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Formalin-evoked pain triggers sex-specific behavior and spinal immune response

ABSTRACT: Formalin-evoked pain triggers sex-specific behavior and spinal immune response

PROVIDER: PRJNA940216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23677142_1.fastq.gz	Fastqsanger.gz
	SRR23677142_2.fastq.gz	Fastqsanger.gz
	SRR23677143_1.fastq.gz	Fastqsanger.gz
	SRR23677143_2.fastq.gz	Fastqsanger.gz
	SRR23677144_1.fastq.gz	Fastqsanger.gz

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Formalin-evoked pain triggers sex-specific behavior and spinal immune response

Project description:Mounting evidence shows sex-related differences in the experience of pain with women suffering more from chronic pain than men. Yet, our understanding of the biological basis underlying those differences remains incomplete. Using an adapted model of formalin-induced chemical/inflammatory pain, we report here that in contrast to male mice, females distinctly display two types of nocifensive responses to formalin, distinguishable by the duration of the interphase. This could be explained by female gonadal hormones fluctuating across the estrus cycle, rather than by the transcriptional content of the dorsal horn of the spinal cord (DHSC). Additionally, deep RNA-sequencing of DHSC showed that formalin-evoked pain was accompanied by a male-preponderant enrichment in genes associated with the immune modulation of pain, revealing an unanticipated contribution of neutrophils. Taking advantage of the male-enriched transcript encoding the neutrophil associated protein Lipocalin 2 (Lcn2) and using flow cytometry, we confirmed that formalin triggered the recruitment of LCN2-expressing neutrophils in the pia mater of spinal meninges, preferentially in males. Our data consolidate the contribution of female estrus cycle to pain perception and provide evidence supporting a sex-specific immune regulation of formalin-evoked pain.

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Loss of bhlha9 impairs thermotaxis and formalin-evoked pain in a sexually dimorphic manner

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Loss of bhlha9 impairs thermotaxis and formalin-evoked pain in a sexually dimorphic manner

Project description:This RNA-Seq experiment aims at unraveling the sets of genes that may be deregulated in a specific subset of sensory neurons (the C-Low Threshold MechanoReceptors or C-LTMRs), in absence of transcription factor bhlha9. In this study, we show that the transcription factor bhlha9 is expressed in a subset of adult C-LTMRs. Moreover, we show that bhlha9 KO males but not female displayed impaired thermotaxis behavior in the temperature gradient paradigm and exhibited exacerbated pain hypersensitivity in the formalin test. To address this question, we FACS-sorted C-LTMRs from adult WT and bhlha9 KO males and females and extracted the total RNA. Further RNA-deep sequencing is a major step to pin-point the sets of genes deregulated selectively in these neurons, in absence of bhlha9.

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Project description:It remains unknown why upon similar acute/subacute painful conditions, pain persists in some individuals while in others it resolves. Genetic factors, mood, and functional alterations, particularly involving the mesolimbic network, appear to be key. In order to explore potential susceptibility/resistance factors, we screened a large population of rats with a peripheral neuropathy, and we isolated a small subset (<15%) that presented high thresholds (HT) to mechanical allodynia (reduced pain manifestation). The phenotype was sustained over 12 weeks and was associated with higher hedonic behavior when compared with low threshold subjects (LT). The nucleus accumbens (NAc) of HT and LT animals were isolated for proteomic analysis by Sequential Window Acquisition of All Theoretical Mass Spectra (SWATH-MS). Two hundred and sevety-nine proteins proteins displayed different expression between LT and HT animals/subjects.

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