Survival and neurotransmitter plasticity in cultured rat colonic myenteric neurons

Kristensson, Elin; Themner-Persson, Anna; Ekblad, Eva

doi:10.1016/j.regpep.2006.11.024

Cited by 8 publications

(6 citation statements)

References 21 publications

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“…Our finding of a modest increase in VIP-IR neurons after colonic ischemia is in contrast to a previous study on I/R-exposed rat small intestine in which the number of VIP-IR neurons was found to markedly increase as compared to sham-operated intestine [9]. This discrepancy probably illustrates differences in neuronal plasticity between small and large intestine, in accordance with previous findings [37]. The finding of an increased VIP expression also in shamoperated small intestine [9] is in line with our present finding on the colon and provides further support to the theory that myenteric neurons with the ability to express VIP do so in stressful situations as a neuroprotective mechanism.…”

Section: Discussionsupporting

confidence: 77%

“…This since enteric neuronal VIP expression is upregulated in several pathophysiological situations, such as blockade of axonal transport or axotomy [24], intestinal hypertrophy [25], or ischemia [9], and in patients with Crohn's disease [34]. Furthermore, in vitro studies, e.g., primary culture of myenteric neurons from porcine or rat small and large intestine, show that the proportion of neurons expressing VIP markedly increases compared to in vivo [23,[35][36][37]. Addition of VIP to cultured rat small intestine myenteric neurons promotes neuronal survival [35,36] and recently it was shown that VIP, when added to cultured myenteric neurons from rat small intestine in combination with lipopolysaccharide (LPS), markedly reduces LPS-induced neuronal cell death [38].…”

Section: Discussionmentioning

confidence: 99%

“…Studies performed on intestinal I/R have shown that inhibition of NO synthesis causes tissue dysfunction in certain models and provides benefit in others [9,40]. The controversy on NO neuroprotection is also reflected in in vitro studies where addition of a NO donor to primary myenteric neuronal cultures from rat small intestine increases neuronal survival [35] while cultured myenteric neurons from porcine small intestine [41] and rat colon [37] are unaffected. The present study revealed increased number of colonic myenteric neurons expressing NOS one day after exposure to ischemia, as compared to sham.…”

Section: Discussionmentioning

confidence: 99%

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Infiltration of Mast Cells in Rat Colon Is a Consequence of Ischemia/Reperfusion

2008

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Intestinal ischemia as well as mastocytosis occur in patients with inflammatory bowel disease and irritable bowel syndrome. Our aim was to clarify how ischemia with reperfusion (I/R) affects the structure, enteric neurons, and immune cells in the colon. Rats were subjected to colon ischemia for 1 h and reperfused for 1 day up to 20 weeks; sham-operated rats were used as controls. No structural remodeling of the intestinal segment was detected after I/R. The number and distribution of eosinophils were not affected by I/R. Local areas containing numerous mast cells were detected in the muscle layers, the serosa, and in and around the myenteric ganglia 4-20 weeks post ischemia. It was notable that myenteric ganglionic formations within mast-cell-rich areas virtually lacked neurons. Mast cells were rarely found in controls. In conclusion, I/R of the colon attracts mast cells, and death of myenteric neurons occurs in such locations.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Infiltration of Mast Cells in Rat Colon Is a Consequence of Ischemia/Reperfusion

2008

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“…LMMP neurons were cultured using slightly modified method (35). CRF 1 and CRF 2 receptors expression was determined using RT-PCR on 0.1 μg of poly A + RNA isolated from non-fixed 5 days old primary culture cells by oligo-dT cellulose spin column (FastTrack 2.0 Kit, Invitrogen).…”

Section: Methodsmentioning

confidence: 99%

Activation of Corticotropin-Releasing Factor Receptor 2 Mediates the Colonic Motor Coping Response to Acute Stress in Rodents

Gourcerol

Yuan

et al. 2011

Gastroenterology

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Background & Aims Corticotropin-releasing factor receptor-1 (CRF1) mediates the stress-induced colonic motor activity. Less is known about the role of CRF2 in the colonic response to stress. Methods We studied colonic contractile activity (CCA) in rats and CRF2-/-, CRF-overexpressing, and wild-type mice using still manometry; we analyzed defecation induced by acute, partial-restraint stress (PRS), and/or intraperitoneal (IP) injection of CRF ligands. In rats, we monitored activation of the colonic longitudinal muscle myenteric plexus (LMMP) neurons and localization of CRF1 and CRF2 using immunohistochemical and immunoblot analyses. We measured phosphorylation of ERK1/2 by CRF ligands in primary cultures of LMMP-neurons (PC-LMMPn) and cAMP production in HEK-293 cells transfected with CRF1 and/or CRF2. Results In rats, a selective agonist of CRF2 (urocortin 2) reduced CRF-induced defecation (>50%), CCA, and Fos expression in the colonic LMMP. A selective antagonist of CRF2 (astressin2-B) increased these responses. Urocortin 2 reduced PRS-induced CCA in wild-type and CRF-overexpressing mice, whereas disruption of CRF2 increased PRS-induced CCA and CRF-induced defecation. CRF2 co-localized with CRF1 and neuronal nitric oxide synthase in the rat colon, LMMP, and PC-LMMPn. CRF-induced phosphorylation of ERK in PC-LMMPn; this was inhibited or increased by a selective antagonist of CRF1 (NBI35965) or astressin2-B, respectively. The EC50 for the CRF-induced cAMP response was 8.6 nM in HEK-293 cells that express only CRF1; this response was suppressed 10-fold in cells that express CRF1 and CRF2. Conclusions In colon tissues of rodents, CRF2 activation inhibits CRF1 signaling in myenteric neurons and the stress-induced colonic motor responses. Disruption of CRF2 function impairs colonic coping responses to stress.

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“…In general, the expression of somatostatin in the gastrointestinal tract has been studied in various animal species and in humans [31][32][33][34][35][36]. One of the first animal species in which the distribution of SOM in the digestive tract was described was the guinea pig [14].…”

Section: Discussionmentioning

confidence: 99%

The Influence of a Hyperglycemic Condition on the Population of Somatostatin Enteric Neurons in the Porcine Gastrointestinal Tract

Bulc

Palus

Całka

2020

Animals

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Somatostatin (SOM) is the most common agent in the gastrointestinal (GI) tract that is involved in the regulation of several gastric functions, as well as in gastric disorders. Hyperglycemia, which develops as a consequence of improperly treated diabetes, can cause numerous disturbances in the appropriate functioning of the gastrointestinal tract. High glucose level is toxic to neurons. One of the lines of defense of neurons against this glucotoxicity are changes in their chemical coding. To better understood the role of SOM secreted by enteric neurons in neuronal response on elevated glucose level, pancreatic β cells were destroyed using streptozotocin. Due to the close similarity of the pig to humans, especially the GI tract, the current study used pigs as an animal model. The results revealed that the number of enteric neurons immunoreactive to SOM (SOM-IR) in a physiological state clearly depend on the part of the GI tract studied. In turn, experimentally induced diabetes caused changes in the number of SOM-IR neurons. The least visible changes were observed in the stomach, where an increase in SOM-IR neurons was observed, only in the submucosal plexus in the corpus. However, diabetes led to an increase in the population of myenteric and submucosal neurons immunoreactive to SOM in all segments of the small intestine. The opposite situation occurred in the descending colon, where a decrease in the number of SOM-IR neurons was visible. This study underlines the significant role of SOM expressed in enteric nervous system neurons during diabetes.

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Survival and neurotransmitter plasticity in cultured rat colonic myenteric neurons

Cited by 8 publications

References 21 publications

Infiltration of Mast Cells in Rat Colon Is a Consequence of Ischemia/Reperfusion

Infiltration of Mast Cells in Rat Colon Is a Consequence of Ischemia/Reperfusion

Activation of Corticotropin-Releasing Factor Receptor 2 Mediates the Colonic Motor Coping Response to Acute Stress in Rodents

The Influence of a Hyperglycemic Condition on the Population of Somatostatin Enteric Neurons in the Porcine Gastrointestinal Tract

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