Different polysialic acid-neural cell adhesion molecule expression patterns in distinct types of mossy fiber boutons in the adult hippocampus

Seki, Tatsunori; Arai, Yasumasa

doi:10.1002/(sici)1096-9861(19990719)410:1<115::aid-cne10>3.0.co;2-c

Cited by 80 publications

(42 citation statements)

References 58 publications

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“…In rodents, the strongest PSA-NCAM staining was detected on growing axon bundles (Daston et al, 1996;Seki and Arai, 1999), in agreement with our findings in the human fetal brain. Expression of PSA-NCAM by various progenitor cell populations in the central nervous system was reported (Gascon et al, 2007;Vitry et al, 2001;Allan and Greer, 1998;Oumesmar et al, 1995), including in vivo expression by glial restricted progenitors in the perinatal mouse subvetricular zone (Marshall and Goldman, 2002).…”

Section: Discussionsupporting

confidence: 92%

Down-regulation of the axonal polysialic acid–neural cell adhesion molecule expression coincides with the onset of myelination in the human fetal forebrain

Jakovčevski

Zečević

2007

Neuroscience

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The polysialic acid (PSA) modification of neural cell adhesion molecule, which reduces NCAMmediated cell adhesion, is involved in several developmental processes, such as cell migration, axonal growth, pathfinding, and synaptic plasticity. It has been suggested that PSA-NCAM expression may inhibit myelination. To clarify the relationship between myelination and the expression of PSA-NCAM we systematically investigated its expression in the human forebrain from embryonic stage to midgestation (19-24 gestation weeks, gw). Immunofluorescence on cryosections showed that PSA-NCAM is expressed at the earliest stage studied (5.5 gw) in the primordial plexiform layer of the telencephalon, which mainly consists of neuronal processes. At midgestation, cortical axonal tracts in the emerging white matter were PSA-NCAM+, but they were not yet myelinated, based on the lack of myelin basic protein (MBP) immunoreaction. To follow the progression of myelination we developed organotypic slice cultures that included the subventricular and intermediate zones of the fetal forebrain. In freshly prepared slices, similar to cryosections, axonal tracts were PSA-NCAM + but did not express MBP. After 5 days in culture there was a dramatic increase in MBP expression around the axons of the intermediate zone, which suggested the onset of myelination. Simultaneously with MBP up-regulation PSA-NCAM expression in axons was completely lost, as demonstrated both with immunofluorescence and Western blot analysis. These results support the idea that in the human fetal forebrain axonal PSA-NCAM expression is inversely related to primary myelination.

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Section: Discussionsupporting

confidence: 92%

Down-regulation of the axonal polysialic acid–neural cell adhesion molecule expression coincides with the onset of myelination in the human fetal forebrain

Jakovčevski

Zečević

2007

Neuroscience

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“…In the adult brain, PSA-NCAM is still present in a few restricted areas, including the hippocampus. 48 The presence of PSA-NCAM in the adult hippocampus has been associated with neural plasticity 49 involved in learning processes. 50 In the hippocampus, PSA-NCAM may support migration of newly formed neurons that will settle in the dentate granular layer.…”

Section: Discussionmentioning

confidence: 99%

Neuronal mechanism of nociceptin-induced modulation of learning and memory: Involvement of N-methyl-D-aspartate receptors

et al. 2003

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Nociceptin (also called orphanin FQ) is an endogenous heptadecapeptide that activates the opioid receptor-like 1 (ORL 1 ) receptor. Nociceptin system not only affects the nociception and locomotor activity, but also regulates learning and memory in rodents. We have previously reported that long-term potentiation and memory of ORL 1 receptor knockout mice are enhanced compared with those in wild-type mice. Here, we show the neuronal mechanism of nociceptin-induced modulation of learning and memory. Retention of fear-conditioned contextual memory was significantly enhanced in the ORL 1 receptor knockout mice without any changes in cued conditioned freezing. Inversely, in the wild-type mice retention of contextual, but not cued, conditioning freezing behavior was suppressed by exogenous nociceptin when it was administered into the cerebroventricle immediately after the training. ORL 1 receptor knockout mice exhibited a hyperfunction of N-methyl-D-aspartate (NMDA) receptor, as evidenced by an increase in [ 3 H]MK-801 binding, NMDA-evoked 45 Ca 2 þ uptake and activation of Ca 2 þ /calmodulin-dependent protein kinase II (CaMKII) activity and its phosphorylation as compared with those in wild-type mice. The NMDA-induced CaMKII activation in the hippocampal slices of wild-type mice was significantly inhibited by exogenous nociceptin via a pertussis toxin-sensitive pathway. However, the a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor GluR1 subunit at Ser 831 and Ser 845, and NMDA receptor subunit NR2B at Thr 286 were phosphorylated similarly after NMDA receptor stimulation in both type of mice. The expressions of GluR1 and GluR2 also did not change, but the levels of polysialylated form of neuronal cell adhesion molecule (N-CAM) were reduced in the ORL 1 receptor knockout as compared with wild-type mice. These results suggest that nociceptin system negatively modulates learning and memory through the regulation of NMDA receptor function and the expression of N-CAM. Molecular Psychiatry (2003Psychiatry ( ) 8, 752-765. doi:10.1038 Keywords: nociceptin/orphanin FQ; ORL 1 receptor; Knockout mice; hippocampus; NMDA Opioid receptors are negatively coupled to adenylate cyclase through Gi/o proteins and mediate the inhibition of forskolin-induced cAMP accumulation by morphine and endogenous opioid peptides. Opioid receptor agonists have receptor subtypespecific actions on not only the nociceptive thresholds but also synaptic transmission and long-term potentiation (LTP) in the hippocampus. Thus, opioid system modulates certain forms of learning and memory.

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“…PSA-NCAM is associated with granule neurons and mossy fiber boutons in the adult hippocampus, and is thought to participate in the formation and remodeling of synapses between granule neurons and CA3 pyramidal neurons (Seki and Arai, 1999). The expression of doublecortin, a marker of dendritic growth in newly generated neurons (Rao and Shetty, 2004), also increased in the hippocampus in a pattern similar to that of PSA-NCAM.…”

Section: Dexefaroxan May Also Enhance Neuronal Plasticitymentioning

confidence: 91%

The Alpha2-Adrenoceptor Antagonist Dexefaroxan Enhances Hippocampal Neurogenesis by Increasing the Survival and Differentiation of New Granule Cells

Rizk

Salazar

Raisman‐Vozari

et al. 2005

Neuropsychopharmacol

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The generation of new neurons in the hippocampus is a dynamic process regulated by environmental, endocrine, and pharmacological factors. Since enhancement of hippocampal neurogenesis has been associated with learning and memory, and the locus coeruleusnoradrenergic system has been shown to modulate these cognitive functions, we hypothesized that activation of noradrenergic neurotransmission might enhance neurogenesis in the adult hippocampus. To test this hypothesis in vivo, we induced the release of noradrenaline in the hippocampus by blocking presynaptic inhibitory autoreceptors with the selective alpha2-adrenoceptor antagonist dexefaroxan. Confocal microscopy showed that noradrenergic afferents make contact with proliferating and differentiating cells, suggesting a direct noradrenergic influence on neurogenesis. Chronic systemic treatment of rats with dexefaroxan did not affect cell proliferation per se in the dentate gyrus (as monitored by bromodeoxyuridine-labeling), but promoted the long-term survival of newborn neurons by reducing apoptosis. Dexefaroxan treatment also enhanced the number and complexity of the dendritic arborizations of polysialated neural cell adhesion molecule-positive neurons. The trophic effects of dexefaroxan on newborn cells might involve an increase in brain-derived neurotrophic factor, which was upregulated in afferent noradrenergic fiber projection areas and in neurons in the granule cell layer. By promoting the survival of new endogenously formed neurons, dexefaroxan treatment represents a potential therapeutic strategy for maintaining adult neurogenesis in neurodegenerative conditions, such as Alzheimer's disease, that affect the hippocampus.

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Different polysialic acid-neural cell adhesion molecule expression patterns in distinct types of mossy fiber boutons in the adult hippocampus

Cited by 80 publications

References 58 publications

Down-regulation of the axonal polysialic acid–neural cell adhesion molecule expression coincides with the onset of myelination in the human fetal forebrain

Down-regulation of the axonal polysialic acid–neural cell adhesion molecule expression coincides with the onset of myelination in the human fetal forebrain

Neuronal mechanism of nociceptin-induced modulation of learning and memory: Involvement of N-methyl-D-aspartate receptors

The Alpha2-Adrenoceptor Antagonist Dexefaroxan Enhances Hippocampal Neurogenesis by Increasing the Survival and Differentiation of New Granule Cells

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