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R Martini

Publications and source records attributed to R Martini.

At least 109 records · Page 6Linked to original sources
PubMed1992

Immunocytochemical localization of the L1 and N-CAM cell adhesion molecules and their shared carbohydrate epitope L2/HNK-1 in the developing and differentiated gustatory papillae of the mouse tongue.

The localization of the cell adhesion molecules L1 and N-CAM, and their shared carbohydrate epitope L2/HNK-1, was investigated at the light and electron microscopic levels in developing and adult fungiform and circumvallate gustatory papillae of the mouse tongue. At embryonic day 13, the earliest stage investigated, the tongue epithelium was still undifferentiated and was not yet innervated by sensory fibres. At this stage none of the three molecules was detectable within the tongue epithelium. At embryonic day 15 the primordia of the gustatory papilla became unequivocally discernible when the papillary epithelium was already innervated by few sensory axons. At this stage N-CAM was the first molecule expressed on epithelial cells and was confined to those parts of the papillary epithelium destined to become the chemosensory cells of the taste buds. The sensory axons were N-CAM-, L1- and L2/HNK-1-positive when fasciculating or contacting their accompanying Schwann cells or the cells of the papillary epithelium. Contacts between Schwann cells were also prominently labelled by antibodies to the three antigens. The mesenchymal tissue underlying the prospective sensory epithelium expressed N-CAM at all embryonic stages, but ceased to be N-CAM positive within the first six postnatal days. From embryonic day 16 onward a weak L1 immunoreactivity was detectable within the basal and intermediate layers of the lingual epithelium and remained present in adulthood. Cytodifferentiation of epithelial cells into spindle-shaped sensory cells and organization into taste buds began at postnatal day two. Simultaneously, L1 and L2/HNK-1 immunoreactivity increased on taste bud cells and N-CAM disappeared from the non-sensory extragemmal parts of the papillary epithelium. At approximately postnatal day six, taste bud formation was complete and the pattern of cell adhesion molecule expression was comparable to that found in the adult in that L1 was strongly expressed on the apposing surfaces of all cells, whereas N-CAM was confined to cell contacts between a subpopulation of intragemmal cells. The L2/HNK-1 epitope was visible on the surfaces of taste bud cells, on intragemmal axons, and in a small portion of extracellular matrix directly underlying the taste buds, but was no longer expressed on those parts of the sensory fibres embedded in the subepithelial mesenchyme. The L2/HNK-1 epitope may thus be regarded as a cell surface marker for the cellular elements of mature taste buds. The highly sialylated form of N-CAM was not detectable at any stage investigated.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Shear bond strength of a 4-META adhesive system.

This study evaluated the shear bond strength between amalgam and amalgam, amalgam and composite resin, and amalgam and dentin using a 4-META adhesive. Eighty samples were divided into four groups of 20 and were then divided into subgroups of 10 samples for thermocycling procedures. This study indicated that amalgam bonded to amalgam with a 4-META adhesive yielded bond strengths that were weaker than the shear strength of amalgam itself (p less than 0.05), and that thermocycling appeared to significantly weaken bond values (p less than 0.02).

Adhesives↗
PubMed1991

Increased expression of cytochrome P450 IIIA2 in male rat liver after dietary vitamin A supplementation.

In this study dietary vitamin A supplementation (25 IU/g diet) was assessed for its effect on hepatic microsomal P450 content and on P450 enzyme-specific drug oxidase activities in rats. Intake of the supplemented diet by male rats over a 15-week period resulted in a fivefold increase in hepatic vitamin A stores over those measured in control liver from rats that received a balanced diet without vitamin A supplementation. Serum retinol was unchanged and there was no evidence of hepatocellular injury in any of the animals. There was a 26% increase in P450 content in vitamin A-supplemented rat liver and regioselective androst-4-ene-3,17-dione (androstenedione) and progesterone hydroxylation revealed changes in several P450 pathways. Thus, androstenedione 16 alpha-hydroxylation (P450 IIC11-mediated) and progesterone 21-hydroxylation (P450 IIC6-mediated) were decreased slightly to 80 and 74% of respective control activities while P450 IIA1/2-dependent androstenedione 7 alpha-hydroxylation was slightly increased. In contrast, the 6 beta-hydroxylations of androstenedione and progesterone were increased to 169 and 152% of control following dietary supplementation. Kinetic analysis of androstenedione 6 beta-hydroxylation revealed an increase in maximal reaction velocity (Vmax 4.00 +/- 0.47 vs 2.20 +/- 0.10 nmol/min/mg protein) but the Km was unchanged, suggesting an increase in enzyme concentration. Consistent with this assertion, immunoquantitation of the steroid 6 beta-hydroxylase, P450 IIIA2, revealed a 158% increase in the microsomal expression of this enzyme (9.8 +/- 2.7 vs 6.2 +/- 1.3 ng/micrograms microsomal protein). From these studies it now seems clear that vitamin A, as a dietary additive in nontoxic doses, has the capacity to alter the activity of hepatic microsomal drug oxidases by modulating the expression of P450 enzymes.

Androstenedione↗
PubMed1991

Complex expression pattern of tenascin during innervation of the posterior limb buds of the developing chicken.

The histological localization of the extracellular matrix glycoprotein tenascin was studied during the formation of peripheral nerves in the developing chick hindlimb (embryonic stages 21.5 to 30) by light and electron microscopic immunological methods to obtain insights into the molecule's functional role in the pathway formation by motor and sensory nerves. At stages 21.5 and 23, nerve roots and plexus were surrounded by high tenascin-immunoreactivity, whereas the not yet innervated limb bud was not immunoreactive. During innervation of the limb bud at stages 24.5 and 25, tenascin was detectable at the limb bud base and restricted in its expression to the proximal nerve regions. The nerve tips did not contact areas of elevated tenascin-immunoreactivity. At stages 26 to 28 the dorsal and ventral trunks of the crural and sciatic nerves were surrounded by tenascin-immunoreactivity, which was localized between Schwann and mesenchymal cells. The tips of the growing nerve had now reached the tenascin-positive interface between bone and muscle anlagen. This interface was contacted tangentially rather than penetrated by the nerve tips. The medial and lateral femoral cutaneous nerves were surrounded by high and weak tenascin-immunoreactivity, respectively. In both nerves, tenascin-immunoreactivity was absent where the nerves branched extensively to innervate the skin. The cutaneous nerves diverging from the sciatic nerve were of very low tenascin-immunoreactivity or tenascin-negative at all developmental stages tested. At stages 29 and 30, muscle nerves, having just entered the tenascin-negative muscles, exhibited strong immunoreactivity, whereas the more proximally situated trunks of the sciatic nerve were weakly and discontinuously labeled, particularly at sites where smaller nerves were branching off. Since the cutaneous branches of the sciatic nerve were always of low tenascin-immunoreactivity, the question was raised whether tenascin expression in the sciatic nerve depended on the presence of motor axons. Spinal cords of stage 19 or 20 embryos were therefore removed and tenascin expression was investigated at stages 26 and 27. Some of the residual nerves were weakly tenascin-immunoreactive, whereas others were tenascin-negative. Our observations suggest that tenascin is not involved in the initial guidance of peripheral nerves to their targets. Rather, neuron-induced tenascin appears to stabilize the proximal nerve trunks during a transient time period, possibly by preventing axons and Schwann cells from intermingling with the surrounding mesenchyme, thus contributing to nerve fiber compaction. Conversely, nerve branching may be elicited by reduced levels of tenascin. Furthermore, tenascin may divert growth cones from the developing bone tissue and direct muscle afferents to their appropriate targets.

Animals↗
PubMed1991

Expression of carbohydrate epitopes L2/HNK-1 and L3 in the larva and imago of Drosophila melanogaster and Calliphora vicina.

The carbohydrate epitopes L2/HNK-1 and L3 belong to two overlapping families of adhesion molecules in the vertebrate, and probably the invertebrate nervous systems. To investigate their pattern of expression during the development of insects, cryosections of late third instar larvae and imagoes of Drosophila melanogaster and Calliphora vicina were studied by indirect immunofluorescence using several monoclonal antibodies to the L2/HNK-1 and one monoclonal antibody to the L3 epitope. Each monoclonal antibody to the L2/HNK-1 epitope showed a different immunohistological staining pattern, which differed from that of the L3 monoclonal antibody. In both insect species the immunohistological staining patterns for the two carbohydrate epitopes were similar at the two developmental stages, with immunoreactivity not confined to the nervous system. In larvae, immunoreactivities of the monoclonal antibodies L2.334 and L3.492 were predominantly associated with the extracellular matrix as indicated by co-localization with laminin, particularly in the imaginal discs, while L2.349 revealed a more cell surface-associated distribution. In imagoes, immunoreactivities were detectable in most organs studied.

Animals↗
PubMed1990

Changes in expression of mRNA specific for cell adhesion molecules (L1 and NCAM) in the transected peripheral nerve of the adult rat.

The relative amounts of transcripts specific for the adhesive molecule L1 and the neural cell adhesion molecule (NCAM) in the distal stump of transected rat sciatic nerves were determined by quantitative Northern blot analysis during the first four weeks after injury. Two days after operation, transcript levels were approximately 50% lower in the lesioned than in the unsevered control nerve reaching maximum values 2 and 3 times over control for L1 and NCAM mRNAs, respectively, after 3 weeks. In contrast, expression of the mRNAs specific for the myelin-associated glycoprotein (MAG) and for the major myelin protein of the peripheral nervous system, P0, dropped to 10% or less of the control after nerve injury and did not exceed 30 and 20%, respectively, 3 weeks after the lesion. The up-regulation of L1- and NCAM-specific mRNAs in distal nerve stump parallels the induction of L1 and NCAM protein expression by Schwann cells of lesioned nerves as revealed by previous immunocytochemical studies and may reflect the Schwann cells' capacity to recapitulate development and to promote axonal regrowth.

Animals↗
PubMed1990

Immunological evidence that the neural adhesion molecule L1 is expressed in fish brain and optic nerve: possible association with optic nerve regeneration.

In the mammalian peripheral nervous system (PNS), expression of the neural adhesion molecule L1 on Schwann cells and neurons has been correlated with axonal growth during development and regeneration. The present study was undertaken to examine whether a similar correlation exists between a lesion-induced increase of L1 expression and regenerative capacity in the central nervous system (CNS). The fish optic nerve was used as a model for a successfully regenerating region of the CNS. Immunochemical and immunohistological experiments carried out with immunoaffinity purified polyclonal antibodies, generated against L1 from mouse brain, showed that carp optic nerve and brain, but not liver, contained L1 immunoreactivity. Western blot analysis of brain tissue yielded one distinct band at 200 kDa, while a double band at 200 kDa and two low-molecular weight bands at 120 and 100 kDa, possibly degradation products, were seen in the optic nerve. Immunohistological examination of normal optic nerves revealed L1 immunoreactivity, predominantly associated with connective tissue boundaries of nerve fascicles and with blood vessels, as well as inside axonal fascicles. L1 immunoreactivity was increased by 25%, 8 days after crushing of the optic nerve, as determined by radioimmunoassay on a nerve segment distal to the site of injury and compared with untreated control nerves. Increased levels of L1 were also seen by immunohistology and found to be predominantly associated, as in the normal nerve, with connective tissue boundaries and blood vessels. These observations suggest that a lesion-induced increase in L1 expression in the fish optic nerve is associated with axonal regrowth in the CNS.

Animals↗
PubMed1990

Enhanced expression of the extracellular matrix molecule J1/tenascin in the regenerating adult mouse sciatic nerve.

We have investigated the expression of J1/tenascin in the sciatic nerve of the adult mouse under normal and regenerating conditions by immunocytological and immunochemical methods. In the normal nerve, J1/tenascin expression was confined to the extracellular matrix at the node of Ranvier and in the perineurium. At 2 days after nerve transection, J1/tenascin was detectable in the fibroblast-containing caps of the distal and proximal nerve stumps, in the distal nerve stump along its entire length and in the distal end of the proximal nerve stump. In the nerve stumps immunoreactivity was predominantly associated with extracellular matrix consisting of collagen fibrils and Schwann cell basal laminae. Approximately 7 days after transection, the caps of the nerve stumps had usually grown together forming a bridge. This bridge consisted of a J1/tenascin-negative perineurium-like structure and an inner part of predominantly fibroblasts, endothelial cells and macrophages. All cell types in this inner part were embedded in a J1/tenascin-positive matrix of collagen fibrils indicating the prospective direction of growth of neural elements. A few days later, J1/tenascin in the bridge was confined to the extracellular matrix around small Schwann cell-containing nerve fascicles. In nerves chronically denervated for 19 days, J1/tenascin was poorly detectable in the cap of the distal stump, although Schwann cells had infiltrated this cap. Approximately 19 days after the lesion, J1/tenascin expression returned to control levels in the proximal nerve stump. In the distal nerve stump, J1/tenascin immunoreactivity reached a peak at approximately 14 days after nerve transection and vanished only at approximately 35 days, thus correlating with the time of active regrowth of axons into the distal nerve stump. This reduction was prevented by chronic denervation, suggesting that reinnervation of target structures may be related to the down-regulation of J1/tenascin. These combined observations suggest that J1/tenascin is differentially regulated in the individual parts of the regenerating nerve, possibly triggered by different cellular and molecular signals.

Animals↗
PubMed1990

Expression of the adhesion molecules L1, N-CAM and J1/tenascin during development of the murine small intestine.

We have previously studied the immunohistological localization of the three adhesion molecules L1, N-CAM and J1/tenascin in adult mouse small intestine and shown that L1 expression in epithelial crypt cells underlies the adhesion of these cells to one another [63]. To obtain further insight into the functional roles of L1, N-CAM and J1/tenascin in this organ we studied their expression starting at embryonic day 14 during embryonic and early postnatal morphogenesis and during epithelial cell migration in the adult. Expression of L1 was restricted to neural cells until approximately postnatal day 5, when L1 started to be detectable on crypt but not on villus cells, predominantly on the basolateral membrane infoldings. As in brain, L1-specific mRNA was approximately 6 kb in size. L1 from intestine appears to differ from the brain-derived equivalent in possessing a higher level of glycosylation. N-CAM was detectable from embryonic day 14 onward in neural and also in mesenchymal cells. Expression by smooth muscle cells decreased during development. In the villus core, N-CAM was strongly detectable at contact sites between smooth muscle cells forming the cellular scaffold of the villus. From embryonic day 14 onward, N-CAM appeared in both 180- and 140-kDa forms. J1/tenascin was present in both neural and mesenchymal cells from embryonic day 14 onward. Starting at embryonic day 17, J1/tenascin appeared concentrated at the boundary between mesenchyme and epithelium in an increasing gradient from the crypt base to the villus top. From embryonic day 14 onward J1/tenascin consisted of the 190- and 220-kDa components. J1/tenascin from intestine differed from brain-derived J1 in its carbohydrate composition. These observations show that the three adhesion molecules are expressed by distinct cell populations and may serve as cell-type-specific markers in pathologically altered intestinal tissue.

Animals↗
PubMed1990

Expression of J1/tenascin in the crypt-villus unit of adult mouse small intestine: implications for its role in epithelial cell shedding.

The localization of the extracellular matrix recognition molecule J1/tenascin was investigated in the crypt-villus unit of the adult mouse ileum by immunoelectron microscopic techniques. In the villus region, J1/tenascin was detected strongly in the extracellular matrix (ECM) between fibroblasts of the lamina propria. It was generally absent in the ECM at the interface between subepithelial fibroblasts and intestinal epithelium, except for some restricted areas along the epithelial basal lamina of villi, but not of crypts. These restricted areas corresponded approximately to the basal part of one epithelial cell. In J1/tenascin-positive areas, epithelial cells contacted the basal lamina with numerous microvillus-like processes, whereas in J1/tenascin-negative areas the basal surface membranes of epithelial cells contacted their basal lamina in a smooth and continuous apposition. In order to characterize the functional role of J1/tenascin in the interaction between epithelial cells and ECM, the intestinal epithelial cell line HT-29 was tested for its ability to adhere to different ECM components. Cells adhered to substratum-immobilized fibronectin, laminin and collagen types I to IV, but not to J1/tenascin. When laminin or collagen types I to IV were mixed with J1/tenascin, cell adhesion was as effective as without J1/tenascin. However, adhesion was completely abolished when cells were offered a mixture of fibronectin and J1/tenascin as substratum. The ability of J1/tenascin to reduce the adhesion of intestinal epithelial cells to their fibronectin-containing basal lamina suggests that J1/tenascin may be involved in the process of physiological cell shedding from the villus.

Animals↗
PubMed1989

Immunocytochemical localization of the neural cell adhesion molecules L1, N-CAM, and J1 in Pacinian corpuscles of the mouse during development, in the adult and during regeneration.

The immunocytochemical localization of the neural cell adhesion molecules L1, N-CAM and J1/tenascin was investigated by light and electron microscopical techniques in murine Pacinian corpuscles during development, in the adult and in the regenerating state. In adult corpuscles, L1 was present only at contact sites between the sensory axon and inner core lamellae. From birth, the earliest stage tested, until day 7, L1 was additionally expressed on lamellar processes of the inner core cells. N-CAM was expressed in developing and adult corpuscles on lamellae and somata of the inner and outer core cells at their contact sites but was hardly detectable at contact sites between axolemma and inner core lamellae. J1/tenascin was found only in association with the extracellular material of the inner core, especially with the two radial clefts and the boundary space between inner and outer core. In developing corpuscles, J1/tenascin became detectable on extracellular material with the onset of inner core differentiation at approximately day 2. After transection or crush of the sciatic nerve, L1 disappeared from the corpuscles but reappeared with regrowing axons at contact sites between axonal membranes and inner core cells. At any regenerative stage inner core cells remained L1-negative. In denervated and reinnervated corpuscles the expression pattern of N-CAM and J1/tenascin did not differ from the normal adult. These observations suggest that a sensory organ, the Pacinian corpuscle, differs from the sciatic nerve and the neuromuscular junction in that its expression of adhesion molecules remains the same in the denervated state as in the innervated adult. Furthermore, in the denervated Pacinian corpuscle, adhesion molecule expression does not resemble that of any developmental stage tested. Thus, other cures than regulation of adhesion molecule expression patterns might be involved in the successful reinnervation of sensory corpuscles.

Aging↗
PubMed1989

Antibodies to the mammalian adhesion molecule J1/tenascin and its carbohydrate epitope L2/HNK-1 label the receptor lymph cavities of insect sensilla.

Data from light- and electronimmunocytochemistry gave evidence that the antibodies to the mammalian adhesion molecule J1/tenascin and its carbohydrate structure L2/HNK-1 react with immunoreactive structures present in the inner and outer receptor lymph cavities of antennal sensilla of the honey bee. Immunoreactivity was additionally present in the cytoplasm of the enveloping cells surrounding the receptor lymph cavities. Cell contacts between enveloping cells and between dendrites and enveloping cells were never observed to be antigen positive.

Animals↗
PubMed1988

Immunocytological localization of the major peripheral nervous system glycoprotein P0 and the L2/HNK-1 and L3 carbohydrate structures in developing and adult mouse sciatic nerve.

Immunocytological localization of the major glycoprotein of peripheral myelin P0 and its associated carbohydrate structures L2/HNK-1 and L3 was performed at the light- and electron-microscopic levels in mouse sciatic nerves at several developmental stages and in adulthood. P0 was first expressed on Schwann cells at the time that Schwann cells associated with axons on a 1:1 basis. P0 remains expressed at all times of myelin formation and in compact myelin. After cessation of myelination P0 is no longer detectable in the uncompacted parts of myelin, i.e., Schmidt-Lanterman incisures, paranodal loops, and outer and inner mesaxons. P0 is not detectable on basement membranes, interstitial collagens, and non-myelin-forming Schwann cells. The associated carbohydrate epitope L2 does not follow the expression of P0 at any developmental or adult stage. Until 21 days the L2 epitope is confined to nonmyelinated fibers. In sciatic nerves of mice older than 8 weeks, however, only a few nonmyelinated fibers remain L2-positive. L2 immunoreactivity is clearly seen in a subpopulation of compact myelin figures largely associated with motor fibers. The L3 epitope is never detectable on nonmyelinated fibers and becomes first visible when compact myelin is discerned. Unlike the L2 epitope L3 is present in most, if not all, compact myelin figures. These observations suggest that P0 may be involved in ensheathment of axons by Schwann cells at the decisive stages of initiation of myelination and later on, possibly in conjunction with the L3 carbohydrate structure, in maintenance of compact myelin. The appearance of the L2 carbohydrate epitopes in compact myelin of largely motor and fewer sensory nerve fibers at times when morphogenesis of myelin has ceased remains to be elucidated in functional terms.

Animals↗
PubMed1988

Immunoelectron microscopic localization of neural cell adhesion molecules (L1, N-CAM, and myelin-associated glycoprotein) in regenerating adult mouse sciatic nerve.

The localization of the neural cell adhesion molecules L1, N-CAM, and the myelin-associated glycoprotein was studied by pre- and postembedding staining procedures at the light and electron microscopic levels in transected and crushed adult mouse sciatic nerve. During the first 2-6 d after transection, myelinated and nonmyelinated axons degenerated in the distal part of the proximal stump close to the transection site and over the entire length of the distal part of the transected nerve. During this time, regrowing axons were seen only in the proximal, but not in the distal nerve stump. In most cases L1 and N-CAM remained detectable at cell contacts between nonmyelinating Schwann cells and degenerating axons as long as these were still morphologically intact. Similarly, myelin-associated glycoprotein remained detectable in the periaxonal area of the degenerating myelinated axons. During and after degeneration of axons, nonmyelinating Schwann cells formed slender processes which were L1 and N-CAM positive. They resembled small-diameter axons but could be unequivocally identified as Schwann cells by chronical denervation. Unlike the nonmyelinating Schwann cells, only few myelinating ones expressed L1 and N-CAM. At the cut ends of the nerve stumps a cap developed (more at the proximal than at the distal stump) that contained S-100-negative and fibronectin-positive fibroblast-like cells. Most of these cells were N-CAM positive but always L1 negative. Growth cones and regrowing axons expressed N-CAM and L1 at contact sites with these cells. Regrowing axons of small diameter were L1 and N-CAM positive where they made contact with each other or with Schwann cells, while large-diameter axons were only poorly antigen positive or completely negative. 14 d after transection, when regrowing axons were seen in the distal part of the transected nerve, regrowing axons made L1- and N-CAM-positive contacts with Schwann cells. When contacting basement membrane, axons were rarely found to express L1 and N-CAM. Most, if not all, Schwann cells associated with degenerating myelin expressed L1 and N-CAM. In crushed nerves, the immunostaining pattern was essentially the same as in the cut nerve. During formation of myelin, the sequence of adhesion molecule expression was the same as during development: L1 disappeared and N-CAM was reduced on myelinating Schwann cells and axons after the Schwann cell process had turned approximately 1.5 loops around the axon. Myelin-associated glycoprotein then appeared both periaxonally and on the turning loops of Schwann cells in the uncompacted myelin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Microcythemia from anemic hypoxia and normal erythropoiesis in the newt.

Specimens of the newt, Triturus cristatus carnifex (Laurenti), rendered totally anemic, restore erythron by cyclic waves of erythropoietic activity that alternate with intervals of stasis. Hemolysis is obtained by administering 25 mg/liter of acetylphenylhydrazine in the breeding water for 36 h. The first cycle of erythropoietic activity produces microcytes, which have completely differentiated by 8 weeks after treatment. However, if the animals are raised in a hyperbaric chamber at a pressure of 1.5 atmospheres, in order to compensate for hypoxia, normocytes are produced. In both cases the hematocrit and hematic concentration of hemoglobin reach analogous values, so microcythemia appears to be the only effect of hypoxia. The hemoglobin, hematocrit values, and normocyte counts in hyperbaric animals are about one-half those of the controls newts. These data, together with those on the life span of red blood cells (RBC) and time span between two successive erythropoietic cycles (2 months and 1 month, respectively), indicate that the newts normally keep only two sets (one new, one old) of RBC in circulation, whose approximate parameters can be defined as RBC count: 60,000/mm3, hematocrit: 17%, and hemoglobin: 5.4 g/100 ml.

Anemia, Hemolytic↗
PubMed1986

Immunoelectron microscopic localization of neural cell adhesion molecules (L1, N-CAM, and MAG) and their shared carbohydrate epitope and myelin basic protein in developing sciatic nerve.

The cellular and subcellular localization of the neural cell adhesion molecules L1, N-CAM, and myelin-associated glycoprotein (MAG), their shared carbohydrate epitope L2/HNK-1, and the myelin basic protein (MBP) were studied by pre- and post-embedding immunoelectron microscopic labeling procedures in developing mouse sciatic nerve. L1 and N-CAM showed a similar staining pattern. Both were localized on small, non-myelinated, fasciculating axons and axons ensheathed by non-myelinating Schwann cells. Schwann cells were also positive for L1 and N-CAM in their non-myelinating state and at the onset of myelination, when the Schwann cell processes had turned approximately 1.5 loops. Thereafter, neither axon nor Schwann cell could be detected to express the L1 antigen, whereas N-CAM was found in the periaxonal area and, more weakly, in compact myelin of myelinated fibers. Compact myelin, Schmidt-Lanterman incisures, paranodal loops, and finger-like processes of Schwann cells at nodes of Ranvier were L1-negative. At the nodes of Ranvier, the axolemma was also always L1- and N-CAM-negative. The L2/HNK-1 carbohydrate epitope coincided in its cellular and subcellular localization most closely to that observed for L1. MAG appeared on Schwann cells at the time L1 expression ceased. MAG was then expressed at sites of axon-myelinating Schwann cell apposition and non-compacted loops of developing myelin. When compaction of myelin occurred, MAG remained present only at the axon-Schwann cell interface; Schmidt-Lanterman incisures, inner and outer mesaxons, and paranodal loops, but not at finger-like processes of Schwann cells at nodes of Ranvier or compacted myelin. All three adhesion molecules and the L2/HNK-1 epitope could be detected in a non-uniform staining pattern in basement membrane of Schwann cells and collagen fibrils of the endoneurium. MBP was detectable in compacted myelin, but not in Schmidt-Lanterman incisures, inner and outer mesaxon, paranodal loops, and finger-like processes at nodes of Ranvier, nor in the periaxonal regions of myelinated fibers, thus showing a complementary distribution to MAG. These studies show that axon-Schwann cell interactions are characterized by the sequential appearance of cell adhesion molecules and MBP apparently coordinated in time and space. From this sequence it may be deduced that L1 and N-CAM are involved in fasciculation, initial axon-Schwann cell interaction, and onset of myelination, with MAG to follow and MBP to appear only in compacted myelin. In contrast to L1, N-CAM may be further involved in the maintenance of compact myelin and axon-myelin apposition of larger diameter axons.

Aging↗