Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.3 (diaphorase)
 5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By 8 wk gestation, the human fetal oesophagus is identifiable as a hollow epithelium-lined tube with primitive nerve and muscle precursors present. From 8-16 wk gestation, the muscle layers and innervation mature until fetal swallowing commences at 16 wk. This study examines quantitatively the development and maturation of nerve fibres and cell bodies within the oesophagus using histochemistry. Oesophageal samples (n = 35) from 8 wk gestation to 28 months of age and adults (n = 3) were immunostained using antisera for the general nerve marker, protein gene product (PGP 9.5), the glial tissue marker S100, and the synaptic vesicle protein synaptophysin (p38). Histochemical staining for NADH diaphorase enzyme activity was also used to identify neurons. Computer-assisted image analysis of the muscularis externa permitted detailed quantification of cell size, nerve density and myenteric (plexus) fraction. At 8 wk gestation, PGP and synaptophysin were present in immature neurons throughout the cytoplasm, but from 10 wk synaptophysin was localised solely at nerve synapses. S100 immunoreactivity was also detected from 8 wk gestation onwards and was confined to glial tissue. Nerve cell size increased with maturation from 6 microns at 8 wk gestation to 20 microns at term and 21 microns at 28 months. The numbers of cells, nerve density (% area occupied by nerves throughout section) and myenteric fraction (% area occupied by ganglion cells and nerve fibres within the myenteric plexus) all peaked at 16-20 wk gestation and, whereas the number and density then fell towards adult levels, the myenteric fraction fell during the late second trimester and became constant from 30 wk gestation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative study of the development and maturation of human oesophageal innervation. 145 73

We recently described a parasagittal patchy organisation of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity in the granular layer of the rat cerebellum. We now report the pattern of NADPH-d distribution in the primate cerebellum and its relationship to two synaptic proteins, synaptophysin and synaptosomal associated protein 25 kDa (SNAP-25), using histochemistry and immunocytochemistry. NADPH-d reactivity was localised in the molecular and granular layers (ML, GL) and a subset of infraganglionic plexuses (IGPs), but not in the Purkinje cell layer and the white matter. In ML, the histochemical reactivity was dense and relatively homogeneous in the neuropil, and moderate in the stellate cells. A patchy organisation of NADPH-d in GL was detected in both horizontal and parasagittal sections. In the IGPs staining for NADPH-d revealed modular positive zones alternating with negative ones. The positive and negative IGP zones were usually congruent with the high and low NADPH-d reactivity in GL, respectively. Both synaptic proteins were strongly expressed in the neuropil in ML and GL, and their patterns were relatively homogeneous. However, synaptophysin was present in a subpopulation of IGPs organised in modules which corresponded to those expressing NADPH-d. Our results indicate that the NADPH-d modular system is more complicated in the primate cerebellum than in the rat. In addition, we have provided suggestive evidence of a co-expression of NADPH-d and synaptophysin in selected IGP modules in primate cerebellum, which suggests that nitric oxide may be involved in the activity of the Purkinje cells by affecting the basket cell synaptic input.
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PMID:Spatial periodicity of NADPH-diaphorase and synaptophysin, but not SNAP-25, reactivity in the monkey cerebellar cortex. 771 84

Spinal cord injury results in abnormal sympathetic control of the cardiovascular system, perhaps because of reactions of sympathetic preganglionic neurons to loss of their supraspinal afferent inputs. We investigated morphological changes in sympathetic preganglionic neurons in rats one week after midthoracic spinal cord hemisection or complete transection and one month after complete transection. Morphological changes in adrenal sympathetic preganglionic neurons retrogradely-labelled by cholera toxin were examined as well as changes in other thoracic preganglionic neurons identified by their expression of reduced nicotinamide adenine dinucleotide phosphate-diaphorase. Reactive astrogliosis around these neurons was determined by assessing changes in immunoreactivity to glial fibrillary acidic protein. Changes in immunoreactivity to the synaptic vesicular protein synaptophysin were also evaluated in these areas. One week after transection, a comparison of sympathetic preganglionic neurons rostral and caudal to the lesion revealed significant loss of dendrites and decreased cell size caudal to the injury. Reactive astrocytes surrounded sympathetic preganglionic neurons as far as six segments below the transection. Constitutive expression of synaptophysin was observed rostral to the cord hemisection and synaptophysin expression was increased caudal to the lesion by seven days after the injury. One month after transection, the dendritic arbor of preganglionic neurons was re-established and the intensity of the reactive gliosis around the preganglionic neurons was diminished throughout the thoracic cord. These findings demonstrate that sympathetic preganglionic neurons undergo significant atrophy within a week after deafferentation and that this reaction is reversed within one month. Reactive astrogliosis could contribute to plastic changes in the neuropil that affect the sympathetic neurons, and the enhanced expression of synaptophysin in the gray matter caudal to a cord injury is consistent with fibre outgrowth leading to new synapse formation. Such re-organization could be one of the mechanisms for disorders in blood pressure control that occur after spinal cord injury.
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PMID:Morphological changes in sympathetic preganglionic neurons after spinal cord injury in rats. 884 26