The H2S-producing enzyme CSE is dispensable for the processing of inflammatory and neuropathic pain

• Published in: Brain research Vol. 1624; pp. 380 - 389
• Main Authors: Syhr, Katharina M.J., Boosen, Meike, Hohmann, Stephan W., Longen, Sebastian, Köhler, Yvette, Pfeilschifter, Josef, Beck, Karl-Friedrich, Geisslinger, Gerd, Schmidtko, Achim, Kallenborn-Gerhardt, Wiebke
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 22.10.2015
• Subjects: Animals; Chronic pain; CSE; CTH; Cystathionine gamma-Lyase - genetics; Cystathionine gamma-Lyase - metabolism; Disease Models, Animal; Dorsal root ganglia; Formaldehyde - toxicity; Ganglia, Spinal - metabolism; Gene Expression Regulation - genetics; Hydrogen sulfide; Hydrogen Sulfide - metabolism; Hyperalgesia - etiology; Hyperalgesia - metabolism; Inflammation - chemically induced; Inflammation - metabolism; Inflammation - pathology; Knockout mice; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Motor Activity - physiology; Neuralgia - metabolism; Neuralgia - pathology; Pain Measurement; Spinal Cord - metabolism; Up-Regulation; Zymosan - pharmacology; MPST; BCA; PGE2; Knockout mice; PPG; H2S; LPS; Chronic pain; SNI; Hydrogen sulfide; KATP; TRP; Dorsal root ganglia; CSE; CBS; PLP; CTH; CAT; DRGs; WT
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2015.07.058

Accumulating lines of evidence indicate that hydrogen sulfide (H2S) contributes to the processing of chronic pain. However, the sources of H2S production in the nociceptive system are poorly understood. Here we investigated the expression of the H2S releasing enzyme cystathionine γ-lyase (CSE) in the nociceptive system and characterized its role in chronic pain signaling using CSE deficient mice. We show that paw inflammation and peripheral nerve injury led to upregulation of CSE expression in dorsal root ganglia. However, conditional knockout mice lacking CSE in sensory neurons as well as global CSE knockout mice demonstrated normal pain behaviors in inflammatory and neuropathic pain models as compared to WT littermates. Thus, our results suggest that CSE is not critically involved in chronic pain signaling in mice and that sources different from CSE mediate the pain relevant effects of H2S. •CSE expression is induced in inflammatory and neuropathic pain models in dorsal root ganglia.•Acute pain behavior is not affected by CSE deficiency.•CSE knockout mice show normal inflammatory and neuropathic pain behavior .