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PubMed2006

Increased polysialic acid neural cell adhesion molecule expression in human hippocampus of heroin addicts.

Chronic exposure to heroin is known to cause cognitive deficits. However, little is known about the underlying molecular mechanisms. It has been suggested that opiate-induced neurotoxicity as well as impaired plasticity and regeneration may be relevant. One of the target regions where regeneration still can be observed in the adult brain is the hippocampus. Since polysialic acid neural cell adhesion molecule is regarded as one of the key players involved in plasticity and regeneration of neural tissue, we analyzed polysialic acid neural cell adhesion molecule expression in the fascia dentate hilus of the human hippocampus of 29 lethally intoxicated heroin addicts and matched controls. Immunohistochemistry with an antibody directed against polysialic acid neural cell adhesion molecule revealed its expression in differently sized cells which could be identified as neurons and glial cells. We observed an increase in the percentage of polysialic acid neural cell adhesion molecule positive neurons in hippocampal hilus of heroin addicts compared with controls (P = 0.001).Interestingly, we also observed polysialic acid neural cell adhesion molecule expression in glial cells as evidenced by double immunofluorescence with glial fibrillary acidic protein and polysialic acid neural cell adhesion molecule using confocal laser scanning microscopy. The fraction of polysialic acid neural cell adhesion molecule positive glial cells was also higher in heroin addicts compared with controls (P = 0.009). In addition, within the group of addicts morphine blood concentrations showed a positive correlation with the percentage of polysialic acid neural cell adhesion molecule positive neurons (P = 0.04; r = 0.547). In conclusion, we observed an increase in polysialic acid neural cell adhesion molecule positive neurons and glial cells in hippocampi of heroin addicts. This might reflect an attempt to repair cell damage due to heroin exposure.

Adolescent↗
PubMed1992

Use of the neural cell adhesion molecule VASE exon by neurons is associated with a specific down-regulation of neural cell adhesion molecule-dependent neurite outgrowth in the developing cerebellum and hippocampus.

The development of the CNS is associated with an increasing use of the 30-bp variable alternative, spliced exon (VASE) in neural cell adhesion molecule (NCAM). We have assessed the relative usage of VASE by reverse transcriptase-linked polymerase chain reaction in the developing cerebellum and hippocampus at times when neurons isolated from these tissues can respond to substrate-associated NCAM by increased axonal growth and also at later developmental stages, when they are no longer responsive to substrate-associated NCAM. Neurons isolated from the developing cerebellum at postnatal day 6 respond to NCAM with increased neurite growth. NCAM transcripts from these cells were found to have negligible levels of VASE usage. In contrast, neurons that are isolated at later stages of development (postnatal days 8, 10, and 11) and do not respond to NCAM were found to synthesise a much higher proportion of NCAM transcripts containing VASE. In the hippocampus, embryonic day 18 neurons, which are responsive to NCAM, express low levels of VASE, whereas postnatal days 4 and 5 neurons, which are not responsive to NCAM, have a greater proportion of transcripts containing VASE. Thus, the level of NCAM VASE exon usage by neurons appears to be a good indicator of the ability of these cells to respond to non-VASE-containing NCAM (expressed in a cellular substratum) by increased neurite outgrowth.

Alternative Splicing↗
PubMed1996

Dorsal rhizotomy induces transient expression of the highly sialylated isoform of the neural cell adhesion molecule in neurons and astrocytes of the adult rat spinal cord.

Expression of the weakly adhesive, highly sialylated isoform of the neural cell adhesion molecule is a feature common to cell capable of migration and conformation changes. 11,18,19 Polysialylated neural cell adhesion molecule also intervenes in axonal outgrowth and synaptogenesis during development and after lesion. 11,13 High levels of polysialylated neural cell adhesion molecule immunoreactivity are normally visible in laminae I,II and X of the adult rat spinal cord. 2,15 We how here that unilateral cervical dorsal rhizotomy induced no detectable changes in immunoreactivity in these areas. However, 24 h after lesion, polysialylated neural cell adhesion molecule immunoreactivity appeared in neurons scattered in laminae III-IX, ipsi-and contralateral to lesion. This reaction increased particularly on the contralateral side, became maximal at four days and disappeared eight days later. At this time, there was immunolabelling of astrocytes with an activated morphology. The astrocytic labelling, predominant on the side ipsilateral to the lesion, was strongest 12 days after rhizotomy, then diminished progressively. Deafferentation thus causes a transient expression of polysialylated neural cell adhesion molecule within areas of the spinal cord distinct from those which permanently express this adhesion molecule. Such expression occurs both in neurons and glial cells, with a temporal pattern specific to each type of cell.

Afferent Pathways↗
PubMed1991

Distribution of the neural cell adhesion molecule (NCAM) during heart development.

The neural cell adhesion molecule, NCAM, was localized in the embryonic chick heart from Hamburger-Hamilton stage 14 up to hatching and in the adult heart. A monoclonal antibody directed to NCAM was used with the indirect antibody technique to stain frozen sections with immunoperoxidase. The myocardium showed immunoreactivity at stages 15 and 21, with little to no staining of epicardium, endocardium or atrioventricular endocardial cushion tissue. At stage 22, additional immunoreactivity was found in the endocardium of both the atrial septum and the atrial and ventricular surfaces of the atrioventricular cushions. Endocardial-derived mesenchymal cells within the cushions were also immunostained for NCAM. A gradient of NCAM staining was evident in the ventricular wall by stage 16. The staining intensity in the myocardium subjacent to the epicardium was less than found near the ventricular lumen. Biochemical analyses revealed that the embryonic heart expresses polysialylated NCAM. Upon desialylation with the endoneuraminidase Endo-N, the predominant heart NCAM has an apparent molecular weight of 155 to 160 kDa, which is distinct in size from the predominant forms found in embryonic chick nervous system (180, 140 and 120 kDa). NCAM expression is regionally regulated in the heart. The pattern of its expression is consistent with our hypothesis that it is involved in (1) differentiation of the atrial and ventricular walls, (2) fusion of the atrial septum with the endocardial cushions, (3) fusion of the endocardial cushions, and (4) formation and remodeling of ventricular trabeculae.

Animals↗
PubMed1990

Expression of neural cell adhesion molecule immunoreactivity in hypertrophic myocardium.

Myocardial neural cell adhesion molecule (N-CAM) is temporally regulated, being expressed during cardiac morphogenesis and innervation and suppressed in the adult heart. We have investigated the plasticity of N-CAM expression in hypertrophic muscle using the rat model of chronic hypoxia to selectively induce right ventricular hypertrophy over a 14 day time course. Sarcolemmal and intercalated disc N-CAM immunostaining was more extensive in the ventricular myocardium of hypoxic rats compared to normoxic controls. Quantitative assessment of the immunoreactivity in tissue extracts demonstrated a selective increase in the amount of N-CAM immunoreactivity in the hypertrophic myocardium of the right ventricle of rats exposed to hypoxia and this was associated with an increase of the 125 kDa isoform. We conclude that myocardial hypertrophy may be a factor influencing N-CAM expression in the heart and adhesion molecules may have a role in cardiac remodelling.

Animals↗
PubMed1991

Molecular and functional analysis of human natural killer cell-associated neural cell adhesion molecule (N-CAM/CD56).

The neural cell adhesion molecule (N-CAM/CD56) is a member of the Ig supergene family that has been shown to mediate homophilic binding. Several isoforms of N-CAM have been identified that are expressed preferentially in different tissues and stages of embryonic development. To examine the primary structure of N-CAM expressed in leukocytes, N-CAM cDNA were generated by polymerase chain reaction from RNA isolated from normal human NK cells and the KG1a hematopoietic leukemia cell line. The sequence of leukocyte-derived N-CAM cDNA was essentially identical with N-CAM cDNA from human neuroblastoma cells that encode the 140-kDa isoform of N-CAM. Inasmuch as N-CAM is preferentially expressed on human NK cells and a subset of T lymphocytes that mediate MHC-unrestricted cell-mediated cytotoxicity, we examined the potential role of N-CAM in cell-mediated cytotoxicity and heterotypic lymphocyte-tumor cell adhesion. N-CAM loss mutants were established from the human N-CAM+ KG1a leukemia cell line, and N-CAM cDNA was transfected into a human colon carcinoma cell line and murine L cells. Using this panel of mutants and transfectants, it was determined that expression of N-CAM on these target cells does not affect susceptibility to resting or IL-2-activated NK cell-mediated cytotoxicity. Moreover, expression of N-CAM in these transfectants failed to induce homotypic or heterotypic cellular adhesion. Collectively, these studies indicate that homophilic N-CAM interactions probably do not mediate a major role in the cytolytic interaction between NK cells and N-CAM+ tumor cell targets.

Antigens, CD↗
PubMed1991

Enhanced expression of neural cell adhesion molecules and tenascin (cytotactin) during wound healing.

Both neural cell adhesion molecules (N-CAM) and tenascin (cytotactin) are important in embryonic morphogenesis but their expression is reduced greatly in adults. This study examined whether they are induced during wound healing. The spatial and temporal expression patterns of these two and other adhesion molecules in the healing of skin, cartilage, and tendon were compared. Neural cell adhesion molecules, tenascin, and fibronectin are induced in the granulation tissue but the order of prevalence is fibronectin, tenascin, N-CAM. The order of appearance is N-CAM and fibronectin, and then tenascin. The order of disappearance is N-CAM, tenascin, fibronectin. Liver cell adhesion molecules are present in the epidermis undergoing re-epithelization. Explant cultures showed that N-CAM and tenascin are synthesized by wound fibroblasts. These results suggest that N-CAM and tenascin, widely used in embryonic morphogenesis, are induced in a variety of connective tissues during wound healing.

Animals↗
PubMed1987

Changes in neural cell adhesion molecule (NCAM) structure during vertebrate neural development.

Changes in carbohydrate and polypeptide form of the neural cell adhesion molecule (NCAM) have been documented during the development of central nervous system tissue in both chicken and frog. The carbohydrate variations reflect a high and low content of polysialic acid, and for the two vertebrates examined the expression of these forms is similar. At very early stages of neural development NCAM with a low content of polysialic acid is present, during histogenesis of the central nervous system NCAM with a high content of polysialic acid dominates, and there is a gradual return to NCAM with a low content of polysialic acid as the animals approach maturity. In contrast, the order of expression of the major NCAM polypeptide forms is different in the chicken and frog. These findings suggest that changes in sialic acid are a fundamental aspect of the function of NCAM in development, whereas NCAM polypeptide differences may affect events associated with a particular vertebrate. Studies have demonstrated that a decreased sialic acid content enhances the adhesion properties of NCAM. On this basis, we propose that NCAM with a low content of polysialic acid functions both to maintain integrity of neuroepithelium during morphogenesis of the early embryo and to stabilize differentiated structures in the adult, while the decreased adhesive function of NCAM with a high content of polysialic acid provides more plasticity in cell interactions during cell migration, axon outgrowth, and formation of neural circuits.

Animals↗
PubMed2004

Correlations among neural cell adhesion molecule, nerve growth factor, and its receptors, TrkA, TrkB, TrkC, and p75, in perineural invasion by basal cell and cutaneous squamous cell carcinomas.

BACKGROUND: Neural cell adhesion molecule; nerve growth factor; and its receptors TrkA, TrkB, TrkC, and p75(NGFR) regulate unique survival pathways in the cells of different noncutaneous malignancies exhibiting a perineural invasive phenotype. Their expression is currently unknown in basal cell carcinoma and cutaneous squamous cell carcinoma exhibiting perineural invasion. OBJECTIVE: The objective was to evaluate neural cell adhesion molecule, nerve growth factor, TrkA, TrkB, TrkC, and p75(NGFR) expression when perineural invasion occurs in basal cell carcinoma and cutaneous squamous cell carcinoma. METHODS: Four basal cell carcinomas and five cutaneous squamous cell carcinomas that were perineural invasion-positive and four basal cell carcinomas and three cutaneous squamous cell carcinomas that were perineural invasion-negative were evaluated for the expression of neural cell adhesion molecule, nerve growth factor, TrkA, TrkB, TrkC, and p75(NGFR) by immunohistochemical staining. RESULTS: For neural cell adhesion molecule, six of eight basal cell carcinomas and two of eight cutaneous squamous cell carcinomas stained positive. For nerve growth factor, seven of nine perineural invasion-positive and six of seven perineural invasion-negative tumors stained moderately or greater. For TrkA, B, and C, the perineural invasion-positive cutaneous squamous cell carcinomas generally stained darker than the perineural invasion-negative cutaneous squamous cell carcinomas. For p75(NGFR), four of five perineural invasion-positive cutaneous squamous cell carcinoma stain patterns indicated that p75(NGFR) expression was higher perineurally than elsewhere in the tumor. CONCLUSION: In basal cell carcinoma and cutaneous squamous cell carcinoma, the presence of neural cell adhesion molecule may determine tumor aggression and increased levels of nerve growth factor and TrkA, B, and C may reflect unique survival pathways. Higher levels of expression of Trk receptors in cutaneous squamous cell carcinoma cells may predict perineural invasion and the increased p75(NGFR) expression found in cutaneous squamous cell carcinoma perineurally may allow p75(NGFR) immunohistochemical staining to be used for detecting sites of perineural invasion.

Aged↗
PubMed1995

Regulated expression of the neural cell adhesion molecule L1 by specific patterns of neural impulses.

Development of the mammalian nervous system is regulated by neural impulse activity, but the molecular mechanisms are not well understood. If cell recognition molecules [for example, L1 and the neural cell adhesion molecule (NCAM)] were influenced by specific patterns of impulse activity, cell-cell interactions controlling nervous system structure could be regulated by nervous system function at critical stages of development. Low-frequency electrical pulses delivered to mouse sensory neurons in culture (0.1 hertz for 5 days) down-regulated expression of L1 messenger RNA and protein (but not NCAM). Fasciculation of neurites, adhesion of neuroblastoma cells, and the number of Schwann cells on neurites was reduced after 0.1-hertz stimulation, but higher frequencies or stimulation after synaptogenesis were without effect.

Animals↗
PubMed1997

Tumor suppressor activity of neural cell adhesion molecule in colon carcinoma.

BACKGROUND AND AIMS: Neural Cell Adhesion Molecule (NCAM) is a well-characterized member of the immunoglobin superfamily. The structure of NCAM is similar to the tumor suppressor Deleted in Colon Carcinoma (DCC). NCAM has been found in some epithelial tissues and plays a role in tumorigenesis of some cancers. The purpose of the present study was to determine if NCAM is present in normal human colon. Once its presence was established, its function as a tumor suppressor was investigated. METHODS: Colon tumors and normal proximal margins were processed for reverse transcription-polymerase chain reaction (RT-PCR) of the NCAM-180 message. Immunohistochemistry of the tissue was performed to determine the distribution of NCAM. RESULTS: RT-PCR analysis demonstrated the presence of the NCAM-180 kD isoform in normal colonic epithelia. Immunohistochemistry showed NCAM on the basolateral surface of colonic epithelial cells of the villous tips. Tumors from 15 patients followed up for 4 years were studied. All seven tumors expressing NCAM-180 were from patients having a benign clinical course. Seven of eight tumors that lacked NCAM-180 were associated with aggressive clinical behaviors (presenting with obstruction, perforation or metastatic disease, or patient death within 18 months of presentation). The sole exception was in a villous adenoma excised from a patient who has had multiply recurrent polyps on follow-up. CONCLUSION: We conclude that like DCC, NCAM is an important colonic adhesion molecule that functions as a tumor suppressor.

Adenocarcinoma↗
PubMedDate not supplied

Developmental biology of a neural cell adhesion molecule.

A membrane glycoprotein isolated from embryonic brain has been shown to be a ligand in the formation of cell-cell bonds. The molecule, called neural cell adhesion molecule (N-CAM), participates in several aspects of neural development, including the formation of plexiform layers, neurite fasciculation and nerve-muscle interactions. Experiments in vivo indicate that N-CAM-mediated adhesion is essential to the orderly assembly of the visual system.

Animals↗
PubMed2001

Immunohistochemical localization of the neural cell adhesion molecule in the rat sciatic nerve.

The neural cell adhesion molecule (NCAM) has been widely studied in the early embryonal development of the nervous system. The data about NCAM distribution in the peripheral nerves during postnatal life are scant and some controversial. In the present study, the NCAM localization in the sciatic nerves of 15-day-old Wistar rats has been studied. Semi-thin sections of the nerves were immunotested with a polyclonal antibody (Santa Cruz Biotechnology) that recognizes rat NCAM. The antibody was visualized with donkey anti-goat IgG, conjugated to 12 nm colloidal gold, and silver amplification. In the myelinated nerve fibres, the immunoreactivity was associated with the axons, mainly with their plasma membrane, which was unstained in the nodes of Ranvier. The myelin sheaths and the myelinating Schwann cells were negative. The extracellular matrix and the bundles of non-myelinated nerve fibres were immunopositive.

Animals↗
PubMed2001

Neural cell adhesion molecule in breast, colon and lung carcinomas.

Neural cell adhesion molecules (NCAM) play an important role in embryogenesis and in some tumors, especially of neuroectodermal origin. In this study, 18 cases of invasive breast carcinoma, 7 cases of sigmoid colon carcinomas and 17 cases of the non-small-cell lung carcinoma were immunostained for NCAM. NCAM expression, usually focal, was observed in some cases only. NCAM was expressed in the membranes, in a fine granular pattern. In 3 cases of breast cancer cytoplasmic localisation of NCAM was also observed, which may suggest its cytoplasmic formation. Furthermore, in 3 cases expression of NCAM in histologically normal ductal lobular units adjacent to invasive breast cancers without the presence of this antigen in cancer tissue was observed. The immunostaining was weak or absent in sigmoid colon carcinomas. In this study we confirm the observation of some authors that NCAM expression occurs in some cases of non-small-cell lung carcinomas.

Breast Neoplasms↗
PubMed1997

Developmental expression of two rat sialyltransferases that modify the neural cell adhesion molecule, N-CAM.

Polysialylation of the neural cell adhesion molecule (N-CAM) reduces the efficacy of N-CAM-mediated homophilic binding and is regulated both during development and in regions undergoing neurogenesis or remodeling in the adult. Hamster PST-1 (PST) and rat STX are two related sialytransferases that catalyze the polysialylation of N-CAM. We have isolated a cDNA clone for the rat homologue of PST and compared its amino acid and nucleotide sequence to that of rat STX. This analysis revealed regions of high sequence similarity corresponding to the enzymatic domains of the two molecules. Other regions of lower similarity were used to generate specific probes for in situ hybridization. The distribution of PST and STX mRNAs, polysialic acid, and N-CAM were analyzed at three developmental stages. PST and STX mRNAs were expressed abundantly throughout the nervous system at embryonic day 15 and postnatal day 4 and were coexpressed in most tissues examined. In the adult brain, STX expression was reduced relative to PST and expression of both mRNAs was restricted to subsets of cells in areas undergoing constant synaptic rearrangement including hippocampus and olfactory system. The results suggest that both PST and STX participate in the polysialylation of N-CAM in vivo and that their expression levels are dynamically controlled during development and regeneration.

Amino Acid Sequence↗
PubMed1998

Increase in proportion of hippocampal spine synapses expressing neural cell adhesion molecule NCAM180 following long-term potentiation.

Neural recognition molecules such as the neural cell adhesion molecule (NCAM) have been implicated in synaptic plasticity, including long-term potentiation (LTP), sensitization, and learning and memory. The major isoform of NCAM carrying the longest cytoplasmic domain of all NCAM isoforms (NCAM180) is predominantly localized in postsynaptic membranes and postsynaptic densities of hippocampal neurons, with only a proportion of synapses carrying detectable levels of NCAM180. To investigate whether this differential expression of NCAM180 may correlate with distinct states of synaptic activity, LTP was induced by high-frequency stimulation of the perforant path and the percentage of NCAM180 immunopositive spine synapses determined in the outer third of the dentate molecular layer of the dentate gyrus by immunoelectron microscopy. Twenty-four hours following induction of LTP by high-frequency stimulation, the percentage of spine synapses expressing NCAM180 increases from 37% (passive control) to 70%. This increase was inhibited by the noncompetitive N-methyl-D-aspartate receptor antagonist MK801. Following repeated LTP induction at 10 consecutive days with one tetanization each day, 60% of all spine synapses were NCAM180 immunoreactive. Compared to passive control animals, the percentage of NCAM180 expressing synapses in low-frequency stimulated animals decreased from 37% to 28%. Spine synapses in the inner part of the dentate molecular layer not contacted by the afferents of the perforant path did not change the percentage of NCAM180-expressing synapses. The results obtained by the postembedding immunogold staining technique confirmed the difference in NCAM180 expression of spine synapses between passive control and potentiated animals. These observations suggest a role for NCAM180 in synaptic remodeling accompanying LTP.

Animals↗
PubMedDate not supplied

Adult and embryonic mouse neural cell adhesion molecules have different binding properties.

Interactions between neural cell surfaces seem to be of prime importance during neuroontogenesis, and responsible for the guidance of migrating neuroblasts and growing axons and for the formation of synapses. Little is known about the underlying molecular mechanisms, but most hypotheses imply the existence of cell-surface molecules that mediate the formation of transient or permanent bonds between neural cells. Recently, a membrane glycoprotein called neural cell adhesion molecule (N-CAM) has been characterized in chick and rodent nervous tissue that appears to act as a ligand in adhesion among neural cell bodies or neurites. We have identified a mouse neural surface glycoprotein, named BSP-2 (ref. 7), which by criteriaof electrophoretic migration, developmental changes, amino acid and sugar composition seems to be closely related or identical to N-CAM. Both BSP-2 (refs 8, 9) and N-CAM undergo conversion from an embryonic to an adult form during brain development and it has been suggested that this transition changes the adhesive properties or the binding specificity of the molecule. Using a neuroblastoma line to study functional differences between embryonic and adult BSP-2/N-CAM molecules, we show here that liposomes bearing adult BSP-2 but not those bearing the embryonic form adhere to neuroblastoma cells, demonstrating that the two forms do indeed possess different binding properties.

Animals↗
PubMed1989

Localization of mRNA for neural cell adhesion molecule (N-CAM) polypeptides in neural and nonneural tissues by in situ hybridization.

The differential expression of the mRNA for the neural cell adhesion molecule (N-CAM) has been studied by in situ hybridization and compared with protein localization analyzed by immunohistochemical staining. The distribution of mRNA during chicken embryonic development was analyzed in neural and nonneural tissues by using an RNA probe that detects all N-CAM mRNAs and a probe specific for the mRNA of the large cytoplasmic domain (ld) of N-CAM. The results provide a detailed description of the mRNA distribution for N-CAM. The distribution of mRNA for total N-CAM generally corresponded to that of protein but differed at a more detailed level of analysis. For example, the mRNA was localized only within the cell bodies of neurons, whereas the protein was also in neuronal processes; this differential localization was most clearly seen in the alternating layers of cell bodies and fibers in the optic tectum and cerebellum. N-CAM ld mRNA, which arises from alternative RNA splicing, was expressed only in neural tissues, confirming previous biochemical and histological studies. Differential expression of the ld mRNA was detected in specific neural cell types: N-CAM mRNA was present in the ependymal cells of the spinal cord and optic tectum, but mRNA for the ld form was absent. In contrast, the ld mRNA was among the N-CAM mRNAs found in the Purkinje cells and internal granule cells in the cerebellum. The differential expression of mRNAs for the N-CAM forms emphasizes the potential importance of alternative mRNA splicing in modulating adhesive events during embryonic development, particularly in the nervous system.

Animals↗