Lister et al. 2024 (PRJNA1105042)

General Details

Title Translational control in the spinal cord regulates gene expression and pain hypersensitivity in the chronic phase of neuropathic pain
Organism
Number of Samples 24
Release Date 2024/04/26 00:00
Sequencing Types
Protocol Details

Study Links

Repository Details

SRA SRP504307
ENA SRP504307
GEO
BioProject PRJNA1105042

Publication

Title
Authors Lister KC,Wong C,Uttam S,Parisien M,Stecum P,Brown N,Cai W,Hooshmandi M,Gu N,Amiri M,Beaudry F,Jafarnejad SM,Tavares-Ferreira D,Inturi NN,Mazhar K,Zhao HT,Fitzsimmons B,Gkogkas CG,Sonenberg N,Price TJ,Diatchenko L,Atlasi Y,Mogil JS,Khoutorsky A
Journal bioRxiv : the preprint server for biology
Publication Date 2024 Jun 28
Abstract Sensitization of spinal nociceptive circuits plays a crucial role in neuropathic pain. This sensitization depends on new gene expression that is primarily regulated via transcriptional and translational control mechanisms. The relative roles of these mechanisms in regulating gene expression in the clinically relevant chronic phase of neuropathic pain are not well understood. Here, we show that changes in gene expression in the spinal cord during the chronic phase of neuropathic pain are substantially regulated at the translational level. Downregulating spinal translation at the chronic phase alleviated pain hypersensitivity. Cell-type-specific profiling revealed that spinal inhibitory neurons exhibited greater changes in translation after peripheral nerve injury compared to excitatory neurons. Notably, increasing translation selectively in all inhibitory neurons or parvalbumin-positive (PV + ) interneurons, but not excitatory neurons, promoted mechanical pain hypersensitivity. Furthermore, increasing translation in PV + neurons decreased their intrinsic excitability and spiking activity, whereas reducing translation in spinal PV + neurons prevented the nerve injury-induced decrease in excitability. Thus, translational control mechanisms in the spinal cord, particularly in inhibitory neurons, play a role in mediating neuropathic pain hypersensitivity.
PMC PMC11230214
PMID 38979173
DOI
Run Accession Study Accession Scientific Name Cell Line Library Type Treatment GWIPS-viz Trips-Viz Reads BAM BigWig (F) BigWig (R)
SRR28817149 PRJNA1105042 Mus musculus all cells
SRR28817147 PRJNA1105042 Mus musculus all cells
SRR28817145 PRJNA1105042 Mus musculus all cells
SRR28817143 PRJNA1105042 Mus musculus all cells
SRR28817141 PRJNA1105042 Mus musculus all cells
SRR28817139 PRJNA1105042 Mus musculus all cells
SRR28817137 PRJNA1105042 Mus musculus inhibitory neurons
SRR28817135 PRJNA1105042 Mus musculus inhibitory neurons
SRR28817117 PRJNA1105042 Mus musculus all cells
SRR28817114 PRJNA1105042 Mus musculus all cells
SRR28817112 PRJNA1105042 Mus musculus all cells
SRR28817111 PRJNA1105042 Mus musculus excitatory neurons
SRR28817109 PRJNA1105042 Mus musculus excitatory neurons
SRR28817107 PRJNA1105042 Mus musculus excitatory neurons
SRR28817105 PRJNA1105042 Mus musculus excitatory neurons
SRR28817103 PRJNA1105042 Mus musculus excitatory neurons
SRR28817085 PRJNA1105042 Mus musculus excitatory neurons
SRR28817083 PRJNA1105042 Mus musculus excitatory neurons
SRR28817081 PRJNA1105042 Mus musculus excitatory neurons
SRR28817079 PRJNA1105042 Mus musculus excitatory neurons
SRR28817077 PRJNA1105042 Mus musculus excitatory neurons
SRR28817075 PRJNA1105042 Mus musculus excitatory neurons
SRR28817073 PRJNA1105042 Mus musculus inhibitory neurons
SRR28817066 PRJNA1105042 Mus musculus inhibitory neurons
Run Accession Study Accession Scientific Name Cell Line Library Type Treatment GWIPS-viz Trips-Viz Reads BAM BigWig (F) BigWig (R)

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