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Menthol-induced Ca2+ release from presynaptic Ca2+ stores potentiates sensory synaptic transmission
Kenzo Tsuzuki1, Hong Xing, Jennifer Ling
1Department of Oral and Maxillofacial Surgery, McKnight Brain Institute and College of Dentistry, University of Florida, Gainesville, Florida, 32610, USA.
Summary
Menthol enhances sensory synaptic transmission by triggering calcium release from intracellular stores in sensory neurons. This action, mediated by the TRPM8 receptor, facilitates glutamate release and modulates neuronal signaling.
Area of Science:
- Neuroscience
- Molecular Biology
- Sensory Physiology
Background:
- Menthol elicits significant sensory and mental effects.
- The menthol receptor, transient receptor potential channel M8 (TRPM8), has been identified.
- Sensory synaptic transmission is crucial for processing sensory information.
Purpose of the Study:
- To investigate the effects of menthol on sensory synaptic transmission.
- To elucidate the underlying mechanisms of menthol's action at sensory synapses.
- To explore the role of TRPM8 in modulating neuronal signaling.
Main Methods:
- Utilized a dorsal root ganglion (DRG) and dorsal horn (DH) coculture system.
- Performed electrophysiological recordings, including miniature and evoked excitatory postsynaptic currents (mEPSCs and eEPSCs).
- Conducted intracellular calcium (Ca2+) imaging studies on DRG neurons.
Main Results:
- Menthol increased the frequency of mEPSCs, indicating enhanced neurotransmitter release.
- Menthol directly induced Ca2+ release from intracellular stores in DRG neurons.
- Menthol potentiated eEPSCs and altered paired-pulse ratios, suggesting presynaptic modulation.
Conclusions:
- Menthol acts presynaptically on sensory neurons to release intracellular Ca2+ via TRPM8.
- This Ca2+ release facilitates glutamate release, modulating synaptic transmission.
- Novel localization of TRPM8 on presynaptic Ca2+ stores is suggested.