The neural cell adhesion molecule (NCAM) in development and plasticity of the nervous system

Rønn, Lars Christian B.; Hartz, Barbara P.; Bock, Elisabeth

doi:10.1016/s0531-5565(98)00040-0

Cited by 174 publications

(120 citation statements)

References 88 publications

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“…So far, FasciclinII and its homologs N-CAM (vertebrates) and apCAM (Aplysia) have been shown to play important roles during different kinds of neuronal growth events. They have been shown to regulate synaptic terminal size and branching in the embryo or during plastic structural reorganization at later stages, but they also play roles during axonal growth (e.g., during the processes of nerve defasciculation or target recognition) (for review, see Goodman et al, 1997;Schachner, 1997;Ronn et al, 1998;Crossin and Krushel, 2000). The function of FasciclinII during pioneer-follower interactions clearly falls into the second context.…”

Section: Discussionmentioning

confidence: 99%

The Influence of Pioneer Neurons on a Growing Motor Nerve inDrosophilaRequires the Neural Cell Adhesion Molecule Homolog FasciclinII

Sánchez‐Soriano¹,

Prokop²

2005

J. Neurosci.

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The phenomenon of pioneer neurons has been known for almost a century, but so far we have little insights into mechanisms and molecules involved. Here, we study the formation of the Drosophila intersegmental motor nerve (ISN). We show that aCC/RP2 and U motor neurons grow together at the leading front of the ISN. Nevertheless, aCC/RP2 neurons are the pioneers, and U neurons are the followers, because only aCC/RP2 neurons effectively influence growth of the ISN. We also show that this influence depends on the neural cell adhesion molecule homolog FasciclinII. First, ablation of aCC/RP2 has a stronger impact on ISN growth than U ablation. Second, strong growth-influencing capabilities of aCC/RP2 are revealed with a stalling approach we used: when aCC/RP2 motor axons are stalled specifically, the entire ISN (including the U neurons) coarrests, demonstrating that aCC/RP2 neurons influence the behavior of U growth cones. In contrast, stalled U neurons do not have the same influence on other ISN motor neurons. The influence on ISN growth requires FasciclinII: targeted expression of FasciclinII in U neurons increases their influence on the ISN, whereas a FasciclinII loss-of-function background reduces ISN coarrest with stalled aCC/RP2 axons. The qualitative differences of both neuron groups are confirmed through our findings that aCC/RP2 growth cones are wider and more complex than those of U neurons. However, U growth cones adopt aCC/RP2-like wider shapes in a FasciclinII loss-of-function background. Therefore, FasciclinII is to a degree required and sufficient for pioneerfollower interactions, but its mode of action cannot be explained merely through an equally bidirectional adhesive interaction.

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Section: Discussionmentioning

confidence: 99%

The Influence of Pioneer Neurons on a Growing Motor Nerve inDrosophilaRequires the Neural Cell Adhesion Molecule Homolog FasciclinII

Sánchez‐Soriano¹,

Prokop²

2005

J. Neurosci.

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“…The equilibrium between the expression levels of PSA-NCAM and NCAM changes gradually from high levels of PSA-NCAM and low levels of NCAM in early postnatal development to the opposite in adulthood (Doyle et al, 1992b;R nn et al, 1998;R nn et al, 2000). These changes are regulated, on the one hand, by varying dynamics in the activity of ST8SIAIV/PST, a prominent polysialyltransferase (PST) in the postnatal brain, which binds the PSA-branched moieties to NCAM, and on the other hand, by a counteracting depolysialylation process which reduces expression of PSA-NCAM (Doyle et al, 1992b;R nn et al, 2000).…”

Section: Exposure To Stress During Juvenility Alters Emotional Responmentioning

confidence: 99%

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

Tsoory

Guterman

Richter‐Levin

2007

Neuropsychopharmacol

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Childhood trauma is associated with higher rates of both mood and anxiety disorders in adulthood. The exposure of rats to stressors during juvenility has comparable effects, and was suggested as a model of induced predisposition for these disorders. The neural cell adhesion molecule (NCAM) and its polysialylated form PSA-NCAM are critically involved in neural development, activity-dependent synaptic plasticity, and learning processes. We examined the effects of exposure to stressors during juvenility on coping with stressors in adulthood and on NCAM and PSA-NCAM expression within the rat limbic system both soon after the exposure and in adulthood. Exposure to stressors during juvenility reduced novel-setting exploration and impaired two-way shuttle avoidance learning in adulthood. Among naive rats, a development-related decrease of about 50% was evident in the PSA-NCAM to NCAM expression ratio in the basolateral amygdala, in the CA1 and dentate gyrus regions of the hippocampus, and in the entorhinal cortex. In juvenile-stressed rats, we found no such decrease, but rather an increase in the polysialylation of NCAM (B50%), evident soon after the exposure to juvenile stress and also in adulthood. Our results suggest that exposure to stressors during juvenility alters the maturation of the limbic system, and potentially underlies the predisposition to exhibit stress-related symptoms in adulthood.

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“…NCAMmediated adhesion plays a critical role in the nervous system during development, neurite outgrowth, neuronal differentiation, and plasticity [9,10]. Alternative splicing results in three isoforms: one linked to the cell membrane via a glycosylphosphatidylinositol anchor of 120 kDa and two transmembrane isoforms of 140 kDa and 180 kDa.…”

Section: Introductionmentioning

confidence: 99%

IL-1β-induced pro-apoptotic signalling is facilitated by NCAM/FGF receptor signalling and inhibited by the C3d ligand in the INS-1E rat beta cell line

et al. 2006

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Aims/hypothesis: IL-1β released from immune cells induces beta cell pro-apoptotic signalling via mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB). In neurons, the neural cell adhesion molecule (NCAM) signals to several elements involved in IL-1β-induced pro-apoptotic signalling in beta cells. Pancreatic beta cells express NCAM, but its biological effects in these cells are unclear. The aim of this study was to investigate whether there is cross-talk between NCAM signalling and cytokine-induced pro-apoptotic signalling. Materials and methods: Western blotting was used to investigate levels of NCAM and inducible nitric oxide synthase, phosphorylation of Src and MAPKs, and cleavage of caspase-3. MAPK activity was investigated with an in vitro kinase assay. Apoptosis was detected by cleaved caspase-3 and a Cell Death Detection ELISA plus assay. NCAM-induced fibroblast growth factor receptor (FGFR) activation was investigated in NCAM −/− Trex293 cells where FGFR phosphorylation was measured by Western blotting after NCAM transfection. Results: Preexposure of INS-1E cells to the FGFR-inhibitor SU5402, but not to the Src-inhibitor PP2, dose-dependently inhibited IL-1β-mediated MAPK activity. A synthetic peptide, C3d, reported to bind NCAM, did not activate MAPK or Akt as reported in neurons but inhibited IL-1β-induced MAPK activity, thereby mimicking the effect of SU5402. Furthermore, C3d inhibited NCAM-induced FGFR phosphorylation and apoptosis induced by IL-1β plus IFN-γ, but did not affect IL-1β-induced NF-κB signalling. Conclusions/interpretation: We suggest that NCAM signalling through FGFR is required for efficient IL-1β pro-apoptotic signalling by facilitating IL-1β-induced MAPK activation downstream of the NF-κB-MAPK branching point. Further, these data identify a novel function of C3d as an inhibitor of NCAM-induced FGFR activity and of IL-1β-induced MAPK activation in beta cells.

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The neural cell adhesion molecule (NCAM) in development and plasticity of the nervous system

Cited by 174 publications

References 88 publications

The Influence of Pioneer Neurons on a Growing Motor Nerve inDrosophilaRequires the Neural Cell Adhesion Molecule Homolog FasciclinII

The Influence of Pioneer Neurons on a Growing Motor Nerve inDrosophilaRequires the Neural Cell Adhesion Molecule Homolog FasciclinII

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

IL-1β-induced pro-apoptotic signalling is facilitated by NCAM/FGF receptor signalling and inhibited by the C3d ligand in the INS-1E rat beta cell line

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