ArticleThe journal of pain2022
The Double Insult of Neonatal Cystitis Plus Adult Somatic Inflammation Results in Corticotropin Releasing Factor Type II Receptor-Dependent Bladder Hypersensitivity in Female Rats.
Article in The journal of pain, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Spinal CRH facilitates the micturition reflex via the CRH2 receptor in rats with normal bladder and bladder outlet obstruction.Scientific reports · 2025Article
- Latent bladder hypersensitivity induced by neonatal cystitis in rats unmasked by segmental but not hetero-segmental inflammation.Neuroscience letters · 2025Article
- Stress-induced bladder hypersensitivity: Effect of corticotropin releasing factor receptors assessed by spinal neurophysiology and neurochemistry.Neuropharmacology · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
The spinal mechanisms of visceral hypersensitivity are poorly understood, particularly when there is an interaction with somatic systems. Recently we demonstrated that rats which were pretreated with neonatal bladder inflammation (NBI) and subsequently pretreated as adults with bladder re-inflammation had augmented reflex and neuronal responses to urinary bladder distension via a corticotropin-releasing factor receptor type II (CRFR2) mechanism. Another insult producing similar augmented responses is somatic inflammation induced by Complete Freund's Adjuvant (CFA) in the hindlimb. Using neurochemical measures and both reflex and neuronal responses to urinary bladder distension as endpoints, the present study probed the role of CRFR2-related mechanisms in bladder hyperalgesia secondary to NBI and CFA-induced hindlimb inflammation. ELISA measures of the lumbosacral spinal cord demonstrated increased CRFR2 protein following pretreatment with NBI+CFA. Intrathecal CRFR2 antagonists blocked the augmentation of visceromotor responses to distension following pretreatment with both NBI+CFA. Lumbosacral dorsal horn neuronal responses to bladder distension in rats pretreated with NBI+CFA were attenuated by the spinal topical administration of a CRFR2 antagonist. These findings are the first demonstration of a somatovisceral interaction working via CRFR2 receptors and support the therapeutic value of these agents in the treatment of painful bladder disorders, particularly when triggered by somatic events. (Word Count 199). PERSPECTIVE: Bladder hypersensitivity occurs following neonatal cystitis and an adult insult such as somatic inflammation. This paper demonstrates that CRFR2-related mechanisms are associated with this hypersensitivity. This supports the therapeutic value of these agents in the treatment of painful bladder disorders, particularly when triggered by somatic events.
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