Choline acetyltransferase and inducible nitric oxide synthase are increased in myenteric plexus of diabetic guinea pig

LePard, Kathy J.

doi:10.1016/j.autneu.2004.12.002

Cited by 29 publications

(44 citation statements)

References 58 publications

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“…Previously, a similar shrinkage in ganglia was seen in the diabetic guinea pig (LePard 2005). Mean ganglionic sizes were not significantly different between 8-week SC diet, 8- week HF diet, and 20-week SC diet-ingesting mice (8-week data not shown), showing that the shrinkage was independent of age.…”

Section: Discussionsupporting

confidence: 77%

Prolonged high fat diet ingestion, obesity, and type 2 diabetes symptoms correlate with phenotypic plasticity in myenteric neurons and nerve damage in the mouse duodenum

et al. 2015

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Symptoms of diabetic gastrointestinal dysmotility indicate neuropathy of the enteric nervous system. Long-standing diabetic enteric neuropathy has not been fully characterized, however. We used prolonged high fat diet ingestion (20 weeks) in a mouse model to mimic human obese and type 2 diabetic conditions, and analyzed changes seen in neurons of the duodenal myenteric plexus. Ganglionic and neuronal size, number of neurons per ganglionic area, density indices of neuronal phenotypes (immunoreactive nerve cell bodies and varicosities per ganglion or tissue area) and nerve injury were measured. Findings were compared with results previously seen in mice fed the same diet for 8 weeks. Compared to mice fed standard chow, those on a prolonged high fat diet had smaller ganglionic and cell soma areas. Myenteric VIP- and ChAT-immunoreactive density indices were also reduced. Myenteric nerve fibers were markedly swollen and cytoskeletal protein networks were disrupted. The number of nNOS nerve cell bodies per ganglia was increased, contrary to the reduction previously seen after 8 weeks, but the density index of nNOS varicosities was reduced. Mice fed high fat and standard chow diets experienced an age-related reduction in total neurons, biasing towards neurons of sensory phenotype. Meanwhile ageing was associated with an increase in excitatory neuronal markers. Collectively, these results support a notion that nerve damage underlies diabetic symptoms of dysmotility, and reveals adaptive ENS responses to the prolonged ingestion of a high fat diet. This highlights a need to mechanistically study long-term diet-induced nerve damage and age-related impacts on the ENS.

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Section: Discussionsupporting

confidence: 77%

Prolonged high fat diet ingestion, obesity, and type 2 diabetes symptoms correlate with phenotypic plasticity in myenteric neurons and nerve damage in the mouse duodenum

et al. 2015

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“…Participation of Ca þ þ -independent NOS, such as iNOS, is also possible (Starkey et al, 2001). Spontaneous NO release from the guinea pig ileum, human colon and mouse ileum involves both nNOS and iNOS (LePard, 2005;Bagyánski et al, 2011;Giaroni et al, 2013). It is, thus, possible that, in guinea pig ileum, NMDA receptors modulate NO production from myenteric neurons by activating both nNOS and iNOS.…”

Section: Discussionmentioning

confidence: 94%

Interaction between NMDA glutamatergic and nitrergic enteric pathways during in vitro ischemia and reperfusion

Filpa

Carpanese

Marchet

et al. 2015

European Journal of Pharmacology

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“…A decrease in neuronal density is paralleled by an increase in the area occupied by the tertiary plexus composed of axons that innervate the longitudinal muscular tunica located between the primary and secondary components of the myenteric plexus (Lepard 2005). Vitamin E treatment in group DE resulted in a 12% higher number of myosin-V immunoreactive myenteric neurons compared with group D. The neuronal density in group DE was preserved at 50% compared with the neuronal loss exhibited by group D. Cotter et al (1995), using a vitamin E dosage similar to the present study, reported that vitamin E treatment prevented the decrease of motor nerve conduction velocity caused by DM.…”

Section: Discussionmentioning

confidence: 98%

Vitamin E supplementation in rats with experimental diabetes mellitus: analysis of myosin-V and nNOS immunoreactive myenteric neurons from terminal ileum

et al. 2008

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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.

show abstract

Choline acetyltransferase and inducible nitric oxide synthase are increased in myenteric plexus of diabetic guinea pig

Cited by 29 publications

References 58 publications

Prolonged high fat diet ingestion, obesity, and type 2 diabetes symptoms correlate with phenotypic plasticity in myenteric neurons and nerve damage in the mouse duodenum

Prolonged high fat diet ingestion, obesity, and type 2 diabetes symptoms correlate with phenotypic plasticity in myenteric neurons and nerve damage in the mouse duodenum

Interaction between NMDA glutamatergic and nitrergic enteric pathways during in vitro ischemia and reperfusion

Vitamin E supplementation in rats with experimental diabetes mellitus: analysis of myosin-V and nNOS immunoreactive myenteric neurons from terminal ileum

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