Lactobacillus reuteri ingestion and IK(Ca) channel blockade have similar effects on rat colon motility and myenteric neurones.
ABSTRACT We have previously shown that ingestion of Lactobacillus reuteri may modulate colonic enteric neuron activity but with unknown effects on colon motility. The aim of the present report was to elucidate the neuronal mechanisms of action of the probiotic by comparing the effects on motility of L. reuteri ingestion with blockade of a specific ionic current in enteric neurons.
We have used intraluminal pressure recordings from ex vivo rat colon segments and whole cell patch clamp recordings from neurons of rat longitudinal muscle myenteric plexus preparations to investigate the effects of L. reuteri and TRAM-34 on colon motility and neurophysiology. The effects of daily feeding of 10(9) L. reuteri bacteria or acute application of TRAM-34 on threshold fluid filling pressure or pulse pressure was measured.
Lactobacillus reuteri increased intraluminal fluid filling pressure thresholds for evoking pressure pulses by 51% from 0.47 +/- 0.17 hPa; the probiotic also decreased the pulse pressure amplitudes, but not frequency, by 18% from 3.91 +/- 0.52 hPa. The intermediate conductance calcium-dependent potassium (IK(Ca)) channel blocker TRAM-34 (3 micromol L(-1)) increased filling threshold pressure by 43% from 0.52 +/- 0.22 hPa and reduced pulse pressure amplitude by 40% from 2.63 +/- 1.11 hPa; contraction frequency was unaltered. TRAM-34 (3 micromol L(-1)) reduced membrane polarization, leak conductance and the slow afterhyperpolarization current in 16/16 myenteric rat colon AH cells but 19/19 S cells were unaffected.
The present results are consistent with L. reuteri enhancing tonic inhibition of colon contractile activity by acting via the IK(Ca) channel current in AH cells.
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ABSTRACT: Twenty one male Wistar albino rats each weighing approximately 280 g were used in this study. Animals were divided into three groups. The first group (n = 7) consisted of sham controls, in the second (n = 7), rats were administrated 0.1 g/1 ml/galactooligosaccharide by by oral gavage for 4 weeks. In the third group (n = 7), rats were administrated 10 9 CFU/1ml/day Bifidobacterium lactis by oral gavage for 4 weeks. After 4 weeks, rats were sacrified; ileum and proximal colon segments were removed. The spontaneous contractions of ileum and proximal colon were evaluated by using organ bath. It has been detected that both prebiotics and probiotics increased intestinal motility. While probiotics have effects on both ileum and proximal colon, prebiotics seem to be effective in colon. All data are expressed as mean ± SEM (standard error of mean). Statistical comparisons between groups were performed using general linear models of analysis of variance (ANOVA) followed by the Turkey test.African journal of microbiology research 12/2011; 5(32). DOI:10.5897/AJMR11.801 · 0.54 Impact Factor
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ABSTRACT: Stress associated with parturition, transport or mixing has long been correlated with enhanced faecal excretion of diarrhoeal zoonotic pathogens in animals such as Salmonella enterica and Escherichia coli. It may also predispose humans to infection and/or be associated with more severe outcomes. One possible explanation for this phenomenon is the ability of enteric bacterial pathogens to sense and respond to host stress-related catecholamines. This article reviews evidence of the ability of catecholamine hormones to modulate interactions between Gram-negative diarrhoeal pathogens and intestinal mucosa, as well as the molecular mechanisms that may be at work.04/2010: pages 111-134;
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ABSTRACT: This chapter examines and critiques the different methodological approaches, which have been adopted to investigate the interactions of catecholamine neurohormones with bacteria. Adrenergic catecholamines have been shown to promote the in vitro growth of a wide range of both gram-positive and gram-negative bacterial species using growth media, which are designed to mimic the hostile bacteriostatic environment in the host. However, in recent years, it has become apparent that neurohormones are doing more than just alleviating the iron restriction caused by the mammalian transferrin in these media. In fact, it is clear that there are specific receptors in many bacteria, which can recognise epinephrine and norepinephrine resulting in increased virulence determinant expression and alterations in bacterial transcription on a global scale. Furthermore, there is now evidence that “adrenergic” signalling events may also be involved in the bacterial growth responses to catecholamines that have been observed previously. This analysis of the currently used methodologies is intended to assist in a more concerted approach to in vitro microbial endocrinology experiments, which identifies further bacterial genes and molecules the roles of which can be verified in future in vivo investigations.04/2010: pages 291-308;