神经细胞粘附分子在癫痫形成过程中的表达

目的　探讨癫痫发生前即癫痫形成过程中神经细胞粘附分子 (neural cell adhesion m olecule,NCAM)的作用。方法　以戊四氮 (pentylenetetrazol,4 0 mg/ kg,腹腔注射 ,每日一次 )点燃 Wistar大鼠为对象 ,取在点燃前不同时间点的大鼠海马为标本 ,运用 RT- PCR技术测定对照组、苯巴比妥干预组和非苯巴比妥药物干预组在点燃前各时间点大鼠海马 NCAM m RNA表达。结果　非苯巴比妥药物干预组大鼠均于 17～ 2 3d点燃 ,而药物干预组在 30～ 38d点燃 ,且行为学和 EEG痫样放电均低于非药物干预组 ,苯巴比妥药物干预组 NCAM m RNA表达明显低于非干预组相应时间点 NCAM m RNA表达 ,有明显差异 (P<0 .0 1)。非干预组 NCAM m RNA表达明显高于对照组 ,有显著性差异 (P<0 .0 1)。结论　点燃前 NCAM m RNA表达量与点燃过程呈正相关 ,说明 NCAM在癫痫形成过程中起重要作用。     

Inverse expression of olfactory cell adhesion molecule in a subset of olfactory axons and a subset of mitral/tufted cells in the developing rat main olfactory bulb

The projection of olfactory sensory neuron (OSN) axons from the olfactory epithelium (OE) to the olfactory bulb (OB) is highly organized but topographically complex. Evidence suggests that odorant receptor expression zones in the OE map to the OB about orthogonal axes. One candidate molecule for the formation of zone-specific targeting of OSN axon synapses onto the OB is the olfactory cell adhesion molecule (OCAM). OCAM(+) OSNs are restricted to three of the four zones in the OE and project their axons to the ventral OB where they form synapses with mitral/tufted (M/T) cells. To determine when this zonal connection is established, we have examined OCAM expression in rat olfactory system, during seminal periods of glomerular formation. OCAM(+) axons sort out in the ventral olfactory nerve layer of the OB before glomerular formation. Surprisingly, OCAM was also expressed transiently by subsets of M/T cell dendrites located in the dorsal OB. The expression of OCAM by OSN axons and M/T dendrites was asymmetrical; in the dorsal OB, OCAM(-) OSN axons synapsed on OCAM(+) M/T dendrites, whereas in the ventral OB, OCAM(+) OSN axons synapsed on OCAM(-) M/T dendrites. The restricted spatial map of OCAM(+) M/T cells appeared earlier in development than the zonal segregation of OCAM(+) OSN axons. Thus, OCAM on M/T cell dendrites may act in a spatiotemporal window to specify regions of the developing rat OB, thereby establishing a foundation for mapping of the OE zonal organization onto the OB.     

条件性恐惧消退过程中大鼠边缘下区突触素和神经细胞黏附分子的变化

目的 研究条件性恐惧消退过程中,内侧前额叶边缘下区突触素、神经细胞黏附分子免疫反应阳性物质的动态变化.方法 将72只成年雄性SD大鼠随机分为自然消退组(条件恐惧建立后不进行消退训练,n=24)、立即消退组(条件恐惧建立后15 min进行消退训练,n=24)和24 h消退组(条件恐惧建立后24 h进行消退训练,n=24),采用声音提示的足底电击建立大鼠恐惧记忆,然后单独给声音信号进行恐惧消退训练.在条件恐惧建立后(立即消退组和24 h消退组在消退训练后)第1,3,7和20天分别进行消退保持测验,并在各时间点取边缘下区标本进行突触素、神经细胞黏附分子的免疫组化研究.结果 在恐惧消退过程中,(1)3组大鼠消退成绩整体呈上升趋势,其中24h消退组在第7天最高[(79±17)%],且在各时间点消退保持成绩最好(P<0.01);(2)3组大鼠边缘下区突触素免疫反应阳性物质逐渐增加而后减少,第7天最高(P<0.01);(3)3组大鼠边缘下区神经细胞黏附分子免疫反应阳性物质逐渐增加,其中自然消退组在消退后第3天最高,其余2组在消退后第7天最高(P<0.01).结论 恐惧消退后3～7 d,边缘下区突触可塑性相关物质水平能较好地反映消退记忆的保持情况.     

Structure, expression, and function of Ng-CAM, a member of the immunoglobulin superfamily involved in neuron-neuron and neuron-glia adhesion.

The neuron-glia cell adhesion molecule (Ng-CAM) mediates neuron-neuron adhesion by a homophilic mechanism and neuron-astrocyte adhesion by a heterophilic mechanism. The protein is expressed on neurons and Schwann cells but not on astrocytes. It is most prevalent during development on cell bodies of migrating neurons and on axons during formation of nerves. Ng-CAM expression is greatly increased following nerve injury. Anti-Ng-CAM antibodies inhibited migration of granule cells along Bergmann glia in cerebellar explants and fasciculation of neurites in outgrowths from explants of dorsal root ganglia. The combined results indicate that Ng-CAM on neurons binds to Ng-CAM on adjacent neurons and to as yet unidentified ligands on astrocytes. Ng-CAM is synthesized in chicken neurons from a 6 kb mRNA as Mr approximately 200,000 forms which are cleaved to yield two components of Mr 135,000 and 80,000. It is glycosylated and can be phosphorylated. Amino acid sequence analysis indicates that it contains six immunoglobulin domains, five fibronectin type III repeats, a transmembrane domain and a cytoplasmic region. Structural analyses indicate that Ng-CAM is most closely related to the mammalian glycoprotein L1 but significant differences between them strongly suggest that they are not equivalent molecules. The recent identification of another structurally related molecule in the chicken called Nr-CAM underscores the notion that these molecules are members of a subfamily of neural cell adhesion molecules within the immunoglobulin superfamily that have related or complementary functions in the nervous system.     

Cannabinoids modulate Olig2 and polysialylated neural cell adhesion molecule expression in the subventricular zone of post-natal rats through cannabinoid receptor 1 and cannabinoid receptor 2

The subventricular zone (SVZ) is a source of post-natal glial precursors that can migrate to the overlying white matter, where they may differentiate into oligodendrocytes. We showed that, in the post-natal SVZ ependymocytes, radial glia and astrocyte-like cells express cannabinoid receptor 1 (CB1), whereas cannabinoid receptor 2 (CB2) is found in cells expressing the polysialylated neural cell adhesion molecule. To study CB1 and CB2 function, post-natal rats were exposed to selective CB1 or CB2 agonists (arachidonyl-2-chloroethylamide and JWH-056, respectively) for 15 days. Accordingly, we found that CB1 activation increases the number of Olig2-positive cells in the dorsolateral SVZ, whereas CB2 activation increases polysialylated neural cell adhesion molecule expression in this region. As intense myelination occurs during the first weeks of post-natal development, we examined how modulating these factors affected the expression of myelin basic protein. Pharmacological administration of agonists and antagonists of CB1 and CB2 showed that the activation of both receptors is needed to augment the expression of myelin basic protein in the subcortical white matter.     

Expression of the immunoglobulin superfamily neuroplastin adhesion molecules in adult and developing mouse cerebellum and their localisation to parasagittal stripes

Neuroplastin (np) 55 and 65 are immunoglobulin superfamily members that arise by alternative splicing of the same gene and have been implicated in long-term activity-dependent synaptic plasticity. Both biochemical and immunocytochemical data suggest that np55 is the predominant isoform (>95% of total neuroplastin) in cerebellum. Neuroplastin immunoreactivity is concentrated in the molecular layer and synaptic glomeruli in the granule cell layer. Expression in the molecular layer appears to be postsynaptic. First, neuroplastin is associated with Purkinje cell dendrites in two mouse granuloprival cerebellar mutants, disabled and cerebellar deficient folia. Second, in an acid sphingomyelinase knockout mouse with widespread protein trafficking defects, neuroplastin accumulates in the Purkinje cell somata. Finally, primary cerebellar cultures show neuroplastin expression in Purkinje cell dendrites and somata lacking normal histotypic organization and synaptic connections, and high-magnification views indicate a preferential association with dendritic spines. In the molecular layer, differences in neuroplastin expression levels present as a parasagittal array of stripes that alternates with that revealed by the expression of another compartmentation antigen, zebrin II/aldolase c. Neuroplastin immunoreactivity is first detected weakly at postnatal day 3 (P3) in the anterior lobe vermis. By P5, parasagittal stripes are already apparent in the immature molecular layer. At this stage, punctate deposits are also localised at the perimeter of the Purkinje cell perikarya; these are no longer detected by P15. The data suggest a role for neuroplastins in the development and maintenance of normal synaptic connections in the cerebellum.     

慢性应激对大鼠学习记忆功能和海马神经细胞粘附分子表达的影响

目的观察慢性应激对大鼠学习记忆功能和海马神经细胞粘附分子（NCAM）表达的影响,探讨海马NCAM表达在慢性应激影响学习记忆机制的作用。方法20只SD大鼠随机被分为对照组（10只）和慢性应激组（10只）,后者以束缚浸水应激方式连续应激21天,三周后行水迷宫实验,并用免疫组化法测定大鼠的脑海马区NCAM的表达。结果应激组在水迷宫测试中寻找水中隐藏平台的潜伏期为（7．1±8．9）秒,对照组为（12．3±4．2）秒,差异有统计学意义;穿越平台次数：应激组为（8．4±1．1）次,对照组为（12．5±1．9）次,差异有统计学意义。应激组海马CA3区NCAM的表达：25．2％±3．6％,对照组为37．9％±5．1％,差异有统计学意义。结论慢性应激对大鼠的学习记忆功能有抑制作用。其机制可能与应激抑制海马CA3区NCAM表达有关。     

Serotonin depletion in the adult rat produces differential changes in highly polysialylated form of neural cell adhesion molecule and tenascin‐C immunoreactivity

Levels of immunoreactivity for highly polysialylated neural cell adhesion molecule (PSA‐NCAM), NCAM, and tenascin‐C (TN‐C), were examined in the basal ganglia regions and hypothalamic nuclei of adult rats after serotonergic (5‐HT) lesions induced by 5,7‐dihydroxytryptamine injections in the dorsal and medial raphe nuclei. Decreases in the density of serotonin fibers were associated with no changes in NCAM and general decreases in PSA‐NCAM staining, the time‐course of changes being selective for each region. Taken that the confocal analysis indicated that serotonin neurons do not express PSA‐NCAM and that similar decreases in PSA‐NCAM staining were observed after inhibition of 5‐HT synthesis induced by parachlorophenylalanine administration, these results suggest that 5‐HT may reduce adhesion by acting on PSA‐NCAM expression in its environment, and thus facilitate plasticity in adult brain. Two months after the neurotoxin lesions, a normalization of PSA‐NCAM staining was associated with a partial restoration in 5‐HT fiber density in the nucleus accumbens and the supraoptic nucleus, suggesting that PSA‐NCAM may facilitate sprouting of 5‐HT fibers. Since a similar normalization was also detected in the suprachiasmatic nucleus, which remained deprived of serotonin fibers, negative factors are likely to be involved in regeneration processes. Indeed, increases in glial fibrillary acidic protein (GFAP) followed by increases in TN‐C were observed in these areas, suggesting that the secretion of TN‐C by astrocytes may have negative consequences on the sprouting of 5‐HT fibers. Finally, the lack of changes in striatal PSA‐NCAM or TN‐C staining observed after selective lesions of the dopaminergic pathway induced by intranigral injections of 6‐hydroxydopamine indicates that 5‐HT has a selective and critical role in adult brain plasticity. J. Neurosci. Res. 55:54–70, 1999. © 1999 Wiley‐Liss, Inc.     

Reduction of hippocampal long-term potentiation in transgenic mice ectopically expressing the neural cell adhesion molecule L1 in astrocytes

The influence of the neural cell adhesion molecule L1 on hippocampal long-term potentiation (LTP) was investigated using transgenic mice ectopically expressing L1 in astrocytes (GFAP-L1). L1 is a member of the immunoglobulin superfamily of homophilic adhesion molecules predominantly expressed in neurones. Previously, it has been demonstrated that local application of L1 antibodies and recombinant L1 fragments impair the expression of LTP. Here, we show that LTP induced by theta-burst stimulation or by pairing presynaptic stimulation with postsynaptic depolarisation was strongly reduced in GFAP-L1 mice, whereas basal synaptic transmission, post-tetanic potentiation, and paired-pulse facilitation were not modified. These results further support the idea that L1 is involved in synaptic plasticity and suggest that adhesion molecule-dependent changes in synaptic morphology contribute to the expression of LTP. © 1996 Wiley-Liss, Inc.     

Expression of 3-fucosyl-N-acetyllactosamine on glia cells and its putative role in cell adhesion

Summary Mouse monoclonal antibodies from five clones (MMA, 1G10, VIM C6, MC-1 and Tü9), elicited to human myeloid cells and reactive with the 3-fucosyl-N-acetyllactosamine sequence (also termed X-determinant), cross-react with glia cells from human and rat brain. In brain cell cultures from neonatal rats both astrocytes and oligodendrocytes express the X-determinant during the first period of the culture as shown by immunofluorescence tests. While the astrocytes, which exhibit signs of adhesion, permanently express the X-determinant, the oligoden-drocytes lose the epitope nearly completely during culture. The oligodendrocytes preferentially grow on top of the astrocytic layer. After about 8–10 days of culture, numerous X-determinant-positive astrocytic membranes show oligodendrocyte-shaped negative print images underneath the galactocerebroside-positive oligodendrocytes. At this time, the oligodendrocytes are relatively firmly attached to the astrocytic layer. Since participation of the X-determinant in the compaction of the mouse 8–32 cell stage is being discussed, we conclude from our observations that the X-determinant may also play a role in the astrocyte-astrocyte and astrocyte-oligodendrocyte adhesion. It may represent the functionally active carbohydrate moiety of a heterotypic cell adhesion molecule of glia cells.Supported by the Gemeinnützige Hertie-Stiftung, Frankfurt/Main. The Heinrich-Pette-Institut is financially supported by Freie und Hansestadt Hamburg and Bundesministerium für Jugend, Familie, Frauen und Gesundheit     

Identification of a cDNA clone specific for the neural cell adhesion molecule AMOG

A cDNA clone of the neural cell adhesion molecule AMOG was isolated from a lambda gt10 library constructed from 8-day-old mouse brain poly(A) + RNA with a 17mer oligonucleotide probe designed from a nonapeptide sequence obtained from tryptic peptides of AMOG. The cDNA clone expressed as a fusion protein that is recognized by polyclonal AMOG antibodies; conversely, polyclonal antibodies prepared against the fusion protein react with AMOG. The clone contains the full sequence derived from the nonapeptide. Of all tissues tested, only brain expresses detectable levels of AMOG by ELISA and Northern blot analyses, indicating a high correlation in expression at the protein and mRNA levels. Both brain and astrocytes express a 3 kb long mRNA, which appears to be encoded by a single gene.     

Expression of cell adhesion molecules by microvascular endothelial cells in the cortical and subcortical regions of the normal human brain: an immunohistochemical analysis

We studied the repertoire of junctional, cell–matrix and leucocyte–endothelial adhesion molecules normally expressed by cortical and subcortical brain microvessels, as compared with large intracranial vessels. An indirect immunoperoxidase method was applied to acetone‐fixed cryostat sections of normal brain tissue obtained from 10 adult patients during surgical resections for intracranial aneurysms or at autopsy. Like large intracranial vessels, brain microvessels expressed the two endothelial‐specific junctional cell adhesion molecules VE‐cadherin and platelet–cell adhesion molecule‐1. We verified that they also expressed the molecular components of adherens‐type junctions, including catenins, plakoglobin, vinculin and α‐actinin. Brain microvessels expressed a large repertoire of integrin molecules of the β1, β3 and β4 subfamilies. However, they displayed apparently lower levels of α2, α5, αV and β3 integrin chains than large intracranial vessels. Brain microvessels constitutively expressed large amounts of the leucocyte–endothelial adhesion molecules, intercellular adhesion molecule (ICAM)‐2 and CD34 and very low amounts of ICAM‐1 and lymphocyte function‐associated antigen‐3. In contrast to large intracranial vessels, brain microvessels presented no constitutive expression of P‐selectin. Our study shows that, in contrast to their highly specific structural and functional characteristics, brain microvascular endothelial cells present a repertoire of cell adhesion molecules very similar to that of most other capillary vessels in the body.     

Signaling events following the interaction of the neuronal adhesion molecule F3 with the N-terminal domain of tenascin-R

Interaction between the extracellular matrix protein tenascin-R and the neuronal adhesion molecule F3 might be involved in the formation of neuronal networks. In this study, the fragment of tenascin-R comprising epithelial growth factor (EGF)-like repeats and the cysteine-rich NH2 terminal stretch (EGF-L), known to be inhibitory for growing neurites and repellent for growth cones, was used to investigate the signaling events following the F3/EGF-L interaction. We addressed this question using an in vitro test with F3-transfected Chinese hamster ovary (CHO) cells that allowed us to measure the kinetics, magnitude and specificity of the repellent effect resulting from the specific F3/EGF-L interaction. We showed that the repellent effect was counteracted by addition of the serine/threonine kinase and -phosphatase modulators (staurosporine, okadaic acid and H7) but not by modulators of tyrosine kinase or -phosphatases. This result indicates that the intracellular signals activated by the repellent effect involve a serine/threonine kinase pathway. Furthermore, the repellent effect of the EGF-L fragment for growth cones of cultured cerebellar neurons was also abolished by the identical modulators of serine/threonine kinase and -phosphatases. The inhibition of neurite outgrowth from hippocampal neurons by EGF-L was abolished in the presence of the serine threonine-kinase inhibitor H7. These results strongly suggest that the F3/tenascin-R interaction through EGF-L involves an intracellular activation of serine/threonine kinase(s) in all F3-expressing cells tested. J. Neurosci. Res. 49:698–709, 1997. © 1997 Wiley-Liss, Inc.     

Neural cell adhesion molecule and D3 protein in the cerebellum of weaver mutant mice

Weaver (wv/wv) mutant mice are characterized by extensive granule cell degeneration and can therefore be used as a model for brain degeneration that does not involve blood-brain barrier damage. The ontogeny of the neural cell adhesion molecule (NCAM) and the neuronal antigen D3 protein were investigated in cerebellum and forebrain of weaver mutant mice up to post-natal day 60. In the forebrain the concentration of both proteins was virtually unchanged. In cerebellum, in contrast, the concentration of D3 decreased markedly whereas that of NCAM remained unchanged. Similar findings were obtained at post-natal day 30 in the cerebellum of other neurologic mutants, namely the staggerer (sg/sg) and reeler (rl/rl). At this age the concentration of a synaptic vesicle marker, synaptophysin. was severely decreased in the cerebellum of all three mutants. The concentration of neuron-specific enolase was less affected, whereas the concentrations of the glial markers glutamine synthetase and glial fibrillary acidic protein were both increased. The concentration ratio, which probably reflects the ongoing rate of synaptic remodelling, was increased during the whole ontogeny of weaver mutant mice as compared with heterozygous controls. At post-natal day 30, the ratio was increased by 180% in weaver, by 170% in staggerer and by 60% in reeler cerebellum. These findings lend further support to the usefulness of the ratio as a marker of neural plasticity and synaptic remodelling in both animals and man.     

Astrocyte activation by Sindbis virus: Expression of GFAP,cytokines, and adhesion molecules

Sindbis virus (SV) is a member of the alphaviruses which has served as a model system for studying viral encephalitis. Although astrocytes are reported to be involved in the pathogenesis of various virus-related diseases, the effects of SV on astrocyte function have not been reported. In this study we compared the effects of two strains of SV, SVA, and SVNI, which differ in their neurovirulent properties, on astrocytes with the use of cultured mouse astrocytes and the rat C6 glial cell line. We found that although both strains can similarly infect and replicate in astrocytes, they induced different changes in the function of these cells. The neurovirulent strain, SVNI, induced a decrease in cell number and a marked increase in the expression of GFAP, whereas SVA did not alter these parameters. In addition, SVNI induced the secretion of the cytokines TNF-α and IL-6, the expression of adhesion molecules, and the production of the neurotrophic factor NGF. In contrast, SVA induced smaller increases in the secretion of IL-6 and NGF but did not alter the secretion of TNF-α and the expression of the adhesion molecules. Neither virus induced the secretion of IL-2, IL-4, IL-10 and IFN-γ or the expression of iNOS in the cells. These results indicate that astrocytes, similar to neurons, can serve as target cells to SV infection in the CNS. Moreover, the infection of astrocytes by SVNI leads to changes characteristic of reactive astrogliosis which may contribute to the pathogenesis of SV-induced encephalitis by enhancing the local immune response in the CNS. Glia 19:275–285, 1997. © 1997 Wiley-Liss, Inc.     

Expression of four immunoglobulin superfamily adhesion molecules (L1, Nr-CAM/Bravo,neurofascin/ABGP,and N-CAM)in the developing mouse spinal cord

To identify cell adhesion molecules (CAMs) expressed by mammalian motoneurons, we applied the polymerase chain reaction to a murine motor neuron-like cell line, NSC-34. Using primers derived from a group of Ll-related CAMs, we cloned two alternatively spliced forms of mouse L1, which differ by a 12-base-pair insert, plus putative murine orthologs of the chicken cell adhesion molecules Nr-CAM/Bravo and neurofascin. All four mRNAs are expressed in NSC-34 cells, but only neurofascin and the insert-minus form of Ll are expressed in its neuroblastoma parent, N18TG2. Analysis of RNA in neonatal tissues reveals expression largely restricted to the brain and spinal cord. In situ hybridization histochemistry of spinal cord shows that motoneurons express L1, Nr-CAM, and neurofascin as well as N-CAM. Ll and N-CAM RNAs are detected throughout the period studied (from embryonic day,[E]11 to postnatal day [P]28), whereas Nr-CAM is expressed only at early ages (<E15) and neurofascin is predominantly expressed postnatally. Moreover, each CAM is expressed by distinct subsets of neighboring cells and at distinct times. For example, Nr-CAM mRNA is present in floor plate cells of embryonic spinal cord, whereas neurofascin is expressed by a subset of glia postnatally. Finally, we show that each CAM has a distinct spatiotemporal pattern of expression in dorsal root ganglia. © 1995 Wiley-Liss, Inc.     

GlialCAM, an immunoglobulin-like cell adhesion molecule is expressed in glial cells of the central nervous system

Using structure based genome mining targeting vascular endothelial and platelet derived growth factor immunoglobulin (Ig) like folds, we have identified a sequence corresponding to a single transmembrane protein with two Ig domains, which we cloned from a human brain cDNA library. The cDNA is identical to hepatocyte cell adhesion molecule (hepaCAM), which was originally described as a tumor suppressor gene in liver. Here, we show that the protein is predominantly expressed in the mouse and human nervous system. In liver, the expression is very low in humans, and is not detected in mice. To identify the central nervous system (CNS) regions and cell types expressing the protein, we performed a LacZ reporter gene assay on heterozygous mice in which one copy of the gene encoding the novel protein had been replaced with beta-galactosidase. beta-galactosidase expression was prominent in white matter tracts of the CNS. Furthermore, expression was detected in ependymal cells of the brain ventricular zones and the central canal of the spinal cord. Double labeling experiments showed expression mainly in CNPase positive oligodendrocytes (OL). Since the protein is predominantly expressed in the CNS glial cells, we named the molecule glial cell adhesion molecule (GlialCAM). A potential role for GlialCAM in myelination was supported by its up-regulation during postnatal mouse brain development, where it was concomitantly expressed with myelin basic protein (MBP). In addition, in vitro, GlialCAM was observed in various developmental stages of OL and in astrocytes in processes and at cell contact sites. In A2B5 positive OL, GlialCAM colocalizes with GAP43 in OL growth cone like structures. Overall, the data presented here indicate a potential function for GlialCAM in glial cell biology.     

Cellular localization of the neural cell adhesion molecule L1 in adult rat neuroendocrine and endocrine tissues: comparisons with NCAM.

The tissue distribution and cellular localization of the neural cell adhesion molecule L1 was determined by immunocytochemistry at the optical and ultrastructural levels in adult rat neuroendocrine tissues and pancreatic endocrine cells. L1 was found to be abundant in the neurohypophysis but undetectable in the rest of the pituitary gland. It was barely detectable in the normal rat endocrine pancreas, but a rat pancreatic insulinoma cell line was found by immunofluorescence to express low levels of L1. In the adrenal medulla, it was present on a sub-population of chromaffin cells and its density appeared to be lower on surfaces exposed to the extracellular matrix. Double immunolabelling showed this sub-population to consist of noradrenergic chromaffin cells. Adrenergic chromaffin cells were found not to express L1. In addition, the tissue distribution and cellular localization of NCAM mRNAs was determined by in situ hybridization, extending our previous studies on the cellular expression of NCAM proteins in endocrine and neuroendocrine tissues. This confirmed that the NCAM message has a wider cellular distribution than L1 within the hypophysis and the adrenal gland. In addition to secretory cells, L1 immunoreactivity was detected in glial cells, in particular in the pituicytes of the neurohypophysis, which further distinguishes them from astrocytes, their counterparts in the central nervous system. These data are discussed in terms of the different embryological origins of the various endocrine tissues examined and also in terms of the specific design constraints imposed on these tissues during their development.     

Myelination and glial ensheathment of purkinje cells in cerebellar cultures are not inhibited by antibodies to the neural cell adhesion molecule, N-CAM

Mouse cerebellar cultures were exposed to anti-N-CAM antibodies throughout their in vitro development. Some cultures were stripped of myelinating oligodendrocytes and functionally competent astrocytes by treatment with cytosine arabinoside (Ara C), while others were left untreated and were potentially capable of forming myelin around axons and astrocytic sheaths around Purkinje cell somata and dendrites. As expected, the antibodies inhibited axonal fasciculation in the Ara C treated cultures. However, the same antibodies had no discernible effect on formation of myelin or astrocytic sheaths in cultures not treated with Ara C. N-CAM is expressed on the surfaces of neurons, oligodendroglia and astrocytes, and has been proposed as the signal molecule governing both kinds of neuron-glia interactions. The observations of the present study strongly suggest, however, that N-CAM does not have an indispensable role in such interactions.