Quantitative study of the myenteric plexus of the stomach of rats with streptozotocin-induced diabetes

Abstract

-The purpose of the present study was to investigate the morphological and quantitative alterations of the myenteric plexus neurons of the stomach of rats with streptozotocin-induced chronic diabetes and compare them to those of non-diabetic animals. Samples from the body of the stomach were used for wholemount preparations stained with NADH-diaphorase and for histological sections stained with hematoxylineosin. It was observed that diabetes cause a significant decrease on the number of neurons.KEY WORDS: myenteric plexus, diabetes, rat.Estudo quantitativo do plexo mientérico do estômago de ratos com diabetes induzido por estreptozootocina RESUMO -A proposta deste trabalho foi estudar as alterações morfológicas e quantitativas dos neurônios do plexo mientérico do estômago de ratos com diabetes induzido por estreptozootocina e estabelecer uma comparação com animais não diabéticos. Amostras do corpo do estômago foram submetidas a preparados de membrana corados pelo método da NADH-diaforase e a cortes histológicos corados por hematoxilinaeosina. Observou-se que o diabetes provoca significante redução no número de neurônios. Diabetes mellitus is a pathological condition in which several physiological abnormalities are observed, such as neuropathies that affect the central nervous system, the peripheral nerves and the autonomic nervous system 1 . Streptozotocin-induced diabetes causes a cycle of events in the nerve cells of the myenteric plexus that begins within one to three days, with the development of chromatolysis followed by regenerative changes over the next six weeks, with some continuous, albeit occasional, ganglionic degeneration 2 ; changes in the innervation of the ileum and colon 3 are reported, as well as a decrease on the neuronal activity 4 . Studies on streptozotocininduced diabetic rats have emphasized the alterations that occur in the small and large intestines. However, it should be remembered that alterations in the neurons of the myenteric plexus, in addition to changing intestinal peristalsis, can affect stomach motility, leading to dilation and retarded gastric emptying, interfering with the coordination between stomach and duodenum and impairing the digestive process 5 . PALAVRAS-CHAVEIn a diabetic ketonuric Chinese hamsters examination of the gastrointestinal tract was observed that the animals had distention and atony of the stomach and intestines when compared with control animals 6 . In humans, among the clinical manifestations of autonomic neuropathy, there is motor impairment of the stomach, which can lead to anorexia, nausea, vomiting and persisting fullness, characterizing gastric debilitation 1,5 . It is also noteworthy that diabetic gastric atony is similar to that observed after vagotomy 5 .Considering the extensive development of the myenteric plexus and its importance for the control of gastric and intestinal functions, and suspecting that diabetes may affect these neurons, in this way contributing to the gastric disturbances, we undertook the present study to determine ...

Effect of acetyl-L-carnitine on Vip-ergic neurons in jejunum submucous plexus of diabetic rats

“…The increase in the cellular size that follows denervation suggests that the extrinsic neural pulse has an inhibitory influence on the submucous nerves since, although the myenteric and the submucous plexus are spatially apart, they form an integrated unit 20 . Thus, the reduction of the inhibitory pulse by the neurons of the myenteric plexus, which are reduced in the chronic DM [21][22][23][24][25] for neurons in the submucous plexus, could result in an increase in the VIP production, increasing the area of the cell bodies of the submucous VIP-ergic neurons.…”

GDNF rescues hyperglycemia-induced diabetic enteric neuropathy through activation of the PI3K/Akt pathway

“…Loss of myenteric neurons has been reported in short-term diabetes (13,14). A reduction in specific types of enteric neurons has been noted in several diabetic animal models, including streptozotocin-induced (STZ-induced) diabetic rats (15,16), STZ-induced diabetic mice (12), diabetic Chinese hamsters (6), and the OLETF rat model of type 2 diabetes (11).…”

Morphoquantitative effects of acute diabetes on the myenteric neurons of the proximal colon of adult rats

“…Among those systems under investigation are the gastrointestinal tract and its intrinsic enteric nervous system, the neuronal network responsible for the control of the activities of the bowel. It is reported, for instance, that the myenteric neurons of the stomach, duodenum and cecum are numerically reduced in diabetes [1][2][3] , and that specific neurochemical groups show response patterns to diabetes which depend on the intestinal segment and the duration of the diabetic state [4][5][6][7] . These neuronal changes, as well as those associated to the autonomic innervation of the gut [8][9][10] , stand among the responsible by the clinical gastrointestinal symptoms of diabetes [11][12][13] .…”