Abstract
BackgroundThe gonadotropin-releasing hormone (GnRH) analog buserelin causes enteric neuronal loss. Acute stress or injection of corticotropin-releasing factor (CRF) affects motility, secretion, and barrier function of the gastrointestinal tract. The aim of the study was to characterize the CRF immunoreactivity in enteric neurons after buserelin treatment, and to evaluate possible effects of enteric neuropathy on gut microbiota, intestinal permeability, and stress response behavior.ResultsSixty rats were given buserelin (20 μg) or saline subcutaneously for 5 days, repeated four times with 3 weeks in-between. At the study end, enteric neuronal density, enteric expression of CRF, gut microbial composition, and plasma levels of adrenocorticotropic hormone (ACTH) and CRF were analyzed. Intestinal permeability was examined in Ussing chambers and the reaction to stressful events was measured by behavior tests. Buserelin treatment reduced the number of neurons along the entire gastrointestinal tract, with increased relative numbers of CRF-immunoreactive submucosal and myenteric neurons in colon (p < 0.05 and p < 0.01, respectively). The overall microbial diversity and relative abundance did not differ between groups, but Enterobacteriaceae was decreased in colon in buserelin-treated rats (p = 0.020). Basal intestinal permeability did not differ between groups, whereas carbachol stimulation increased ileum permeability in controls (p < 0.05), but not in buserelin-treated rats. Buserelin did not affect stress behavior.ConclusionsAlthough buserelin treatment leads to enteric neuronal loss along the gastrointestinal tract with an increased percentage of CRF-immunoreactive neurons in colon, the physiology is well preserved, with modest effects on colon microbiota and absence of carbachol-induced permeability in ileum as the only observed changes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13104-015-1800-x) contains supplementary material, which is available to authorized users.
Highlights
The gonadotropin-releasing hormone (GnRH) analog buserelin causes enteric neuronal loss
Studies indicate a role for the reproductive peptide hormones in the gastrointestinal (GI) tract, since Gonadotropin-releasing hormone (GnRH) immunoreactivity is found in human enteric neurons [2, 3], and luteinizing hormone (LH) receptors are expressed in both human and rat myenteric neurons [4,5,6]
The aims of the present study were to characterize corticotropin-releasing factor (CRF) immunoreactivity in enteric neurons in the experimental rat model of repeated treatment with the GnRH analog buserelin, and to evaluate possible effects evoked by enteric neuropathy on gut microbiota, intestinal permeability, and stress response behavior
Summary
The gonadotropin-releasing hormone (GnRH) analog buserelin causes enteric neuronal loss. The aim of the study was to characterize the CRF immunoreactivity in enteric neurons after buserelin treatment, and to evaluate possible effects of enteric neuropathy on gut microbiota, intestinal permeability, and stress response behavior. Studies indicate a role for the reproductive peptide hormones in the gastrointestinal (GI) tract, since GnRH immunoreactivity is found in human enteric neurons [2, 3], and LH receptors are expressed in both human and rat myenteric neurons [4,5,6]. Around 50 % of enteric neurons throughout the GI tract were lost after four treatment sessions with the GnRH analog buserelin, whereas morphological measurements showed normal histology in mucosa, submucosa, and muscle layers [5]. If translated into the clinical setting, it may suggest that patients with diffuse GI complaints can suffer from mild to moderate enteric neuropathy despite normal findings in standardized clinical examinations
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