TABLE 4.
Stress/genetic models for the study of visceral pain
| Animals | Stressor/ Knockout gene | Purpose of the study | Findings | References |
|---|---|---|---|---|
| Adult male rat | ICV cannulated rats were exposed to repeated water avoidance stress and administered with TSA, a potent histone deacetylase inhibitor | To study the importance of epigenetic mechanisms in visceral pain induced by chronic water avoidance stress | Stressed rats exhibited visceral hypersensitivity that was significantly attenuated by TSA. Compared to SHAM controls, methylation of the GR gene was increased following WAS while expression of the GR gene was decreased. Methylation of the CRF promoter was decreased with WAS with a concomitant increase in CRF expression | Tran et al 18 |
| Rat | WRS Model | To test the effect of a bronchodilator, aminophylline on stress‐induced defecation and visceral hypersensitivity and defecation in irritable bowel syndrome | Aminophylline suppressed maternal separation‐ and acetic acid administration‐induced visceral hypersensitivity to CRD, which was mediated by both A2AARs and A2BARs | Asano et al 84 |
| Adult mice | Knockout model | To evaluate the effect of Tetrodotoxin on pure visceral pain induced by intracolonic instillation of capsaicin and mustard oil and its effect in a Nav1.7 Knockout Mice | No differences in pain‐related responses and referred hyperalgesia with respect to their control mice littermates when they were instilled intra‐colonically with capsaicin and mustard oil or treated intraperitoneally with cyclophosphamide | Gonzalez‐Cano et al 92 |
| Male and female rat | Knockout model | To examine the role of NaV1.7 in visceral pain processing and the development of referred hyperalgesia using a conditional nociceptor‐specific NaV1.7 knockout mouse (NaV1.7Nav1.8) and selective small‐molecule NaV1.7 antagonist PF‐5198007 | NaV1.7 (in NaV1.8‐expressing neurons) contributes to defined pain pathways in a modality‐dependent manner, modulating somatic noxious heat pain, but is not required for visceral pain processing, and advocate that pharmacological block of NaV1.7 alone in the viscera may be insufficient in targeting chronic visceral pain | Hockley et al 86 |
Abbreviations: CRD, Colorectal Distension; CRF, Corticotropin Releasing Factor; ICV, Intracerebroventricular; TSA, Trichostatin‐A; WAS, water avoidance stress; WRS, wrap restraint stress.