Rodent Models of Colorectal Distension

O’Mahony, Siobhain M.; Tramullas, Mónica; Fitzgerald, Patrick; Cryan, John F.

doi:10.1002/0471142301.ns0940s61

Cited by 39 publications

(38 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Representative CRD traces at the pressure of 40 mmHg and 65 mmHg for conventional or GF mice are shown in Figure 1—figure supplement 1B–E. Importantly, in line with our previous studies (O'Mahony et al, 2012), there was no significant difference in the basal activity (between distensions) of the abdominal musculature between groups ( F 1,15 = 0.38, p=0.58) or within the same experimental group ( F 4,60 = 1.08, p=0.374). The visceral pain threshold was significantly lower in GF versus CC mice ( t 17 = 2.12, p=0.049; Figure 1B).…”

Section: Resultssupporting

confidence: 88%

See 1 more Smart Citation

Microbiota regulates visceral pain in the mouse

Luczynski

Tramullas

Viola

et al. 2017

eLife

Self Cite

133

View full text Add to dashboard Cite

The perception of visceral pain is a complex process involving the spinal cord and higher order brain structures. Increasing evidence implicates the gut microbiota as a key regulator of brain and behavior, yet it remains to be determined if gut bacteria play a role in visceral sensitivity. We used germ-free mice (GF) to assess visceral sensitivity, spinal cord gene expression and pain-related brain structures. GF mice displayed visceral hypersensitivity accompanied by increases in Toll-like receptor and cytokine gene expression in the spinal cord, which were normalized by postnatal colonization with microbiota from conventionally colonized (CC). In GF mice, the volumes of the anterior cingulate cortex (ACC) and periaqueductal grey, areas involved in pain processing, were decreased and enlarged, respectively, and dendritic changes in the ACC were evident. These findings indicate that the gut microbiota is required for the normal visceral pain sensation.DOI: http://dx.doi.org/10.7554/eLife.25887.001

show abstract

Section: Resultssupporting

confidence: 88%

“…CRD was carried out as previously described (O'Mahony et al, 2012; Tramullas et al, 2012). The CRD-system was composed of a barostat (Distender Series II, G and J Electronics, Toronto, ON, Canada) and a transducer amplifier (LabTrax 4, World Precision Instruments, Sarasota, FL).…”

Section: Materials and Methodsmentioning

confidence: 99%

Microbiota regulates visceral pain in the mouse

Luczynski

Tramullas

Viola

et al. 2017

eLife

Self Cite

133

View full text Add to dashboard Cite

show abstract

“…The VMR can be quantified visually without additional instrumentation in freely moving animals, or as quantification of the electromyogenic (EMG) signal following implantation of electrodes in the overlying abdominal muscle, which requires the animal to be partially restrained to minimize movement artifact with the EMG signal. A nonsurgical assessment of VMR via manometric recordings using sensors within the colon to measure changes in intracolonic pressure has been established in mouse models . This method has the advantage that animals do not have to be restrained while assessing colonic sensitivity; however, the disadvantage is that the measurements can contain artifacts due to colonic contractions during normal colonic motility and unrelated to measures of colonic sensitivity.…”

Section: Visceral Painmentioning

confidence: 99%

“…This method has the advantage that animals do not have to be restrained while assessing colonic sensitivity; however, the disadvantage is that the measurements can contain artifacts due to colonic contractions during normal colonic motility and unrelated to measures of colonic sensitivity. For further reading on rodent CRD, the reader is referred to a review on the assessment of visceral pain in rodent models by O'Mahony and colleagues .…”

Section: Visceral Painmentioning

confidence: 99%

Stress and the Microbiota–Gut–Brain Axis in Visceral Pain: Relevance to Irritable Bowel Syndrome

et al. 2015

Self Cite

View full text Add to dashboard Cite

Visceral pain is a global term used to describe pain originating from the internal organs of the body, which affects a significant proportion of the population and is a common feature of functional gastrointestinal disorders (FGIDs) such as irritable bowel syndrome (IBS). While IBS is multifactorial, with no single etiology to completely explain the disorder, many patients also experience comorbid behavioral disorders, such as anxiety or depression; thus, IBS is described as a disorder of the gut-brain axis. Stress is implicated in the development and exacerbation of visceral pain disorders. Chronic stress can modify central pain circuitry, as well as change motility and permeability throughout the gastrointestinal (GI) tract. More recently, the role of the gut microbiota in the bidirectional communication along the gut-brain axis, and subsequent changes in behavior, has emerged. Thus, stress and the gut microbiota can interact through complementary or opposing factors to influence visceral nociceptive behaviors. This review will highlight the evidence by which stress and the gut microbiota interact in the regulation of visceral nociception. We will focus on the influence of stress on the microbiota and the mechanisms by which microbiota can affect the stress response and behavioral outcomes with an emphasis on visceral pain.

show abstract

“…Colorectal distension was carried out as previously described (O'Mahony et al 2012). Each rat was lightly anaesthetized with isoflourane (5%, gaseous), anaesthezia was monitored by pain response to paw pinch, and a latex balloon (6 cm in length; Durex, Parsippany, NJ, USA) was inserted into the colon, 1 cm from the anus.…”

Section: Colorectal Distensionmentioning

confidence: 99%

Differential visceral pain sensitivity and colonic morphology in four common laboratory rat strains

O’Malley¹,

Julio–Pieper²,

O’Mahony³

et al. 2013

Experimental Physiology

Self Cite

View full text Add to dashboard Cite

New Findings r What is the central question of this study?Does stress sensitivity and susceptibility to inflammation innate to certain rat strains make them vulnerable to bowel dysfunction? r What is the main finding and its importance?Of four different rat strains, the Lewis rat, which displays both susceptibility to gastrointestinal inflammation and sensitivity to stress, exhibits the most aberrant gastrointestinal morphology and visceral pain sensitivity. Given the similarities to human functional bowel disorders, such as irritable bowel syndrome, this may make it a good model of this disease.Irritable bowel syndrome is a common, debilitating gastrointestinal (GI) disorder characterized by episodic exacerbations of symptoms such as abdominal pain, bloating and altered bowel habit. Contributory factors for the development of irritable bowel syndrome include genetics, childhood trauma and prior GI infection leading to chronic low-grade inflammation or immune activation. Additional considerations in comprehending the chronic relapsing pattern that typifies irritable bowel syndrome symptoms are the effects of both psychosocial and infection-related stresses. Background stress and immune profiles can influence gut permeability and visceral pain sensitivity. This study examined whether innate susceptibility to inflammation and stress sensitivity in four rat strains is associated with bowel dysfunction. The pain threshold to colorectal distension was assessed in Lewis, Fischer (F344) and spontaneously hypertensive rats and compared with Sprague-Dawley control animals. Colons were subsequently excised and morphologically assessed for total length, goblet cell hyperplasia and muscle and mucosal thickness. Lewis rats displayed visceral hypersensitivity compared with other strains. At a morphological level, the gastrointestinal tract from these rats displayed mucosal goblet cell hyperplasia and alterations in muscle layer thickness. The Lewis rat strain, which is reported to have increased susceptibility to GI inflammation in addition to stress sensitivity, had the most prominent features of physiological and morphological GI dysfunction. These data support the hypothesis that background strain is a key factor in the development and exacerbation of bowel dysfunction in rodent models.

show abstract

Rodent Models of Colorectal Distension

Cited by 39 publications

References 18 publications

Microbiota regulates visceral pain in the mouse

Microbiota regulates visceral pain in the mouse

Stress and the Microbiota–Gut–Brain Axis in Visceral Pain: Relevance to Irritable Bowel Syndrome

Differential visceral pain sensitivity and colonic morphology in four common laboratory rat strains

Contact Info

Product

Resources

About