Retention of J1/tenascin and the polysialylated form of the neural cell adhesion molecule (N-CAM) in the adult olfactory bulb

Abstract

To gain insight into the cellular and molecular mechanisms underlying neurogenesis in adult mouse olfactory bulb, several adhesion molecules expressed by glial cells and neurons were investigated. In the germinal zone of the olfactory bulb, the subependymal layer of the rostral region of the lateral ventricles, two adhesion molecules are detectable that are characteristic of early morphogenetic events: J1/tenascin and the polysialylated form, the so-called embryonic form, of N-CAM. The polysialylated form of N-CAM is expressed by most cells in the subependymal layer, and by some astrocytes and neurons in the granular layer adjacent to the subependymal layer. This suggests that bipotential precursor cells retain expression of the embryonic form during their migration from the subependymal layer and during the first stages of differentiation into neurons and glia. Expression of the polysialylated form of N-CAM is also retained in monolayer cultures of six-day-old olfactory bulbs, 55 days after seeding in vitro. J1/tenascin was detectable in the subependymal layer using two monoclonal antibodies. The immunostaining pattern was different between the two antibodies and more restricted to the subependymal layer than when staining with polyclonal J1 antibodies was performed, indicating that J1/tenascin exists in distinct isoforms. Finally, our observations suggest that, in the adult olfactory bulb, L1 is not only a neuron-neuron adhesion molecule, but it may also be involved in neuron-glia interactions, since it is found at contact sites between these two cell types. L1, therefore, may be a neuron-glia adhesion molecule in some parts of the CNS, while it is not in others.

A Role for N-Methyl-<i>D</i>-Aspartate Receptors in the Regulation of Synaptogenesis and Expression of the Polysialylated Form of the Neural Cell Adhesion Molecule in the Developing Striatum

“…More likely, the results indicate that those synapses expressing PSA-NCAM were preferentially affected by the NMDA antagonist. This hypothesis is supported by evidence that PSA-NCAM expression is typically associated with synapses which are less mature and retain a higher level of plasticity [Bonfanti et al, 1992;Miragall et al, 1990;Muller et al, 1996;Rousselot and Nottebohm, 1995;Seki and Arai, 1993;Tang and Landmesser, 1993;Williams et al, 1996;Rutishauser and Landmesser, 1996]. Evidence suggests that PSA-NCAM is critical for LTP and that LTP plays a role in synaptic stabilization [Bailey et al, 1992;Edwards, 1995;Buchs and Muller, 1996;Geinisman et al, 1996].…”

“…Indeed, the removal of PSA from NCAM interferes with the induction of LTP and long-term depression (LTD) in the hippocampus and results in a decrease in synapses in developing chick muscle [Tang and Landmesser, 1993]. Accordingly, expression of PSA-NCAM is correlated with a high level of both axonal and synaptic plasticity [Aaron and Chesselet, 1989;Bonfanti et al, 1992;Miragall et al, 1990;Muller et al, 1996;Rousselot and Nottebohm, 1995;Seki and Arai, 1993;Williams et al, 1996; review by Rutishauser and Landmesser, 1996].…”

Expression of the neural cell adhesion molecule and polysialic acid during early mouse embryogenesis

“…As has been shown by Western blot analysis, during early embryogenesis of chicken and frag N-CAM is expressed in its lightly sialylated forms (L-N-CAM), during late embryonie development predominantly in its heavily sialylated forms (H-N-CAM), while during early postnatal development H~N-CAM is again converted to L-N-CAM (Levi et al, 1987;. The scheme foragenerat conversion ofH-to L-N-CAM, at least during postnatal development, is clearly too simplistic as it has been shown that H-N-CAM is also expressed in particular parts of the body during adulthood, for ~xample in the hypothalamo-neurohypophysal system (Theodosis et al, 1991), optie nerve, retina (Bartsch et al, 1990), and the olfactory bulb (Miragall et al , 1988(Miragall et al , , 1990.…”

Defective Postnatal Neurogenesis and Disorganization of the Rostral Migratory Stream in Absence of theVax1Homeobox Gene

“…Besides symmetric divisions, B-cells generate a transit amplifying population of cells (C-cells) that expresses Nestin, Dlx2, and Dlx1 (Doetsch et al, 1999;Saino-Saito et al, 2003). C-cells give rise to a third type of precursor, the migrating neuroblasts (A-cells), which express TUJ1, DLX2, DLX1, and polysialylated-neural cell adhesion molecule (Miragall et al, 1990;Bonfanti and Theodosis, 1994;Ben-Hur et al, 1998;Saino-Saito et al, 2003). These cells delaminate in the anterior SVZ (SVZa) and migrate toward the OB at ϳ30 m/hr, through chain migration (Lois et al, 1996;GarciaVerdugo et al, 1998).…”