Alterations in the duodenum myenteric neurons of Wistar ratsafter ingesting of 2, 4 dichlorophenoxyacetic acid

The 2,4 dichlorophenoxyacetic acid (2,4-D) is a systemic herbicide whose effects in animal organic systemshave been examined in previous studies, being the neurotoxicity considered the predominant effect. However,the studies that detect the 2,4-D neurotoxicity have merely focused in the central nervous system, andtherefore, little is known about the effect of this herbicide in the enteric nervous system. This study aimedto verifying the 2,4-D effects on the myenteric neurons in duodenum of Wistar rats. Ten 60-day-old maleWistar rats (Rattus norvegicus) were divided in two groups: control group (C) that did not receive 2,4-D andexperimental group (E) that received 5.0 mg of 2,4-D/kg for 15 days. At the end of experimental period, theanimal were euthanized, the duodenum was collected and processed for NADPH-diaphorase histochemicalanalysis in order to expose the nitrergic myenteric neurons (NADPH-dp). In the light microscopy analysis, thewhole-mount preparation obtained from duodenum of each animal were image-captured in 120 and 40 fields,for quantitative and morphometric analyses of myenteric neurons, respectively. The neuronal density was notaffected when comparing the two groups, but an increase (p > 0.05) of 8.5% was observed in the cell bodyarea of neurons in the E group. In conclusion, the ingestion of 2,4-D at a dosage of 5.0 mg/kg body weightfor 15 days does not change the neuronal density, but promotes the hypertrophy of NADPH-dp myentericneurons in duodenum of the rats of this study.

Study on the relationship between gastrointestinal mobility dysfunction and myenteric plexus nitrergic neurons in type 2 diabetic rats / 中国医师杂志

ObjectiveTo study the role of the myenteric plexus (ENS) nitrergic neurons in type 2 diabetic rats with gastroparesis.MethodsThiry male 8-week-SD rats were randomly divided into control group (CON),type 2 diabetic group (DM),insulin-treated group ( INS ) and insulin-lipoie acid group( LA ),each 15.The rats were sacrificed at 16 weeks after diabetic model established,the stomach relative residual rate of pigmented was measured and the protein content of neuronal nitric oxide synthase (nNOS) was evaluate,the level of malondialdehyde (MDA) and superoxide dismutase (SOD),were measured,the the morphological changes of gastric antrum nitrergic neurons was observed.ResultsCompared with CON group,gastric motility,gastric antrum nitrergic neuron count,T-SOD and CuZn-SOD,and were significantly decreased in DM group ( P ＜0.05).Compared with the CON group,DM group gastric antrum nitrergic neurons nNOS expression decreased,while MDA levels significantly increased ( P ＜ 0.05 ).Compared with DM group,INS group and LA group has significantly rapider gastric motility than that of DM group ( P＜ 0.05 ),the neuron counting markly increased in nitrergic neuron of gastic sinus ( P ＜ 0.05 ),increased expressions of nNOS in gastric sinus,while still lower than control group( P ＜0.05).compared with the INS group,antrum nitrergic neuron counts of LA group significantly increased ( P ＜ 0.05 ).Conclusion The gastrointestinal dyskinesis of type 2 diabetic rats might be associated with lesions of gastric myenteric plexus nitrergic neuron.Insulin intensive therapy and treated with alpha-lipoic acid as an antioxidant can inhibit the abnormally high levels of oxidative stress,protect gastrointestinal nitrergic neurons,delay the progress of diabetic gastrointestinal motility disorders.Insulin combined with a-lipoic acid treatment is superior to single-use insulin.

Alteration of nitrergic neuromuscular transmission as a result of acute experimental colitis in rat

Nitric oxide (NO) is a non-adrenergic, non-cholinergic neurotransmitter found in the enteric nervous system that plays a role in a variety of enteropathies, including inflammatory bowel disease. Alteration of nitrergic neurons has been reported to be dependent on the manner by which inflammation is caused. However, this observed alteration has not been reported with acetic acid-induced colitis. Therefore, the purpose of the current study was to investigate changes in nitrergic neuromuscular transmission in experimental colitis in a rat model. Distal colitis was induced by intracolonic administration of 4% acetic acid in the rat. Animals were sacrificed at 4 h and 48 h postacetic acid treatment. Myeloperoxidase activity was significantly increased in the acetic acid-treated groups. However, the response to 60 mM KCl was not significantly different in the three groups studied. The amplitude of phasic contractions was increased by Nomega-nitro-L-arginine methyl ester (L-NAME) in the normal control group, but not in the acetic acid-treated groups. Spontaneous contractions disappeared during electrical field stimulation (EFS) in normal group. However, for the colitis groups, these contractions initially disappeared, and then reappeared during EFS. Moreover, the observed disappearance was diminished by L-NAME; this suggests that these responses were NO-mediated. In addition, the number of NADPH-diaphorase positive nerve cell bodies, in the myenteric plexus, was not altered in the distal colon; whereas the area of NADPH-diaphorase positive fibers, in the circular muscle layer, was decreased in the acetic acidtreated groups. These results suggest that NO-mediated inhibitory neural input, to the circular muscle, was decreased in the acetic acid-treated groups.