We carried out this study with the purpose of contributing on the effects of the proteic desnutrition on the morphological aspects and quantitative analysis of the neurons in the myenteric plexus of the ascending colon of adult Rattus norvegicus. Twenty adult rats were divided into two groups: in one of them, we offered a normal ration with proteic level of 22% (control group) and in the other, a ration with a proteic level of 8% (experiment group) during 120 days. We did the whole-mount preparations for the ascending colon and stained them with the Giemsa technique and the histochemical technique of NADH-diaphorase. The rats with proteic desnutrition showed a body weight, on average, to be 35.1% less than those of the control group, and the colon was on average, 26.8% shorter and 6.7% narrower. Thus, it was to be expected that the colon of animals with proteic desnutrition had a neuronal density 31.62% greater than the rats of the control group. Nevertheless, the difference with the Giemsa technique was on average 18.4%, demonstrating a mean neuronal loss of 13.25%.

The purpose of this work was to study the neurons of the myenteric plexus of the cecum of rats with chronic streptozotocin-induced diabetes. We used four experimental groups of animals. In groups D2 and D8 animals were killed two and eight months, respectively, after diabetes induction and groups C2 and C8 were used as controls. We carried out whole-mount preparations stained with Giemsa and NADH-diaphorase. We verified that the diabetes did not alter the shape and disposition of the myenteric ganglia; it provoked decrease on the neuronal density and increase on the incidence of weakly basophilic neurons. The effects of streptozotocin caused dilatation of the cecum still evidenced two months after induction, but no more observed on the eight months after induction. The smaller incidence of neurons in group D8 relative to group C8 was due to the early loss related to the drug toxicity and later to the aging in diabetic condition.

-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 ...

-We carried out this study with the purpose of analyzing the density of neurons of the myenteric plexus in the mesenteric, intermediate and antimesenteric regions of the ileum of rats. We conclude that there is a variation of neuronal density around the intestinal circumference and this fact independs on the technique used to stain the neurons, and that in a single region the neuronal density varies with the technique employed. We also call attention for the identification of the site were countings were carried out, so that the results of research in this area are not compromised.KEY WORDS: myenteric plexus, Giemsa, NADPH-diaphorase, NADH-diaphorase, acetylcholinesterase, rat, ileum.Diferenças regionais no número e tipo de neurônios mientéricos do íleo de ratos: comparação entre técnicas de evidenciação neuronal RESUMO -Realizamos este estudo com o objetivo de analisar a densidade de neurônios do plexo mientérico nas regiões mesentérica, intermediária e antimesentérica do íleo de ratos. Empregamos preparados de membrana corados por 4 diferentes técnicas. Através de contagens sob microscópio óptico em uma área de 8,96 mm 2 encontramos com as técnicas de Giemsa, histoquímica da NADH-diaforase, NADPH-diaforase e acetilcolinesterase, respectivamente as seguintes médias neuronais: região mesentérica 2144, 40±161,05, 1657,80±88,23, 473,80±19,62, 905,25±22,40; região intermediaria 1790,60±128,24, 1265,20±141,17, 371,30±27,84, 770,25±33,12; região antimesentérica 1647,0±76,67, 981,80±68,04, 298,50±22,75, 704,50±69,38. Concluimos que há uma variação na densidade neuronal ao redor da circunferência intestinal, e este fato independe da técnica utilizada para marcar os neurônios, e que em uma mesma região, a densidade neuronal varia com a técnica utilizada. Também chamamos a atenção para que seja indicado o local onde as quantificações serão realizadas, para que não haja comprometimento dos resultados em pesquisa nesta área.

The effect of vitamin E (1 g/kg body weight) supplementation on myosin-V and neuronal nitric oxide synthase (nNOS) immunoreactive myenteric neurons from the ileum of diabetic rats was investigated in the present study. Forty animals were divided into the following groups: normoglycemics (N), normoglycemics treated with vitamin E (NE), diabetics (D), and diabetics treated with vitamin E (DE). Quantitative and morphometric analyses were performed. The area of the tertiary plexus was also determined. Diabetes produced a 24% reduction in the number of myosin-V neurons in group D compared with group N, an effect that was accompanied by an increase in the tertiary plexus area (P < 0.05). Neuronal density was 27% higher in group NE than group N (P < 0.05). Nitrergic neuronal density was not altered as a consequence of either diabetes or vitamin E treatment. Myosin-V and nNOS immunoreactive neuronal cell body area increased significantly in group NE. The area of myosin-V and nNOS myenteric neurons also increased in group D. Vitamin E treatment (group DE) increased only the size of nitrergic neurons. The present results suggest that vitamin E elicited a neuroprotective and neurotrophic effect on the natural aging process, but with regard to diabetes, vitamin E supplementation exerted a neurotrophic effect only on nitrergic neurons.