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RGS4 Maintains Chronic Pain Symptoms in Rodent Models

ABSTRACT: RGS4 Maintains Chronic Pain Symptoms in Rodent Models

PROVIDER: PRJNA574183 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10186410_1.fastq.gz	Fastqsanger.gz
	SRR10186410_2.fastq.gz	Fastqsanger.gz
	SRR10186411_1.fastq.gz	Fastqsanger.gz
	SRR10186411_2.fastq.gz	Fastqsanger.gz
	SRR10186412_1.fastq.gz	Fastqsanger.gz

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RGS4 Maintains Chronic Pain Symptoms in Rodent Models

Project description:There is an imminent need for safe and efficient chronic pain medications. Regulator of G-protein signaling 4 (RGS4) is a multi-functional signal transduction protein, widely expressed in the pain matrix. Here, we demonstrate that RGS4 plays a prominentrole in the maintenance of chronic pain symptoms in male and female mice. Using genetically modified mice, we show a dynamicrole of RGS4 in recovery from symptoms of sensory hypersensitivity deriving from hindpaw inflammation or hindlimb nerveinjury. We also demonstrate an important role of RGS4 actions in gene expression patterns induced by chronic pain states in themouse thalamus. Our findings provide novel insight into mechanisms associated with the maintenance of chronic pain states anddemonstrate that interventions in RGS4 activity promote recovery from sensory hypersensitivity symptoms.

2019-09-26 | GSE138024 | GEO

Algesic MBP peptide induce pain-specific signaling in rodent Schwann Cells

Project description:Algesic MBP peptide induce pain-specific signaling in rodent Schwann Cells

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Tianeptine promotes lasting antiallodynic effects in a mouse model of neuropathic pain

Project description:Tricyclic antidepressants (TCAs), such as desipramine (DMI), are effective at managing neuropathic pain symptoms but often take several weeks to become effective and also lead to considerable side effects. Tianeptine (TIAN) is an atypical antidepressant that activates the mu-opioid receptor but does not produce analgesic tolerance or withdrawal in mice, nor euphoria in humans, at clinically-relevant doses. Here, we evaluate the efficacy of TIAN at persistently alleviating mechanical allodynia in the spared nerve injury (SNI) model of neuropathic pain, even well after drug clearance. After finding an accelerated onset of antiallodynic action compared to DMI, we used genetically modified mice to gain insight into RGS protein-associated pathways that modulate the efficacy of TIAN relative to DMI in models of neuropathic pain. Because we observed similar behavioral responses to both TIAN and DMI treatment in RGS4, RGSz1, and RGS9 knockout mice, we performed RNA sequencing on the NAc of TIAN- and DMI-treated mice after prolonged SNI to further clarify potential mechanisms underlying TIANs faster therapeutic actions. Our bioinformatic analysis revealed distinct transcriptomic signatures between the two drugs, with TIAN more directly reversing SNI-induced differentially expressed genes, and further predicted several upstream regulators that may be implicated in onset of action. This new understanding of the molecular pathways underlying TIAN action may enable the development of novel and more efficacious pharmacological approaches for the management of neuropathic pain.

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Microarray analyses of mouse dorsal root ganglia tissue for six different pain models

Project description:Six different mouse pain models were studied: (1) tumour-injection model for bone cancer pain; (2) partial sciatic nerve ligation (PSL) for neuropathic pain; (3) mechanical joint loading for osteoarthritis pain; (4) oxaliplatin-induced painful neuropathy for chemotherapy-induced pain; (5) hyperalgesic priming model for chronic muscle pain; and (6) complete Freund’s adjuvant (CFA)-injection for inflammatory pain. Transcriptomic microarray analyses were performed using RNA isolated from dorsal root ganglia.

2018-06-11 | E-MTAB-6864 | biostudies-arrayexpress

Epigenetic regulation of beta-endorphin synthesis in hypothalamic arcuate nucleus neurons modulates neuropathic pain in a rodent pain model

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Project description:We demonstrated the pain-specific response to the algesic peptide fragment MBP84-104 of myelin basic protein that induces pain if injected into sciatic nerve of rats and mice. We used the wild-type peptide MBP 84-104, H89G mutant peptide (MBP84-104-H89G), scramble peptide (MBP84-104-SCR) and phosphomimetic peptide MBP84-104-mimTT to stimulate the primary rat Schwann cell cultures. After 24h we isolated total RNA and conducted genome wide RNA-seq. In addition, we performed RNA-seq using Schwann cells constitutively expressing an MBP84-104-mCherry construct. The gene expression data was analyzed using Ingenuity Pathway Analysis software. We conclude that the Schwann cells expressing MBP84-104 constructs stimulate pain-specific signaling pathways thus representing a relevant model to study neuropathic pain.

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Project description:Two out-bred rat selection lines were separated to produce different hypersensitivity phenotypes following nerve injury. These lines were termed High Pain and Low Pain (HP or LP). Each sub-strain was either subject to a Sham surgery or a Spinal Nerve Ligation (SNL) surgery to the L4 and L5 spinal nerves. Three days following surgery L4/L5 Dorsal Root Ganglia (DRG) were dissected from these animals. For the rat line separation protocol see: Devor M, Raber P (1990) Heritability of symptoms in an experimental model of neuropathic pain. Pain 42:51-67. 12 Hybridizations, 3 per condition; Sham HP DRG; 3 day SNL HP DRG; Sham LP DRG; 3 day SNL LP DRG.

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