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Characterization of pain-related behaviors and gene expression profiling of peripheral sensory ganglia of a mouse model of acute ankle sprain

ABSTRACT: Characterization of pain-related behaviors and gene expression profiling of peripheral sensory ganglia of a mouse model of acute ankle sprain

PROVIDER: PRJNA957787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24230400.fastq.gz	Fastqsanger.gz
	SRR24230401.fastq.gz	Fastqsanger.gz
	SRR24230396.fastq.gz	Fastqsanger.gz
	SRR24230397.fastq.gz	Fastqsanger.gz
	SRR24230398.fastq.gz	Fastqsanger.gz

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Characterization of pain-related behaviors and gene expression profiling of peripheral sensory ganglia of a mouse model of acute ankle sprain

Project description:Lateral ankle sprain (LAS) is a very common type of joint injury.Unfortunately, a certain proportion of individuals who once developed LAS may suffer persistent ankle pain and recurrent sprains. However, the molecular pain mechanisms underlying LAS are still not well understood. To investigate the potential mechanisms of pain in LAS model mice, we performed RNA- Seq of ipsilateral DRG of sham and LAS model group mice. GO analysis found that the mostly enriched biological process include immune response and positive regulation of gene expression. Immune response can trigger neuroinflammation, a critical process for peripheral sensitization and contributes to chronic pain mechanisms. Furthermore, our RNA-Seq analysis indicated that LAS modulated the expression of multiple genes and gene networks in the DRGs. Our work may help to further advance the understandings of the molecular pain mechanisms underlying LAS and help to identify novel targets for LAS.

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Project description:Chronic pain is one of the most significant and costly medical problems throughout the world. Recent evidence has confirmed the hippocampus as an active modulator of pain chronicity but the underlying mechanisms remain poorly defined. By means of in vivo electrophysiology together with chemogenetic and optogenetic manipulations in freely behaving mice, we identified a neural ensemble in the ventral hippocampal CA1 (vCA1) that showed inhibitory responses to noxious external stimuli, but not to innocuous stimuli. Following peripheral inflammation, this neuronal ensemble became responsive to innocuous stimuli and causally contributed to sensory hypersensitivity in inflammatory animals. Mimicking this inhibition of vCA1 neurons using chemogenetics in naïve mice induced chronic pain-like behavioral changes, whereas activating these vCA1 neurons in mice with chronic peripheral inflammation resulted in a striking reduction of pain-related behaviors. Pathway-specific manipulation of vCA1 projections to the basolateral amygdala (BLA) and infralimbic cortex (IL) showed that these pathways were differentially involved in pain modulation at different temporal stages of chronic inflammatory pain. These results confirm a crucial role of the ventral hippocampus and its circuits in modulating the development of chronic pain in mice.

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Expression data from FACS purified nociceptor neurons from peripheral sensory ganglia

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Project description:Inflammation plays a role in neuropathic pain conditions as well as in pain induced solely by an inflammatory stimulus. Robust mechanical hyperalgesia and allodynia can be induced by locally inflaming the L5 dorsal root ganglion (DRG) in rat. This model allows investigation of the contribution of inflammation per se to chronic pain conditions. Most previous microarray studies of DRG gene expression have investigated neuropathic pain models involving axon transection. To examine the role of inflammation, we used microarray methods to examine gene expression 3 days after local inflammation of the L5 DRG in rat. We observed significant regulation in a large number of genes (23% of observed transcripts), and examined 221 (3%) with a fold-change of 1.5-fold or more in more detail. Immune-related genes were the largest category in this group and included members of the complement system as well as several pro-inflammatory cytokines. However, these upregulated cytokines had no prior links to peripheral pain in the literature other than through microarray studies, though most had previously described roles in CNS (especially neuroinflammatory conditions) as well as in immune responses. The L5 dorsal root ganglion (DRG) was locally inflamed with zymosan/Incomplete Freund's Adjuvant. DRG were isolated 3 days later. Each sample was RNA extracted from a single DRG. 6 samples from rats with local DRG inflammation were compared with 6 samples from sham-operated rats.

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ALKBH5-mediated m6A modification of 5-HT3A mRNA in primary sensory neurons promotes neuropathic pain behaviors

Project description:ALKBH5-mediated m6A modification of 5-HT3A mRNA in primary sensory neurons promotes neuropathic pain behaviors

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