Background & Aims-Electrophysiological and behavioral studies have demonstrated that increased N-methyl-D-aspartate (NMDA) receptor activation of anterior cingulate cortex (ACC) neurons has a critical role in modulating visceral pain responses in viscerally hypersensitive (VH) rats. This study aimed to identify the NMDA receptor subtypes in perigenual ACC (pACC) neurons involved in the facilitation of visceral nociception.

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Activation of the vagal afferents by noxious gastrointestinal stimuli suggests that vagal afferents may play a complex role in visceral pain processes. The contribution of the vagus nerve to visceral pain remains unresolved. Previous studies reported that patients following chronic vagotomy have lower pain thresholds. The patient with irritable bowel syndrome has been shown alteration of vagal function. We hypothesize that vagal afferent nerves modulate visceral pain. Visceromotor responses (VMR) to graded colorectal distension (CRD) were recorded from the abdominal muscles in conscious rats. Chronic subdiaphragmatic vagus nerve sections induced 470, 106, 51, and 54% increases in VMR to CRD at 20, 40, 60 and 80 mmHg, respectively. Similarly, at light level of anesthesia, topical application of lidocaine to the subdiaphragmatic vagus nerve in rats increased VMR to CRD. Vagal afferent neuronal responses to low or high-intensity electrical vagal stimulation (EVS) of vagal afferent A␦ or C fibers were distinguished by calculating their conduction velocity. Low-intensity EVS of A␦ fibers (40 A, 20 Hz, 0.5 ms for 30 s) reduced VMR to CRD at 40, 60, and 80 mmHg by 41, 52, and 58%, respectively. In contrast, high-intensity EVS of C fibers (400 A, 1 Hz, 0.5 ms for 30 s) had no effect on VMR to CRD. In conclusion, we demonstrated that vagal afferent nerves modulate visceral pain. Low-intensity EVS that activates vagal afferent A␦ fibers reduced visceral pain. Thus EVS may potentially have a role in the treatment of chronic visceral pain. colorectal distension; vagal afferent A␦ or C fibers; visceromotor responses ALTHOUGH IT IS GENERALLY HELD that pain arising from the viscera is mediated exclusively by spinal afferents, vagal afferents primarily convey interoceptive information that is important in regulating autonomic function but do not contribute to the perception of pain. However, there is growing evidence that the vagus nerve may play a complex role in these processes (5,32,35,46). Electrical physiological studies have demonstrated that electrical or chemical stimulation of thoracic vagal and sympathetic afferent fibers activated C1-C3 spinothalamic tract (STT) neurons, which received input from noxious mechanical stimulation of somatic fields including the neck and jaw regions (6, 7). Studies have shown that vagal afferents respond to nociceptive mechanical and chemical stimulation and this leads to brain stem representation of nociceptive signals (35,46,51). Noxious gastric distension resulted in c-Fos expression in the nucleus of the solitary tract (NTS), the location of second order neurons receiving vagal afferent input from the stomach. This increase in c-Fos response is blunted by vagotomy but persists after spinal cord transection (51). Although vagal afferents are activated by gastrointestinal noxious stimuli, the contribution of the vagus nerve to visceral pain remains unresolved. It is well known that a hot drink or a nourishing meal (stimulation of various abdominal receptors) is relaxing and helps to ca...

The objectives of this study were to estimate the herd prevalence of major mastitis pathogens in bulk tank milk (BTM) in China dairy herds, to determine the relationship between the presence of mastitis pathogens and bulk tank milk somatic cell counts (BTSCC), and to investigate the impact of different dairy cattle farming modes and region on bacterial species. BTM samples collected from 894 dairy herds in China were examined for the presence of mastitis pathogens. The Flinders Technology Associates (FTA) cards were used for BTM sample collection, storage, and transportation and bacterial DNA amplification by real-time PCR. Among contagious pathogens, Staphylococcus aureus, Streptococcus agalactiae, and Streptococcus dysgalactiae were detected in 50.1, 92.2, and 72.3% of the 894 BTM samples, respectively. Among environmental pathogens, E. coli, Streptococcus uberis, Enterococcus spp., Klebsiella spp., Serratia marcescens, Corynebacterium bovis, and Arcanobacterium pyogenes were detected in 28.6, 8.9, 35.7, 20.0, 1.3, 17.0, and 67.2% of the BTM samples, respectively. Staphylococcal β-lactamase gene was detected in 61.7% of the BTM samples. The presence of Staphylococcus aureus and Arcanobacterium pyogenes were significantly associated with high BTSCC, respectively. Significant differences were found in presence of Staphylococcus aureus, Streptococcus agalactiae, and Streptococcus dysgalactiae in BTM sampled from the small household farms, dairy-farming communities, and large-scaled dairy farms. There were significant differences in the presence of Streptococcus agalactiae, Streptococcus dysgalactiae, Arcanobacterium pyogenes, staphylococcal β-lactamase gene, Staphylococcus spp., Klebsiella spp., Enterococcus spp., and Streptococcus uberis in BTM among Inner Mongolia, Heilongjiang, and Hebei province. In conclusion, contagious mammary pathogens are predominated among pathogens in BTM samples in China.

Natural antioxidants have drawn growing interest for use in animal feed and the food industry. In the current study, essential oils (EOs) obtained from hydrodistillation of three mentha species, including Mentha piperita (peppermint), Mentha spicata (native spearmint) and Mentha gracilis (Scotch spearmint), harvested in the Midwest region in the United States, were analyzed for their chemical composition using gas chromatography-mass spectrometry, and their antioxidant properties were assessed through chemical assays, in vitro cell culture modeling and in Caenorhabditis elegans (C. elegans). The activity of ferric iron reduction and free-radical scavenging capacity were assessed through chemical-based assays, including the reducing power assay, 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging assay, and Trolox equivalent antioxidant capacity assay (TEAC). Subsequently, the capacity of EOs to mitigate lipid peroxidation was analyzed at various doses using fresh liver homogenates from pigs. A porcine jejunum epithelial cell line (IPEC-J2) was employed as in vitro model to study the cellular antioxidant activity of the mint EOs. Finally, the effectiveness of mint EOs to alleviate acute systemic oxidative damage were evaluated in vivo using C. elegans. Data were analyzed by the MIXED procedure of SAS. Contrast statement was performed to assess linear or quadratic effects of mint EOs given at various doses. All three EOs are mostly composed of monoterpenes and their derivatives (76–90%), but differed in the major compounds, which are menthol and menthone (50%) in peppermint EO and carvone (70%) in spearmint EOs. Three mint EOs demonstrated prominent radical scavenging and Fe3+ reducing activity in chemical-based assays. In comparison with native and Scotch spearmint EOs, peppermint EO had the lowest (p < 0.05) half maximal effective concentration (EC50) in DPPH and TEAC assays and higher efficacy in the reducing power assay. All three EOs exhibited equivalent activity in mitigation of chemical-induced lipid peroxidation in liver tissues in a dose-dependent manner (linear, p < 0.001). The maximal cellular antioxidant activity (CAA) was observed at 5 µg/mL for peppermint, and 100 µg/mL for native and Scotch spearmint EOs. The addition of 25 µg/mL of both spearmint EOs increased (p < 0.05) cellular concentrations of glutathione in H2O2-treated IPEC-J2 cells, suggesting enhanced endogenous antioxidant defense. Supplementation of 100 µg/mL of peppermint or Scotch spearmint EO significantly increased (p < 0.05) the survival rate of C. elegans in response to H2O2-induced oxidative stress. The protective effect is comparable to that of supplementation of 10 µg/mL of ascorbic acid. However native spearmint EO failed to reduce the death rate within the same supplementation dose (10–200 μg/mL).