Early-li
fe stress is a risk
factor
for irritable bowel syndrome (IBS), a common and debilitating
functional gastrointestinal disorder that is o
ften co-morbid with stress-related psychiatric disorders. In the rat, maternal separation (MS) stress has been shown to induce visceral hypersensitivity in adulthood and thus has become a use
ful model o
f IBS. However, development o
f mouse models o
f maternal separation has been di
fficult. Given the advent o
f transgenic mouse technology, such models would be use
ful to
further our understanding o
f the pathophysiology o
f IBS and to develop new pharmacological treatments. Thus, the present study aimed to develop a mouse model o
f MS stress-induced visceral hyperalgesia as measured using manometric recordings o
f colorectal distension (CRD). Moreover, since the GABA
B receptor has been reported to play a role in pain processes, we also assessed its role in visceral nociception using novel GABA
B(1b) receptor subunit knockout mice.
CRD was performed in adult male wildtype and GABAB(1b) receptor knockout mice that had undergone unpredictable MS combined with unpredictable maternal stress (MSUS) from postnatal day 1 through 14 (PND 1-14). MSUS induced visceral hypersensitivity in both wildtype and GABAB(1b) receptor knockout mice when compared with non-stressed mice. Wildtype and GABAB(1b) receptor knockout mice did not differ in baseline or stress-induced visceral sensitivity. To the best of our knowledge, this is the first study to show that early-life stress induces visceral hypersensitivity in a mouse model. These findings may provide a novel mouse model of visceral hypersensitivity which may aid our understanding of its underlying mechanisms in future studies.