In a study, it has been found that the primary somatosensory cortex ( S1 ) contains parvalbumin ( PV ) interneurons that are essential for encoding pain intensity and driving gamma oscillations. Cross-species research demonstrated that beta oscillations in S1 carefully reflect human pain levels and are related to rodent PV interneuron activity.
These cells ‘ ability to modulate pain-related behaviors was demonstrated by optogenetic manipulation, confirming their place in pain control. The research demonstrates the potential of PV interneurons as a marker and goal for pain therapies by establishing a strong link between them and gamma oscillations.
Important Information:
- Pain Encoding: PV cells in S1 carefully record problems power via beta fluctuations.
- Cross-Species Validation: Gamma vibrations linked to PV cells were observed in both humans and mammals.
- Medical Potential: Targeting gamma fluctuations offers a fascinating method for discomfort management.
Origin: Chinese Academy of Sciences
A research team led by Prof. HU Li at the Institute of Psychology , of the , Chinese Academy of Sciences, has revealed that parvalbumin ( PV ) interneurons in the primary somatosensory cortex ( S1 ) preferentially encode pain intensity and drive nociceptive-evoked gamma oscillations ( GBOs ).
Published website in , Neuron , on January 13, the study fills a historic gap in understanding the origins of nociceptive-evoked GBOs and , their , careful marriage with , pain running across different types.
The results point to the potential for using these vibrations as a promising target for therapeutic treatments.
Pain is a major source of human anguish, resulting in economic costs , amounting to hundreds of billions of dollars yearly. Due to the essentially subjective nature of pain, correct assessment and successful treatment of pain are important but challenging.
As a result, experts have engaged in intensive efforts to identify selective neurological markers for , pain perception.
Earlier studies have established that nociceptive-evoked GBOs diligently record anguish and pain-related behaviors , in , both , humans and animals, suggesting their potential as neurological indicators.
However, the synaptic systems underlying GBOs have remained ill understood, limiting the use of GBOs in medical applications.
To address this problem, Prof. HU and his associates conducted a series of cross-species research. The experiments included optogenetic methods ( both alone and together with electrophysiology in mice ), a range of neural recording techniques ( high-density EEG in humans, and silicon probes and calcium imaging in rodents ), as well as nociceptive and non-nociceptive sensory stimuli.
Their findings demonstrated that GBOs in S1 carefully record human pain intensity and are closely related to the rising engagement of PV-positive cells in rodents. Calcium imaging indicated that PV cells, more than pyramid cells, predominantly track pain power.
Follow-up implantable adjustments demonstrated that activating or inhibiting PV cells may affect nociceptive-evoked GBOs and related pain-related activities.
This study strongly establishes PV cells in S1 as the cerebral basis for GBOs ‘ role in encoding pain , power by linking PV interneuron activity at the micro level to GBOs at the mesoscopic level.
According to Prof. HU Li, corresponding author of the study,” These findings are not only important for understanding the biology of cortical nerve digesting but also have far-reaching implications as GBOs are increasingly recognized as a pain biomarker in medical practice and drug development.”
About this news from neuroscience and pain research
Author: LIU Chen
Source: Chinese Academy of Sciences
Contact: LIU Chen – Chinese Academy of Sciences
Image: The image is credited to Neuroscience News
Original Research: Open access.
” Neuronal mechanisms of nociceptive-evokedgamma-band oscillations in rodents” by HU Li et al. Neuron
Abstract
Neuronal mechanisms of nociceptive-evokedgamma-band oscillations in rodents
Gamma-band oscillations ( GBOs ) in the primary somatosensory cortex ( S1 ) play key roles in nociceptive processing. Yet, one crucial question remains unaddressed: what neuronal mechanisms underlie nociceptive-evoked GBOs?
We used a variety of somatosensory stimuli, including nociceptive and non-nociceptive ones, neural recording techniques (electroencephalography in humans and silicon probes and calcium imaging in rodents ), optogenetics ( alone or together with electrophysiology in mice ), and somatosensory stimuli ( nociceptive and non-nociceptive ).
We found that ( 1 ) GBOs encoded pain intensity independent of stimulus intensity in humans, ( 2 ) GBOs in S1 encoded pain intensity and were triggered by spiking of S1 interneurons, ( 3 ) parvalbumin ( PV ) -positive interneurons preferentially tracked pain intensity, and critically, ( 4 ) PV S1 interneurons causally modulated GBOs and pain-related behaviors for both thermal and mechanical pain.
These findings provide direct evidence that PV interneurons in S1 are the source of the preferred nociceptive-evoked GBOs, laying a solid foundation for the development of GBO-based targeted pain therapies.
