• Animal cells and systems
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• v.3 no.3
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• pp.259-267
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• 1999

The expression of the neural cell adhesion molecule-180 (NCAM-180), which accumulates at contact sites between cells and may be responsible for the stabilization of cell contacts, was studied in the olfactory system and retina of developing and adult rats. From embryonic day 12 onwards, which was the earliest stage examined, the NCAM-180 pathway directing to the presumptive olfactory bulb was observed. In later stages, olfactory neurons and fasciculating axons in the olfactory epithelium and nerve fiber layer and glomeruli of the olfactory bulb expressed NCAM-180. From postnatal day 0, immunolabelling pattern of the olfactory epithelium and olfactory bulb were the same as that during later stages. NCAM-180 immunoreactivity was present on differentiating retinal cells and persisted on those cells throughout adulthood. However, contrary to the olfactory nerve which remained detectable in the adult, the optic nerve was only transiently expressed with NCAM-180 and was no longer detectable in the adult. The presence of NCAM-180 in olfactory tissues suggests their possible role in pathfinding, differentiation, fasciculation and synaptic plasticity. The continued presence of NCAM-180 in the olfactory system examined may underlie its continuous cell turnover and regenerative capacity. The continuous expression of NCAM-180 in ganglion cells, bipolar cells and photoreceptor cells, also suggests potential regenerating capability and some plastic functions for these cells in the adult. Since the expression of NCAM-180 by the optic nerve was restricted to the period of special histogenetic events, for example, during axonal growth and synaptogenesis, it is possible that the lack of NCAM-180 in the adult optic nerve might cause a nonpermissive environment for the regeneration and result in regenerative failure of this system.

• The Journal of Korean Physical Therapy
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• v.19 no.2
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• pp.41-55
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• 2007

Purpose: This study aimed to compare the effect on nerve regeneration of ultrasound irradiation in rats with peripheral nerve injury. Methods: To investigate alterations of the NCAM immunoreactivity in non-crushed part and crushed part of the spinal cord, the unilateral sciatic nerve of the rats were crushed. The expression of NCAM was used as the marked of peripheral nerve regeneration, and also plays an important role in developing nerve system. Experimental animals were sacrificed by perfusion fixation at post-injury 1, 3, 7, 14 days after ultrasound irradiation. The pulsed US was applied at a frequency of 1MHz and a spatial average-temporal average Intensity of 0.5W/of (20% pulse ratio) for 1 mins. The Luxol fast blue-cresyl violet stain were also done to observe the morphological changes. Results: Alteration of NCAM immunoreactivity in the crushed part and the non-crushed part of lower lumbar spinal cord were observed. NCAM-immunoreactivity cells were some increased in the dorsal horn lamina I, III and cell ventral horn at 1 day after unilateral sciatic nerve injury. However, there was not significant difference in the relationship between crushed part and non-crushed part. NCAM-inmmunoreactivity was remarkably increased at 3 days after unilateral sciatic nerve injuryin the gray matter and white matter. NCAM-immunoreactivity was increased in the ventral horn and post horn of experimental crushed part. Also, NCAM-immunoreactivity in large motor neurons in ventral horns lamina VIII, IX were increased at 7 days after unilateral sciatic nerve injury. At 14 days after sciatic nerve crushed injury, there was no significant difference. All group were decreased for 14 days. In the time course of NCAM expression, all groups showed a significant difference at 3day groups(p<0.05). Whereas, CC group was noted a significant difference between 3day and 7 day group respectively. In NCAM expression, there were significantly increased in all group. In the relationship between CNC group and ENC group, significant difference was detected among 3, 7, 14 day group(p<0.05). The difference between CC group and ENC group were noted in all groups(p<0.05). Conclusion: It is consequently suggested that the effects of the ultrasound irradiation may increase the NCAM immunoreactive neurons and glial cell in the spinal cord after unilateral sciatic nerve crushed injury. Therefore, the increased NCAM immunoreactivity in the spinal cord may reflect the neuronal damage and healing process induced by a ultrasound irradiation after peripheral nerve injury in rat.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.8
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• pp.3131-3135
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• 2015

Objective: To investigate whether the expression of serum soluble neural cell adhesion molecule (sNCAM) is associated with hepatic encephalopathy (HE) in hepatocelular carcinoma (HCC) patients. Materials and Methods: The Oncomine Cancer Microarray database was used to determine the clinical relevance of NCAM expression in different kinds of human cancers. Sera from 75 HCC cases enrolled in this study were assessed for expression of sNCAM by enzyme linked immunosorbent assay (ELISA). Results: Dependent on the Oncomine Cancer Microarray database analysis, NCAM was down regulated in 10 different kinds of cancer, like bladder cancer, brain and central nervous system cancer, while up-regulated in lung cancer, uterine corpus leiomyoma and sarcoma, compared to normal groups. Puzzlingly, NCAM expression demonstrated no significant difference between normal and HCC groups. However, we found by quantitative ELISA that the level of sNCAM in sera from HCC patients with HE ($347.4{\pm}151.9ng/ml$) was significantly more up-regulated than that in HCC patients without HE ($260.3{\pm}104.2ng/ml$), the p-value being 0.008. sNCAM may be an important risk factor of HE in HCC patients, the correlation coefficients was 0.278 (P<0.05) on rank correlation analysis. Conclusions: This study highlights that up-regulated level of serum sNCAM is associated with HE in HCC patients and suggests that the high expression can be used as an indicator.

• Korean Journal of Biological Psychiatry
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• v.16 no.1
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• pp.5-14
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• 2009

Objectives : Most of the mechanisms reported for antidepressant drugs are the enhancement of neurite outgrowth and neuronal survival in the rat hippocampus. Neural cell adhesion molecule 140(NCAM140) has been implicated as having a role in cell-cell adhesion, neurite outgrowth, and synaptic plasticity. In this report, we have performed to elucidate a correlation among chronic antidepressant treatments, NCAM140 expression, and activation of phosphorylated cyclicAMP responsive element binding protein(pCREB) which is a downstream molecule of NCAM140-mediated intracellular signaling pathway in the rat hippocampus. Methods : Fluoxetine(10mg/kg) was injected acutely(daily injection for 5days) or chronically(daily injection for 14days) in adult rats. RNA and protein were extracted from the rat hippocampus, respectively. Real-time RT-PCR was performed to analyze the expression pattern of NCAM140 gene and western blot analyses for the activation of the phosphorylation ratio of CREB. Results : Chronic fluoxetine treatments increased NCAM140 expression 1.3 times higher than control in rat hippocampus. pCREB immunoreactivity in the rat hippocampus with chronic fluoxetine treatment was increased 4.0 times higher than that of control. Conclusion : Chronic fluoxetine treatment increased NCAM140 expression and pCREB activity in the rat hippocampus. Our data suggest that NCAM140 and pCREB may play a role in the clinical efficacy of antidepressants promoting the neurite outgrowth and neuronal survival.

• Advances in pediatric surgery
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• v.7 no.1
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• pp.15-20
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• 2001

The pathophysiology of Hirschsprung's disease (HD) is not fully understood, but recent studies have disclosed that neural cell adhesion molecule (NCAM) and glial cell line-derived neurotrophic factor (GDNF) play important roles in the formation of aganglionic bowel of Hirschsprung's disease. To evaluate the roles of NCAM and GDNF in HD, immunohistochemical analysis was performed using formalin-fixed and paraffin-embedded tissue sections. On the basis of the results, we tried to evaluate them as diagnostic markers. The specimens were obtained from 7 patients with HD who underwent modified Duhamel operation. The diagnosis was based on the clinical findings and the absence of ganglion cells in the nerve plexuses by routine microscopy. NCAM immunoreactivity was found in the nerve plexuses and scattered nerve fibers in the smooth muscle layers of ganglionic segments. In aganglionic segments, the number of NCAM positive nerve fibers in the smooth muscle layers was significantly reduced compared with ganglionic segments. In two cases the nerve plexuses in aganglionic segments, NCAM was negligible. The smooth muscle cells showed diffuse immunoreactivity for GDNF and the staining intensity was not different in the aganglionic and ganglionic segments. However, higher expression of GDNF in the nerve plexus of the ganglionic segments was noted comparing to aganglionic segments. These data suggest that both NCAM and GDNF may play important roles in pathogenesis of Hirschsprung's disease and immunohistochemical staining for NCAM can be used as an ancillary diagnostic tool for HD.

• Journal of Acupuncture Research
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• v.21 no.3
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• pp.61-81
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• 2004

Background and Objective : The aim of this study was to investigate the effects of acupuncture and electroacupuncture on the DCX, PSA-NCAM, and pCREB expression in the brain of spontaneously hypertensive rats(SHR). Materials and Methods : SHR were divided into five groups: control group, acupuncture group, 2Hz electroacupuncture(EA) group and 100Hz EA group. We evaluated the changes of the DCX, PSA-NCAM, and pCREB positive cells using immunohistochemical method. In the olfactory bulb, we investigate the optical densities of the immunoactive cells. In the dentate gyrus and the piriform cortex, we count the immunoactive cells under the $100{\times}$ visual field optical microscope. Results : 1. The optical densities of DCX-positive cells in the subependymal zone were significantly decreased in all groups, compared to the control group. 2. The counts of DCX-positive cells in the dentate gyrus were significantly increased in all groups, compared to the control group. The counts of DCX-positive cells in the piriform cortex were significantly increased in the acupuncture and 100Hz EA group, compared to the control group. 3. The optical densities of PSA-NCAM-positive cells in the subependymal zone were significantly decreased in the acupuncture and 2Hz EA group, compared to the control group. 4. The counts of PSA-NCAM-positive cells in the dentate gyrus and the piriform cortex were significantly increased in all group, compared to the control group. 5. The counts of pCREB-positive cells in the dentate gyrus were significantly increased in all groups, compared to the control group. The counts of pCREB-positive cells in the piriform cortex were significantly increased in the acupuncture and 100Hz EA group, compared to the control group. Conclusion : We conclude that acupuncture and EA may affect neuronal cell proliferation, differentiation and plasticity in the brain.

• Journal of Ginseng Research
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• v.32 no.1
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• pp.62-66
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• 2008

Non-saponin gingseng fraction components (NSRG) have been known to have a variety of biological activity. However, the effects of these components on the function of brain cell have not been characterized in detail. In this study, we investigated the preventive effect of non-saponin red ginseng components on acrylamide (ACR)-induced suppression of neural cell adhesion molecule (NCAM), which is highly expressed in neuronal cells. The data showed that NSRG blocked the suppression of NCAM expression by ACR in neuroblastoma cells (SK-N-SH). In addition, NSRG significantly increased NCAM expression in ACR-nontreated neuroblastoma cells. NSRG treatment resulted in the increase of cell proliferation in a concentration-dependent manner. We also examined whether NSRG could modulate the NO production of astrocytes. When glioma cells (C6) were treated with various concentrations of NSRG (100-300 ug/ml) in the presence or absence of $IFN-{\gamma}$ for 24 hours, NO production was suppressed in $IFN-{\gamma}-$stimulated C6 cells. Taken together, these results demonstrate that treatment of brain cells with NSRG results in the enhancement of proliferation, the suppression of NO production and the protective effect on NCAM expression impaired by ACR. Thus, the present data suggest that NSRG has proliferative and neuroprotective effects and these effects could be useful in neuronal diseases.

• Journal of Korean Neurosurgical Society
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• v.60 no.4
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• pp.417-423
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• 2017

Objective : Repair of sensorial nerve defect is an important issue on peripheric nerve surgery. The aim of the present study was to determine the effects of sensory-motor nerve bridging on the denervated dermatomal area, in rats with sensory nerve defects, using a neural cell adhesion molecule (NCAM). Methods : We compared the efficacy of end-to-side (ETS) coaptation of the tibial nerve for sural nerve defect repair, in 32 Sprague-Dawley rats. Rats were assigned to 1 of 4 groups : group A was the sham operated group, group B rats had sural nerves sectioned and buried in neighboring muscles, group C experienced nerve sectioning and end-to-end (ETE) anastomosis, and group D had sural nerves sectioned and ETS anastomosis was performed using atibial nerve bridge. Neurological evaluation included the skin pinch test and histological evaluation was performed by assessing NCAM expression in nerve terminals. Results : Rats in the denervated group yielded negative results for the skin pinch tests, while animals in the surgical intervention groups (group C and D) demonstrated positive results. As predicted, there were no positively stained skin specimens in the denervated group (group B); however, the surgery groups demonstrated significant staining. NCAM expression was also significantly higher in the surgery groups. However, the mean NCAM values were not significantly different between group C and group D. Conclusion : Previous research indicates that ETE nerve repair is the gold standard for peripheral nerve defect repair. However, ETS repair is an effective alternative method in cases of sensorial nerve defect when ETE repair is not possible.

• BMB Reports
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• v.41 no.8
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• pp.593-596
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• 2008

ADPKD (Autosomal Dominant Polycystic Kidney Disease) is characterized by the progressive expansion of multiple cystic lesions in the kidneys. ADPKD is caused by mutations in Ed-pl. consider PKD1 and PKD2. Recently a relation between c-myc and the pathogenesis of ADPKD was reported. In addition, c-Myc is a downstream effector of PKD1. To identify the gene regulated by PKD2 and c-Myc, we performed gene expression profiling in PKD2 and c-Myc overexpressing cells using a human 8K cDNA microarray. NCAM (neuronal cell adhesion molecule) levels were significantly reduced in PKD2 overexpressing systems in vitro and in vivo. These results suggest that NCAM is an important molecule in the cystogenesis induced by PKD2 overexpession.

• International Journal of Oral Biology
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• v.33 no.3
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• pp.83-89
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• 2008

Glutamate-induced cobalt uptake reveals non-NMDA glutamate receptors (GluRs) in rat taste bud cells. Previous studies suggest that glutamate-induced cobalt uptake in taste cells occurs mainly via kainate type GluRs. Cobaltstained cells were immunoreactive against GluR6 and KA1 subunits of GluRs. However, the functions of those type of receptors are not known yet. It is important question which types of taste cells are cobalt-stained when stimulated by glutamate and whether they express these kinds of GluRs. Circumvallate and foliate papilla of Sprague-Dawley rats (45-60 days old) were used. A cobalt-staining technique combined with immunohistochemistry against specific markers for taste bud cell types, such as blood group H antigen (BGH), $\alpha$-gustducin (Gus), or neural cell adhesion molecule (NCAM) was employed. We also performed double labeling of GluR6 or KA1 subunits of GluR with each specific marker for taste bud cell types. Lots of cobaltstained taste bud cells expressed Gus-like immunoreactivity, and subsets of the cobalt stained cells appeared NCAM- or BGH-like immunoreactivity. Stimulation with 1 mM glutamate significantly increased the number of cobaltstained cells in Gus-like immunoreactive cells, but not in NCAM- or BGH-like immunoreactive cells. In the double labeling experiments, GluR6 and KA1 subunits of GluRs were mainly expressed with Gus. These results suggest that kainate glutamate receptors preferentially expressed in type II taste bud cells in rat.