O Sistema nervoso entérico está localizados entre as camadas constituintes das paredes do trato gastrintestinal, entre as camadas musculares longitudinal e circular, que se estende por todo o trato digestório, desde o esôfago até o reto. Desordens gastrintestinais são complicações comuns causadas pela lesão térmica. A presente pesquisa avalia, em estômagos de ratos alterações na mucosa e no plexo mioentérico submetidos à lesão térmica corporal. O número de neurônios NADH-d e NADPH-d aumentaram significativamente nos animais queimados. Analisando a média da área do perfil dos neurônios NADH-dr e NADPH-dr evidenciaram uma diminuição significativa de 26% e 24%, respectivamente, na área do perfil dos neurônios dos animais queimados. Assim, associados o VIP o NO e a acetilcolina se apresentaram de maneira a interferir no esvaziamento gástrico causando ulcerações que foram observadas pela técnica da MEV na mucosa gástrica. Com esses dados, pode-se concluir que a LTC interfere no plexo mioentérico do estômago de ratos causando uma gastroparesia. / The enteric nervous system is located among the layer constituents of the gastrintestinal tract. Between the longitudinal and circular muscle layers, which extend throughout the digestory tract from the esophagus to the rectum. Gastrintestinal disorders are common complications caused by burn injury. This research evaluates, in stomach of rats changes in the mucosal and myenteric plexus, subjected burn injury. The number of neurons NADH-d and NADPH-d significantly increased in burned animals. Analyzing the average area of the profile of the neurons NADH-dr and NADPH-dr, showed a significant decrease of 26% and 24%, respectively, in the area of the profile of the neurons of the burned animals. Thus, the association of VIP, NO and acetylcholine is presented so as to interfere with gastric emptying causing changes in the mucosal wich were observed by the technique of MEV. With this data, it can be conclude that the burn injury interferes in the myenteric plexus of the stomach of rats causing a gastroparesis.

A distrofia muscular do Golden Retriever é uma doença degenerativa de caráter hereditário com alterações musculares semelhantes às descritas na distrofia muscular de Duchenne, sendo comprovada a existência de alterações na musculatura lisa do trato gastrointestinal destes animais. Alguns autores sugerem que um dos fatores responsáveis por essas alterações possa estar relacionado com a motililidade intestinal. Este trabalho tem como objetivo estudar os neurônios nitrérgicos e colinérgicos, além da expressão do receptor P2X7, no plexo mioentérico do cólon descendente de cães afetados e não afetados pela distrofia muscular. Foram utilizadas técnicas de imunohistoquímica para marcação das enzimas Óxido Nítrico Sintase (NOS) e Acetilcolina Transferase (ChAT) e da população neuronal total pelo HuC/D e analisada a presença do receptor P2X7. Também foram utilizadas técnicas de microscopia eletrônica de transmissão e histologia básica. Os resultados indicam que neurônios nitrérgicos tendem a ser maiores em cães distróficos e apresentam morfologia Dogiel tipo I; neurônios que expressam o receptor P2X7 colocalizam com neurônios nitrérgicos e colinérgicos. As análises qualitativas demonstram que cães distróficos apresentam maior quantidade de colágeno entre as fibras musculares, entre as camadas musculares circular e longitudinal e, ainda, no interior dos gânglios mioentéricos. Este estudo fornece base para futuras pesquisas e tratamentos da distrofia muscular do Golden Retriever e mais futuramente da Distrofia Muscular de Duchenne, além de poder auxiliar no entendimento das desordens gastrointestinais que são observadas nesta última. / The golden retriever muscular dystrophy is a hereditary degenerative disease characterized by muscle changes similar to those described in Duchenne muscular dystrophy, as well as by alterations in the smooth muscles of the gastrointestinal tract. Some authors suggest that these abnormalities may be associated with intestinal motility. This study evaluated nitrergic and cholinergic neurons in the myenteric plexus of the descending colon of dogs with and without muscular dystrophy, in addition to P2X7 receptor expression. Immunohistochemical techniques were used to label nitric oxide synthase (NOS) and acetylcholine transferase (ChAT), as well as to label total HuC/D-immunoreactive neurons and neurons containing the P2X7 receptor. Transmission electron microscopy and basic histology were used for analysis. Results showed that nitrergic neurons tend to be larger in dystrophic dogs and to be characterized by Dogiel type I morphology, and neurons that express the P2X7 receptor colocalize with nitrergic and cholinergic neurons. Transmission and light microscopy revealed higher collagen density between muscle fibers, between circular and longitudinal muscle layers and within myenteric ganglia of affected dogs. These findings provide support for future research and treatment of the golden retriever muscular dystrophy and hence of the Duchenne muscular dystrophy and contribute to the understanding of the gastrointestinal disorders found in these patients.

For the purpose of developing an effective therapeutic strategy for HSCR, the enteric neural crest stem cells were investigated firstly which were isolated from the E14.5 mouse embryonic gut, cultured as neurospheres and characterized by multiple immunofluorescence and reverse transcription-PCR, population doubling time, frequency of forming secondary neurospheres and limited dilution assay. In the differentiation culture medium, several types of cells were induced to form from the neurospheres derived from single cells. Hence the putative enteric neural crest stern cells, which were isolated from the embryonic mouse gut tube and cultured as neurospheres for many passages ex vivo with the demonstrated capacity of proliferation, self-renewal and differentiation, showed properties of stem cells. / Hirschsprung's disease (HSCR) is caused by the absence of the enteric neural crest-derived neurons at the distal region of the gut. Cell-based therapy using stem cells or progenitors gives the potential to supplement these missing enteric neurons in the gut. Enteric neural crest stem cells isolated from the human or rodent gut can give rise to neurons and glia after they are transplanted into the recipient guts of the mouse or rat. However, numbers of issues are unresolved about the basic biology of the enteric nervous system, the characteristics of the stem cells isolated from the enteric nervous system and the biological significance of these cells in prenatal and postnatal periods. In this study, the characteristics and therapeutic potential on HSCR of the enteric neural crest stem cells were explored. / In addition to the above, a recombination organotypic gut culture ex vivo showed that the colonization of enteric neural crest-derived cells in the recipient gut was influenced not only by the genotypes of enteric neural crest-derived cells themselves but also the microenvironment of the gut through which enteric neural crest-derived cells migrated. For instance, the developmental stage of the recipient gut and also the presence of endogenous enteric neural crest-derived cells along the migratory pathway of neural crest-derived cells both affected the extent of the migration and colonization of exogenous enteric neural crest-derived cells and stem cells. The gradual maturation and differentiation of the neighboring structures, such as the smooth muscle layer, during the time period of the enteric neural crest cells migration, might also suggest that these neighboring tissues may have a role in regulating the neural crest-derived cells migration. / In conclusion, enteric neural crest stem cells isolated from the embryonic mouse gut tube showed properties of stem cells, and had the potential to compensate missing enteric neural crest-derived cells both ex vivo and in vivo. However, the colonization of enteric neural crest-derived cells in the developing gut was affected cell-autonomously and also by the microenvironment of the gut and the presence of existing enteric neural crest-derived cells. / Their potential applications in the transplantation experiments were shown by transplantation of the neurospheres isolated to the gut tube maintained in an organotypic culture or to the descending colon of neonates at postnatal day 7. The development of the enteric neural crest stern cells from the neurospheres was found to be compatible to endogenous enteric neural crest-derived cells in the recipient gut as evidenced by the formation of interconnected cellular networks of donor stem cells and endogenous neural crest-derived cells. The enteric neural crest stem cells also possess the potential to compensate the loss of enteric neural crest-derived cells ex vivo and in vivo in recipient prenatal and postnatal guts. / Bao, Lihua. / Adviser: Wood Yee Chan. / Source: Dissertation Abstracts International, Volume: 73-01, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 208-228). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

A isquemia aguda mesentérica é uma condição de grande emergência vascular, que é fatal na população mundial em 60% a 80% dos casos. O objetivo desse trabalho foi estudar, os efeitos da isquemia/reperfusão intestinal sobre o receptor P2X2 e diferentes classes neuronais no plexo mioentérico. Foram analisados o íleo de ratos: controle, Sham e isquemia/reperfusão intestinal (I/R-i) com de 24h e 1 semana de reperfusão. Foram realizadas colocalização do receptor P2X2 com a NOS, ChAT, Calb, Calr, S100 e anti-HuC/D. Os resultados mostraram diminuição de neurônios P2X2-ir colocalizados com a NOS, ChAT e Hu, e um aumento com S100 no grupo I/R-i 1 semana. A densidade apresentou um aumento de células P2X2-ir e S100 e diminuição de ChAT e Hu no grupo I/R-i de 1 semana. O perfil neuronal apresentou um aumento nos neurônios NOS-ir, ChAT, Calb (Dogiel Tipo II) e Calr. Conclui-se que a isquemia levou a alterações diferenciadas no receptor P2X2, células gliais e neurônios entéricos, que podem causar disfunções gastrintestinais, como por exemplo, problemas na motilidade intestinal. / The acute mesenteric ischemia is a vascular condition of extreme emergency, which is fatal in the world population by 60% to 80% of cases. The aim of this work was to study the effects of intestinal ischemia/reperfusion on the P2X2 receptor and different neuronal classes in the myenteric plexus. We analyzed the ileum of rats: control, Sham and ischemia/reperfusion (I/R-i) with 24 hours and 1 week of reperfusion. The colocalization were performed by P2X2 receptor with NOS, ChAT, Calb, Calr, S100 and anti-HUC/D. The results showed a decrease of P2X2-ir neurons colocalizated with ChAT and Hu, and an increase in the group with S100 in the I/R-i 1 week group. The density of cells showed an increase of P2X2-ir and S100 and a decrease of Hu and ChAT in I/R-i 1 week group. The profile area showed an increase in NOS-ir, ChAT-ir, Calb (Dogiel Type II) and Calr-ir neurons. We conclude that ischemia led to different changes in P2X2 receptor, enteric neurons and glial cells, which can cause gastrointestinal disorders, such as intestinal motility disorder.

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system that causes motor, visual, and sensory symptoms. Patients also experience constipation, which is not yet understood, but could involve dysfunction of the enteric nervous system (ENS). Autoimmune targeting of the ENS occurs in other autoimmune diseases that exhibit gastrointestinal (GI) symptoms, and similar mechanisms could lead to GI dysfunction in MS. Here, we characterize GI dysmotility in the experimental autoimmune encephalomyelitis (EAE) model of MS and test whether autoantibodies targeting the ENS are present in the serum of MS patients. Male SJL or B6 mice were induced with EAE by immunization against PLP139-151, MOG35-55, or mouse spinal cord homogenate, and monitored daily for somatic motor symptoms. EAE mice developed GI symptoms consistent with those observed in MS. In vivo motility analysis demonstrated slower whole GI transit, and decreased colonic propulsive motility. EAE mice had faster rates of gastric emptying, with no changes in small intestinal motility. Consistent with these results, ex vivo evaluation of isolated colons demonstrated that EAE mice have slower colonic migrating myoelectric complexes and slow wave contractions. Immunohistochemistry of EAE colons exhibited a significant reduction in GFAP area of ENS ganglia, with no changes in HuD, S100, or neuron numbers. To test whether antibodies in MS bind to ENS structures, we collected serum samples from MS patients with constipation and without constipation, and healthy control patients without constipation. Immunoreactivity was tested using indirect immunofluorescence by applying serum samples to guinea pig ENS tissue. MS serum exhibited significantly higher immunoreactivity against guinea pig ENS than control patients, which was particularly evident in MS patients who did not experience constipation. There was no significant difference in immunoreactivity between MS patients with and without constipation. Targets of human MS and mouse EAE serum include enteric glia and neurons. Taken together, these data validate EAE as a model for constipation in MS, and support the concept that this symptom involves changes within the neuromuscular system of the colon. EAE mice develop symptoms consistent with constipation that affects functional ENS networks and may result in structural or phenotypic changes at the cellular level. Serum immunoreactivity suggests that autoantibodies could play a role in the development of constipation in MS by targeting the ENS itself.

Orientador: Renata de Britto Mari / Resumo: A leishmaniose visceral é considerada a forma clínica mais grave das leishmanioses. É causada pelo parasita da espécie Leishmania chagasi que pode ser transmitida para animais silvestres, animais domésticos e também para o homem e que vem expandindo seu território. A infecção atinge principalmente o baço, o fígado e a medula óssea, porém, a infecção também atinge outros sistemas do organismo, como o trato gastrointestinal (TGI). O TGI é controlado pelo sistema nervoso entérico (SNE) que tem como função controlar o fluxo sanguíneo, relaxamento e contração da musculatura lisa local, agindo de maneira independente do sistema nervoso central, mas mantendo contato através do eixo cérebro-intestinal. Além disso, tem relação com o sistema imunológico, visto que o intestino é considerado o maior órgão imune do corpo. Os neurônios mioentéricos do SNE são responsáveis por toda motilidade do TGI sofrendo alterações sempre que sofrem algum tipo de estresse, como por envelhecimento, dietas e até mesmo doenças. Essas alterações mostram a plasticidade neuronal para que seja mantida sempre a homeostase do intestino. Portanto, visto a importância do SNE para o funcionamento adequado do organismo, o objeivo desse trabalho foi observar como o parasitismo causado por L. chagasi atinge o intestino delgado de hamsters em diferentes períodos, avaliando a plasticidade neuronal ao decorrer da infecção parasitária. Para isso foram utilizados hamsters dourados que foram divididos em grupo controle e ex... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Visceral leishmaniasis is considered the most severe clinical form of leishmaniasis. It is caused by the parasite of the species Leishmania chagasi that can be transmitted to wild animals, domestic animals and also to the human and, it has been expanding its territory. The infection mainly affects the spleen, liver and bone marrow, but the infection can also affect other systems of the body, such as the gastrointestinal (GI) tract. GI tract is controlled by the enteric nervous system (ENS), whose function is to control blood flow, relaxation and contraction of the local smooth muscle, acting independently of the central nervous system, but maintaining contact through the cerebellar-intestinal axis. In addition, it is related to the immune system, since the intestine is considered the largest immune organ in the body. The myenteric neurons of the ENS are responsible for all the motility of the GI tract undergoing changes whenever they suffer some type of stress, such as by aging, diets and even illnesses. These changes show the neuronal plasticity so that intestinal homeostasis is always maintained. The objective of this work was to observe how the parasitism caused by L. chagasi reaches the small intestine of hamsters in different periods, evaluating the neuronal plasticity during the parasitic infection. For this purpose, golden hamsters were used, which were divided into control and experimental groups. The animals were euthanized after 30, 60 and 90 days of infection and f... (Complete abstract click electronic access below) / Mestre

Made available in DSpace on 2014-06-11T19:33:26Z (GMT). No. of bitstreams: 0 Previous issue date: 2006-01-18Bitstream added on 2014-06-13T21:06:07Z : No. of bitstreams: 1 neves_mf_dr_jabo.pdf: 706059 bytes, checksum: 19061e8d0f78f8eea19e6d3f8b802f9d (MD5) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Para estudar a cinética populacional de células imune/inflamatórias na infecção natural por Toxocara vitulorum em bezerros búfalos, realizou-se a quantificação de mastócitos, eosinófilos, linfócitos intraepiteliais (LIE) e células caliciformes na camada intraepitelial e de macrófagos na parede do intestino delgado. Para isto, amostras de tecidos foram retiradas do duodeno, jejuno e íleo de seis grupos de animais, de acordo com o resultado do exame coprológico, ou seja: animais que estavam no início ou ascensão (1), no pico (2) do parasitismo, durante as fases de declínio ou expulsão (3), e de pós-expulsão dos parasitas (4), além de dois grupos controles de animais não parasitados por T. vitulorum com idades médias entre 30 (C30) e 50 (C50) dias. Pelo estudo morfológico, feito através de mensurações de todas as camadas da parede do intestino delgado, constatou-se somente uma significativa atrofia vilosa no duodeno, durante as fases de ascensão, de pico e de expulsão do parasita, mas a hipertrofia muscular não foi observada. Concluiu-se que a infecção pelo nematódeo T. vitulorum em bezerros búfalos foi responsável pela hiperplasia celular (LIEs, células caliciformes, eosinófilos e mastócitos) na camada intraepitelial e pela interação entre mastócitos e processos nervosos na mucosa, nos plexos submucoso e mioentérico. Como estas alterações celulares predomindando no pico da infecção normalizaram-se após a expulsão, concluiu-se também que elastiveram participação no mecanismo imunológico celular de controle e expulsão do parasita pelo hospedeiro. O macrófago presente em maior quantidade na fase da pós-expulsão sugeriu uma importante participação destas células na recuperação das lesões inflamatórias nesta infecção. / The populational kinetics of immune/inflammatory cells was studied in the wall of the small intestine from buffalo calves naturally infected with Toxocara vitulorum. Samples of tissues were removed from duodenum, jejunum and ileum of four groups of animals during the beginning of the infection, at the peak of egg output, during the period of expulsion and post-expulsion of the worms, as well as from uninfected calves. Cells (mast cells, eosinophils, intraepithelial lymphocytes - IEL and goblet cells) present in the epithelial layer (intraepithelial) of the small intestine were counted. In the duodenum, jejunum and ileum, the population of mast cells, eosinophils and lymphocytes increased significantly during the peak of the infection. Goblet cell numbers increased also during the beginning and at the peak of the infection. The decline of the number of these cells occurred during the periods of expulsion of the worms reaching to uninfected control counts at the post-expulsion period indicated a role of these cells in the process of expulsion of T. vitulorum by the buffalo calves. Morphological examinations showed a significant vilar atrophy, particularly in the duodenum during the beginning, peak and during the phase of expulsion of the worms, but smooth muscle hypertrophy or other alteration was not observed in any phase of the infection. In conclusion, the infection by T. vitulorum in buffalo calves elicited cellular hyperplasy of LIEs, goblet cells, eosinophils and mast cells in the intraepithelial layer of the small intestines and association between mast cells and nervous process in the mucosa and in the submucosal and mioentérico plexa, these cellular changes might be important for the worm expulsion. The macrophages presents in high numbers in the post-expulsion phase might have important role in the recovery of the infection.

Constipation is a serious public health problem that afflicts thousands of patients worldwide. It is believed that with the modern lifestyle, followed by constant stress and inadequate eating habits, the incidence of constipation will increase considerably in coming decades. Constipation is caused by abnormal functioning of the digestive tract which is not yet fully elucidated. It is known that the enteric nervous system is responsible for sensory and motor functions of the digestive tract, which makes it work in perfect sync and perform peristalsis, promoting proper transit of the bolus and subsequently fecal mass. The vast majority of pathologies afflicting the gastrointestinal tract are originated from disturb in specific neurons in the enteric nervous system and probably the same happens with constipation. Hence, the objective of this study was, by immunohistochemistry, to characterize and compare the expression of several neuropeptides of the enteric nervous system in patients with constipation and individuals not constipated. The results showed that among the various types of neurons studied, constipated patients have fewer neurons expressing calretinin and choline acetyltransferase, characteristic neuropeptides from afferent neurons and excitatory neurons engines. We believe that these results can help in future treatment techniques and prevention of constipation. / A constipação intestinal é um problema grave de saúde pública que aflige milhares de pacientes em todo o mundo. Acredita-se que, com o estilo de vida moderno, seguido de constante estresse e inadequação dos hábitos alimentares, a incidência da constipação intestinal aumente consideravelmente nas próximas décadas. A constipação é causada por alterações no funcionamento do trato digestório que ainda não estão completamente elucidadas. Sabe-se que o sistema nervoso entérico é responsável pelas funções sensitivas e motoras do trato digestivo, o que confere a este funcionar sob perfeita sincronia e realizar a peristalse, promovendo o trânsito adequado do bolo alimentar e posteriormente do bolo fecal. A grande maioria das patologias que afligem o trato gastrointestinal são originadas de distúrbios em neurônios específicos do sistema nervoso entérico e, provavelmente, o mesmo ocorre com a constipação intestinal. Diante disto, o objetivo deste trabalho foi, através da técnica de imunohistoquímica, caracterizar e comparar a expressão dos diversos neuropeptídios do sistema nervoso entérico em pacientes portadores de constipação intestinal e indivíduos não constipados. Os resultados demonstraram que, dentre os vários tipos de neurônios estudados, os pacientes constipados apresentam uma menor quantidade de neurônios que expressam calretinina e colina-acetiltransferase, neuropeptídios característicos de neurônios aferentes e de neurônios motores excitatórios. Acreditamos que esses resultados possam colaborar com futuras técnicas de tratamento e com a prevenção da constipação intestinal. / Mestre em Ciências da Saúde

O Sistema nervoso entérico está localizados entre as camadas constituintes das paredes do trato gastrintestinal, entre as camadas musculares longitudinal e circular, que se estende por todo o trato digestório, desde o esôfago até o reto. Desordens gastrintestinais são complicações comuns causadas pela lesão térmica. A presente pesquisa avalia, em estômagos de ratos alterações na mucosa e no plexo mioentérico submetidos à lesão térmica corporal. O número de neurônios NADH-d e NADPH-d aumentaram significativamente nos animais queimados. Analisando a média da área do perfil dos neurônios NADH-dr e NADPH-dr evidenciaram uma diminuição significativa de 26% e 24%, respectivamente, na área do perfil dos neurônios dos animais queimados. Assim, associados o VIP o NO e a acetilcolina se apresentaram de maneira a interferir no esvaziamento gástrico causando ulcerações que foram observadas pela técnica da MEV na mucosa gástrica. Com esses dados, pode-se concluir que a LTC interfere no plexo mioentérico do estômago de ratos causando uma gastroparesia. / The enteric nervous system is located among the layer constituents of the gastrintestinal tract. Between the longitudinal and circular muscle layers, which extend throughout the digestory tract from the esophagus to the rectum. Gastrintestinal disorders are common complications caused by burn injury. This research evaluates, in stomach of rats changes in the mucosal and myenteric plexus, subjected burn injury. The number of neurons NADH-d and NADPH-d significantly increased in burned animals. Analyzing the average area of the profile of the neurons NADH-dr and NADPH-dr, showed a significant decrease of 26% and 24%, respectively, in the area of the profile of the neurons of the burned animals. Thus, the association of VIP, NO and acetylcholine is presented so as to interfere with gastric emptying causing changes in the mucosal wich were observed by the technique of MEV. With this data, it can be conclude that the burn injury interferes in the myenteric plexus of the stomach of rats causing a gastroparesis.

A isquemia aguda mesentérica é uma condição de grande emergência vascular, que é fatal na população mundial em 60% a 80% dos casos. O objetivo desse trabalho foi estudar, os efeitos da isquemia/reperfusão intestinal sobre o receptor P2X2 e diferentes classes neuronais no plexo mioentérico. Foram analisados o íleo de ratos: controle, Sham e isquemia/reperfusão intestinal (I/R-i) com de 24h e 1 semana de reperfusão. Foram realizadas colocalização do receptor P2X2 com a NOS, ChAT, Calb, Calr, S100 e anti-HuC/D. Os resultados mostraram diminuição de neurônios P2X2-ir colocalizados com a NOS, ChAT e Hu, e um aumento com S100 no grupo I/R-i 1 semana. A densidade apresentou um aumento de células P2X2-ir e S100 e diminuição de ChAT e Hu no grupo I/R-i de 1 semana. O perfil neuronal apresentou um aumento nos neurônios NOS-ir, ChAT, Calb (Dogiel Tipo II) e Calr. Conclui-se que a isquemia levou a alterações diferenciadas no receptor P2X2, células gliais e neurônios entéricos, que podem causar disfunções gastrintestinais, como por exemplo, problemas na motilidade intestinal. / The acute mesenteric ischemia is a vascular condition of extreme emergency, which is fatal in the world population by 60% to 80% of cases. The aim of this work was to study the effects of intestinal ischemia/reperfusion on the P2X2 receptor and different neuronal classes in the myenteric plexus. We analyzed the ileum of rats: control, Sham and ischemia/reperfusion (I/R-i) with 24 hours and 1 week of reperfusion. The colocalization were performed by P2X2 receptor with NOS, ChAT, Calb, Calr, S100 and anti-HUC/D. The results showed a decrease of P2X2-ir neurons colocalizated with ChAT and Hu, and an increase in the group with S100 in the I/R-i 1 week group. The density of cells showed an increase of P2X2-ir and S100 and a decrease of Hu and ChAT in I/R-i 1 week group. The profile area showed an increase in NOS-ir, ChAT-ir, Calb (Dogiel Type II) and Calr-ir neurons. We conclude that ischemia led to different changes in P2X2 receptor, enteric neurons and glial cells, which can cause gastrointestinal disorders, such as intestinal motility disorder.