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Abstract
In humans, gamma-band oscillations in the primary somatosensory cortex (S1) correlate with subjective pain perception. However, functional contributions to pain and the nature of underlying circuits are unclear. Here we report that gamma oscillations, but not other rhythms, are specifically strengthened independently of any motor component in the S1 cortex of mice during nociception. Moreover, mice with inflammatory pain show elevated resting gamma and alpha activity and increased gamma power in response to sub-threshold stimuli, in association with behavioral nociceptive hypersensitivity. Inducing gamma oscillations via optogenetic activation of parvalbumin-expressing inhibitory interneurons in the S1 cortex enhances nociceptive sensitivity and induces aversive avoidance behavior. Activity mapping identified a network of prefrontal cortical and subcortical centers whilst morphological tracing and pharmacological studies demonstrate the requirement of descending serotonergic facilitatory pathways in these pain-related behaviors. This study thus describes a mechanistic framework for modulation of pain by specific activity patterns in the S1 cortex.
Gamma oscillations in somatosensory areas in humans correlate with pain perception and pain stimulus intensity, but could also reflect cognitive processes such as attention. Here the authors provide evidence in mice that these oscillations causally contribute to pain perception.
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1 Medical Faculty Heidelberg, Pharmacology Institute, Heidelberg, Germany
2 Medical Faculty Heidelberg and German Cancer Research Center, Department of Clinical Neurobiology, Heidelberg, Germany (GRID:grid.7497.d) (ISNI:0000 0004 0492 0584)
3 Medical Faculty Heidelberg, Pharmacology Institute, Heidelberg, Germany (GRID:grid.7497.d)