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Pain Inhibits GRPR Neurons via GABAergic Signaling in the Spinal Cord
Rita Bardoni1, Kai-Feng Shen2,3,4, Hui Li2,5
1Departments of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, 41125, Italy. rita.bardoni@unimore.it.
Scientific Reports
|November 3, 2019
Summary
Noxious or cooling stimuli inhibit itch by suppressing spinal gastrin releasing peptide receptor (GRPR) neurons. This research reveals a key neural circuit where pain suppresses itch transmission through GABAergic signaling.
Area of Science:
- Neuroscience
- Molecular Biology
- Sensory Physiology
Background:
- Itch sensation is modulated by algogens and cooling, but mechanisms are unclear.
- Spinal circuits involved in itch and pain processing require further elucidation.
Purpose of the Study:
- To investigate the role of gastrin releasing peptide receptor (GRPR) expressing spinal neurons in itch modulation.
- To elucidate the neural pathways and molecular mechanisms by which pain and cooling inhibit itch.
Main Methods:
- Electrophysiological recordings in spinal cord slices.
- Neuronal tracing and immunofluorescence.
- Pharmacological manipulation of neuronal activity.
Main Results:
- GRPR neurons are excitatory interneurons receiving input from C and Aδ fibers.
- Noxious or cooling stimuli inhibit GRPR neuron activity via GABAergic signaling.
- Capsaicin enhances synaptic transmission onto GRPR neurons, suggesting complex modulation.
Conclusions:
- GRPR neurons are crucial for itch transmission.
- Pain inhibits itch through suppression of GRPR neuron activity via GABAergic signaling.
- This study reveals a spinal mechanism for pain-induced itch suppression.
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