| 其他摘要 | The encoding process of pain information in the cerebral cortex is crucial for our understanding of the mechanisms underlying pain perception and the discovery of objective indicators of pain. Among them, the primary somatosensory cortex (S1) in the cerebral cortex receives extensive projections from neurons in the spinal cord, brainstem, and thalamus. It plays a key role in generating sensory awareness and processing pain perception. Pyramidal neurons and interneurons in S 1 are involved in pain-induced brain responses and make distinct contributions to the encoding of pain perception. In this study, multiple experimental techniques were employed, including silicon electrode electrophysiological recording, calcium imaging, optogenetic modulation, pharmacological modulation, and animal behavioral tests, aiming to reveal the neural mechanisms underlying the encoding of pain perception in S1，explore the coding of pain perception by different types of neurons in S 1，and provide new evidence for potential targets for analgesia and objective indicators of pain.
The study first used laser stimulation to induce heat pain in the rat's plantar surface and electrical stimulation to induce tactile sensation. By using silicon electrode electrophysiological recording, the brain responses in S1 were investigated, and it was found that the encoding patterns of pain perception in S1 were distinct from those of tactile perception. Low-frequency event-related potentials (ERPs) played a role in encoding the location and intensity of pain stimuli, while high-frequency gamma band oscillations (GBOs) were only associated with the intensity of pain stimuli. On the other hand, low-frequency ERPs and high-frequency GBOs in tactile perception were only related to the location of the stimuli. Further analysis of neuronal discharge revealed that pain-induced ERPs and GBOs were highly correlated with the activities of pyramidal neurons and interneurons in S 1，with neurons encoding intensity and spatial location attributes showing higher synchronization with ERPs, while interneurons encoding intensity attributes showed higher synchronization with GBOs. ERPs and GBOs induced by tactile stimuli were primarily associated with the activity of pyramidal neurons encoding location information in S1，with pyramidal neurons encoding location attributes exhibiting the highest synchronization with both ERPs and GBOs.
To further investigate the differences in encoding pain perception among different types of neurons in S 1，the study employed free-behavioral calcium imaging to observe and record the response patterns of pyramidal neurons and interneurons in mouse S 1 to laser-induced pain stimuli. The results showed that pyramidal neurons in S1 primarily exhibited stronger responses to location attributes in pain perception, while interneurons primarily exhibited stronger responses to intensity attributes in pain perception.
To elucidate the neural mechanisms underlying pain-induced brain responses, the study utilized techniques such as optogenetic modulation, pharmacological modulation, and optrode recordings to investigate the regulatory mechanisms of neurons in S 1 on pain-induced behaviors and brain responses. First, optogenetic modulation was used to selectively activate or inhibit pyramidal neurons and interneurons in mouse S 1，and their effects on nocifensive behaviors, including laser heat pain scores and mechanical pain thresholds, were observed. The results showed that only when interneurons were modulated, changes in nocifensive behaviors were observed, while modulation of pyramidal neurons had no effect on nocifensive behaviors. Subsequently, pharmacological modulation combined with electrophysiological recordings and optogenetics combined with electrophysiological recordings were used to further verify the effects of modulating these two types of neurons on pain-induced brain responses in S 1 .Electrophysiological results showed that the low-frequency ERP component in S1 was jointly regulated by pyramidal neurons and interneurons, while the high-frequency GBO component was only regulated by interneurons.
In summary, this study revealed the encoding mechanisms of pain information in S1 and the neural mechanisms by which neurons regulate pain perception and pain-induced brain responses. The findings are consistent with previous research and provide causal evidence for the strong correlation between the activity of interneurons in S1 and GBOs as well as nocifensive behaviors. These findings are of significant importance for further understanding the neural encoding principles of pain perception and developing relevant therapeutic approaches. |
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