The Burning Pain Transcriptome in the Mouse Primary Somatosensory Cortex.

Area of Science:

• Neuroscience
• Molecular Biology
• Pain Research

Background:

• Previous studies showed spinal cord changes after burn injury (BI).
• The primary somatosensory cortex (S1) role in pain perception after BI is unknown.
• Investigating S1 transcriptomic changes offers insight into pain processing.

Purpose of the Study:

• To investigate transcriptomic alterations in the S1 cortex following burn injury (BI) and formalin application (FA).
• To compare gene expression profiles between BI and FA in the S1 cortex.
• To identify key molecular pathways involved in the S1 response to different pain types.

Main Methods:

• RNA sequencing (RNA-seq) was used to analyze gene expression in the S1 cortex of mice one hour after BI or FA.
• Differential gene expression analysis identified significant changes in gene activity.
• Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed.

Main Results:

• RNA-seq identified 1116 differentially expressed genes (DEGs) in BI and 136 DEGs in FA.
• A majority of DEGs were downregulated in both conditions (82.4% in BI, 32.4% in FA).
• BI upregulated mitochondrial functions and ribosome synthesis, while downregulating axon guidance and synaptic plasticity; FA primarily impacted metabolic processes.
• Retrograde endocannabinoid signaling (REC) was highlighted in the KEGG analysis for BI response.

Conclusions:

• Transcriptomic remodeling in the S1 cortex differs based on pain sensory modality.
• Burn injury leads to distinct molecular changes in S1 compared to inflammatory pain.
• The retrograde endocannabinoid signaling network is activated during acute pain responses following burn injury.