice have chronic pain, their brain cells release more chemicals that help send pain signals, which can make the pain feel worse.
Methodology
The study used whole-cell patch-clamp recordings from ACC neurons in mice with chronic pain induced by CFA injection and nerve ligation.
Limitations
The study's findings may not fully represent synaptic behavior due to the use of stimulus intensities that could lead to synaptic failures.
Participant Demographics
Adult male mice aged 6-8 weeks.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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