Responses of rat spinal neurones to natural and electrical stimulation of colonic afferents: effect of inflammation

Acute Colitis Enhances Responsiveness of Lumbosacral Spinal Neurons to Colorectal Distension in Rats

“…It is suggested that colonic inflammation decreased response threshold of spinal neurons to CRD. This observation is similar to the results reported for rats that had short periods of colonic inflammation produced by mustard oil or acetic acid [7,11]. These data can account for colonic allodynia, which is observed in patients with ulcerative colitis [1,2,3] and animals with colonic inflammation [10,29].…”

“…In the present study, the ratio of active to silent neurons as well as the average spontaneous activity of lumbosacral spinal neurons excited by CRD was significantly higher in rats with an inflamed colon than in control animals. These observations are similar to previous studies, in which spinal neuronal activity has been examined after administration of different irritants in the colon of rats [4,7,10,11]. For example, acute inflammation of the colon with mustard oil or turpentine induces an increase in spontaneous activity of postsynaptic dorsal column or spinal neurons responding to CRD [10,11].…”

“…However, previous studies that used electrophysiological techniques to examine spinal neuronal responses to noxious colonic stimulation administered short-term (minutes to hours) colonic irritants, which is more comparable to an instant noxious stimulus rather than an inflammatory course similar to a clinical situation. For example, spinal neuronal hyperexcitability or hypersensitivity has been determined in rats after pretreatment with colonic acetic acid for 45 min [7,8]; with colonic turpentine for 2-48 h [9,10], and with colonic mustard oil for 30 min to a few hours [11][12][13]. In these cases, colorectal irritation may not be long enough to allow the colon and pain pathways to fully develop symptomatic and adaptive responses to pathological alterations that are observed clinically.…”

Convergence of sensory pathways in the development of somatic and visceral hypersensitivity

“…However, colonic application of irritants, such as zymosan, leads to a significant activation of spinal neurons in adjacent segments, including L4 and L5, thus providing a neuroanatomic basis for the observed hypersensitivity in both hindpaws during an inflammatory state (16). Similarly, electrophysiological experiments showed an increased size of the cutaneous receptive field after colonic administration of acetic acid (41), a finding consistent with data showing lower sensory thresholds and larger areas of pain referral in patients with functional bowel disorders (31,34). Importantly, the thresholds for mechanical or thermal stimulation did not differ between controls and animals with cystitis when a distant, nonconvergent area (front paw) was tested, arguing against generalized changes in sensory processing.…”

Visceral antinociceptive and proinflammatory effects of proteinase activated receptor-4 and its role in the pathogenesis of ulcerative

“…Inflammatory mediators may sensitize colonic afferents to enhance firing in response to painful stimuli (12). A study on rat spinal neurons showed a significantly increased activity to CRD in acute colonic inflammation (71). Thus, the pathomechanism of hypersensitivity may differ in these two models, but our results demonstrate that Intriguingly, the ic.…”