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At least 19 recordsLinked to original sources
PubMed1985

Parameters of neuritic growth from ciliary ganglion neurons in vitro: influence of laminin, schwannoma polyornithine-binding neurite promoting factor and ciliary neuronotrophic factor.

Ciliary ganglion neurons extend neuritic processes when cultured for 24 h in medium containing ciliary neuronotrophic factor (CNTF) and on a polyornithine substratum precoated with either laminin or a Schwannoma-derived neurite promoting factor (PNPF). We have examined the roles of laminin, PNPF and CNTF for each of four parameters of neuritic growth, including: initiation time, neuronal polarity, neuritic branching and average neurite output (lengths) with time. Increasing laminin and PNPF levels were found to advance the time of neurite initiation as well as shift the majority (70-80%) of the neurons from a unipolar to multipolar neuritic morphology. The polarity imposed by any given concentration of either neurite promoting factor remained constant over the 24 h culture period examined. The average lengths from the longest neurites per neuron over a 10-28 h culture interval were not affected by increasing levels of laminin or PNPF, but total neuritic output per neuron was increased. This increased total neuritic output could be attributed to a combination of earlier neuritic initiation time and an increased neuronal polarity at high laminin or PNPF levels. CNTF at threshold survival levels did not promote initiation time, neuronal polarity or total neuritic output. However, cultures receiving less CNTF than that required for maximal neuronal survival displayed an increased neuronal polarity and a reduced neuritic output before any apparent loss of neurons. Neuritic branching was not affected by either the neurite promoting or trophic factors after 24 h of culture. Laminin and PNPF were found to be indistinguishable in their effects on the ciliary ganglion neurons in each of the four parameters studied.

Animals↗
PubMed1992

[Neuritic degeneration in Alzheimer-type dementia, with special reference to the presence of dark neurites].

Four cases of neuritic degeneration in the cerebral cortex of Alzheimer-type dementia patients have been examined by routine and Gallyas-silver electron microscopy. This examination has revealed neuritic changes described below. (1) Dendrites and axons with an increased electron density (dark neurites) were found scattered throughout the neuropils, these dark neurites thought to be either degraded neurites resulting from simple neuronal atrophy or retrograde and/or transsynaptic degeneration due to an axonal injury within the senile plaques. (2) Both dystrophic neurites and neuropil threads were found scattered throughout the neuropils and showed some similarities in producing abnormal substances in their processes and in their manner of aggregating, especially within the senile plaque region. These degenerated neurites may have been caused by neurotoxicity of the amyloid. On Gallyas electron microscopic inspection, neurites often are found to have small fibrous and sometimes tubular structures on which silver particles are deposited. This finding may represent the initial stage of a neurofibrillary change. (3) The regeneration of neurites though such ultrastructures is not known, but such concept is believed by many authors and is discussed.

Aged↗
PubMed1992

Tangle-associated neuritic clusters. A new lesion in Alzheimer's disease and aging suggests that aggregates of dystrophic neurites are not necessarily associated with beta/A4.

Abnormal (dystrophic) neurites are widespread in the brains of patients with Alzheimer's disease (AD). Subsets of these neurites cluster in intimate association with amyloid deposits, constituting classic senile plaques. Two major markers expressed by many plaque-associated neurites are the microtubule associated protein tau and chromogranin A, a soluble protein of large dense core synaptic vesicles. The authors show a new type of lesion, tangle-associated neuritic clusters (TANCs), in which abnormal neurites form dense aggregates, each centered by an extracellular (ghost) neurofibrillary tangle, rather than an amyloid deposit. Neurites in TANCs are similar to plaque neurites in shape and expression of tau and chromogranin A, and different from a second, nonaggregating subset of dystrophic neurites in AD, neuropil threads. TANCs are abundant in the hippocampus of all patients with AD; a few are found in some aged nondemented people, and in the nucleus basalis of Meynert and occasionally the neocortex of AD patients. Ultrastructurally, the core of a TANC is made up of extracellular bundles of straight filaments. This core is not recognized by antibodies to native or synthetic beta A4 peptide, the major protein of plaque amyloid, thus showing that not all neuritic clusters in AD are associated with this peptide.

Adolescent↗
PubMed1986

Changes in the organization of the neuritic cytoskeleton during nerve growth factor-activated differentiation of PC12 cells: a serial electron microscopic study of the development and control of neurite shape.

After exposure to nerve growth factor, PC12 cells differentiate within a period of only a few days into cholinergic sympathetic neurons. Using computer-assisted three-dimensional serial electron microscopic reconstruction, we describe the progressive cytoskeletal and structural changes of PC12 neurites at different stages in their differentiation. Developmental changes in these neurites can be characterized by two major transitions. First, microtubules (MTs), which define the longitudinal axis of the neurite, increase in number leading to a more cylindrical and uniform neurite shape. Second, there are major changes in the relative numbers of other organelle types, which reflect the functional specialization of the neurite. These changes do not in themselves seriously affect shape change of the neurite during development, however the presence of these organelles and their associated obligatory volumes (volumes surrounding organelle) account for well over 50% of the neurite's volume at all stages of development. The MT-MT distances and obligatory volumes associated with the organelles remain constant throughout development. Thus, we can conclude that many of the observed changes seen in developing PC12 neurites are due simply to the production of a greater number of MTs in the cell, and that many of the other important parameters that can be measured and contribute to neurite shape remain constant during development.

Animals↗
PubMed1989

Analysis of slow-onset neurite formation in NG108-15 cells: implications for a unified model of neurite elongation.

When undifferentiated NG108-15 cells are plated onto polylysine coated Petri dishes in serum-free medium, they form neurites within 1-4 h if plated in the presence of laminin or 5'-deoxy-5'-methylthioadenosine (rapid-onset neurites). In the absence of such agents, serum-deprived NG108-15 cells extend axon-like neurites onto polylysine over several days; here we characterize the dynamic behavior of this slow-onset outgrowth pattern in detail. Individual cells plated on laminin expressed a gradual multipolar-to-unipolar transition due to rapid-onset neurites becoming remodelled into the appearance of slow-onset neurites. This phenomenon reflected the selective stabilization of certain rapid-onset neurites, along with the restriction of motility to their distal tips. Based upon the properties and interactions of both rapid- and slow-onset neurites in NG108-15 cells, a unified model for neurite formation is presented.

Animals↗
PubMed1986

NIF (neurite-inducing factor): a novel peptide inducing neurite formation in PC12 cells.

Neurite-inducing factor (NIF) is a novel protein that has been partially purified from mouse submaxillary glands. NIF induces neurite formation in PC12 pheochromocytoma cells, and the NIF-induced neurites are indistinguishable from NGF-induced neurites in both their morphology and the time course of their formation. Neurite-inducing activity can be recovered at a position corresponding to a molecular weight of 20,000 Da after fractionation of partially purified preparations via SDS-PAGE. Partially purified preparations of NIF are about half as potent as pure beta NGF, and since the neurite-inducing activity does not correspond to any of the major proteins in this fraction, specific activity of purified NIF will probably be significantly greater than the 60 ng/ml found for our partially purified material. NIF is distinct from beta NGF by four criteria: (1) antibodies to beta NGF can block the activity of beta NGF, but not the activity of NIF; (2) beta NGF can induce ornithine decarboxylase (ODC) in PC12 cells at concentrations significantly below those required to induce neurites, while NIF induces ODC only at concentrations greatly in excess of those required to induce neurite formation; (3) by the criterion of SDS-PAGE, there is insufficient beta NGF in our partially purified preparations of NIF to explain the biological activity of this fraction; and (4) the biological activity of NIF has a molecular weight (20,000 Da) that is distinct from beta NGF (13,000 Da). We conclude that NIF is probably a novel peptide that is very active in promoting morphological differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗
PubMed1985

Neurite guidance by non-neuronal cells in culture: preferential outgrowth of peripheral neurites on glial as compared to nonglial cell surfaces.

Growing axons in the peripheral nervous system (PNS) encounter a variety of cellular and extracellular substrates. Since it is difficult to sort out the possible contributions of these diverse components of the extracellular environment to axonal guidance in vivo, I have developed an in vitro system to study neurite outgrowth on two classes of cells which may provide as substrates for growing axons during development or regeneration: glial cells, e.g., astrocytes and Schwann cells, and nonglial cells, e.g., fibroblasts. Although neurites from sympathetic and spinal sensory ganglia explants grew onto preformed monolayers of both glial and nonglial cells, glial cells were a markedly better substrate. On the glial cells the neurites extended at a rate of 25 to 30 micron/hr and traveled singly or in fine fascicles; their growth cones displayed long filopodia and migrated on the upper surface of the monolayer cells. Conditioned media experiments suggested that neurite outgrowth on glial cell monolayers was not mediated by soluble secreted factors. These results indicate that the glial cell surface is an attractive substrate for neurite outgrowth. In contrast, on nonglial cells the rate of outgrowth was only 10 to 15 micron/hr, large neurite fascicles were common, and the growth cones migrated beneath the monolayer cells in contact with the underlying artificial substrate. This location of the growth cone, coupled with the observation that conditioned medium from these cells promoted neurite outgrowth only when bound to artificial substrates, suggests that secreted substrate-associated components may be an important determinant of neurite outgrowth on nonglial cell monolayers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Comparison of the effects of laminin and the polyornithine-binding neurite promoting factor from RN22 Schwannoma cells on neurite regeneration from cultured newborn and adult rat dorsal root ganglion neurons.

We have investigated the effects of two neurite promoting factors (NPFs)--laminin and the semipurified polyornithine-binding neurite promoting factor (PNPF-1) from RN 22 Schwannoma cells--on neurite regeneration from dissociated newborn and adult rat dorsal root ganglion (DRG) neurons during 24 and 48 h culture periods in the absence of exogenous neuronotrophic factors. Both laminin and PNPF, when used to pretreat the polyornithine substratum, significantly enhanced neurite recruitment from surviving newborn and adult DRG neurons as compared to an untreated polyornithine substratum. However, the responses of newborn neurons at saturating concentrations of laminin and PNPF were consistently greater (46% neurite-bearing cells at 24 h, 81% at 48 h) than those of adult neurons (14 and 45%, respectively). The responsive neurons of both newborn and adult DRG displayed extensive neuritic networks at 48 h. The ED50 of laminin, or PNPF was 0.15-0.2 micrograms/ml for both newborn and adult neurons. The similarities in the responses of newborn and adult DRG neurons to NPFs validate the use of neurons from embryonic and newborn animals for the in vitro assays of NPFs that can be collected from injured and regenerating adult peripheral nervous tissues.

Age Factors↗
PubMed1986

Experimental modification of PC12 neurite shape with the microtubule-depolymerizing drug Nocodazole: a serial electron microscopic study of neurite shape control.

The microtubule-depolymerizing drug Nocodazole has been used to experimentally manipulate the form of PC12 neurites. Both time-lapse photography and serial electron microscopy demonstrate that microtubule depolymerization leads to varicosity formation due to a clustering of membranous organelles in young neurites (nerve growth factor activated within 7 d). Neurites that have been nerve growth factor activated 7 or more d before Nocodazole application are resistant to microtubule depolymerization. These data and data from previous papers has been combined in an attempt to predict quantitatively the volume and the shape of a neurite. The relationship is described mathematically by Vn = 4.52 Vo + 0.0054 MTl, where Vn is local neurite volume, Vo is organelle volume, and MTl is MT length (the constant, 0.0054 is micron2), and 4.52 is the obligatory volume constant derived from serial electron microscopic studies. The equation predicts the total volume of neurites despite alterations of morphology due to Nocodazole and despite changes in morphology during development.

Animals↗
PubMed1991

New plastic plates which enhance neurite extension in culture: roles of bisphenol-A and tricyclodecanyl units for growth and orientation of neurites on plastic plates with microstructures.

In order to study molecular mechanisms of contact guidance of neurites, dissociated culture of adult mouse dorsal root ganglion (DRG) cells was performed for 6 species of plastic plates different in monomer compositions. Microstructures (grooves of 5-10 microns wide and 1 micron deep) were grafted on the plates so as to guide neurite growth in their axial direction. Neurites were longer and more oriented on plates with larger water contact angle. The distribution of neurites was uneven between grooves and steps of the microstructures, exhibiting a bell-shaped curve in relation to the water contact angle of the plastic. These indicate that hydrophilic properties of the plastic plate surface, due to the presence of bisphenol-A and tricyclodecanyl units, are crucially involved in the elongation and orientation of neurites.

Animals↗
PubMed1989

Effects of calcium ion on neurite outgrowth of rat spinal cord neurons in vitro: the role of non-neuronal cells in regulating neurite sprouting.

The interactions of nerve cells with their environment and other cells are specific to different stages of cellular differentiation. Neurite outgrowth was measured from cultured spinal cord neurons under the influence of different Ca2+ concentrations. We used fluorodeoxyuridine (FuDr), an antimitotic agent which reduces significantly the proportion of non-neuronal cells in spinal cord cell cultures, to examine the effects of non-neuronal cells on neurite outgrowth. Spinal cord neurons responded to changes in their environment by means of two types of neurite outgrowth: sprouting and elongation. The concurrent presence of non-neuronal cells led to increased sprouting of neurites in certain ionic environments, thus lending support to the idea that non-neuronal cells release diffusible factors which influence sprouting and guide neurite outgrowth.

Animals↗
PubMed1992

Merosin promotes cell attachment and neurite outgrowth and is a component of the neurite-promoting factor of RN22 schwannoma cells.

The laminin-like protein merosin was purified from human placenta in intact form and as pepsin fragments and compared to laminin in heparin affinity chromatography and cell binding assays. Intact merosin and a small fragment of merosin comprising the last two repeats of the heavy chain g domain bind to heparin. Intact merosin and large pepsin fragments of merosin, but not the small C-terminal fragment, mediate the attachment and spreading of several types of cells and promote neurite outgrowth from neuronal cells similar to laminin and its corresponding fragments. Cells with various integrin-type receptors for laminin attached equally well to merosin and laminin, suggesting that several of the known laminin binding receptors also bind to merosin. Antibodies to the beta 1 subunit of integrins inhibited neurite outgrowth on merosin as well as on laminin, confirming the involvement of integrin-mediated interaction of cells with both merosin and laminin. Schwannoma cells, which have previously been shown to produce a laminin-like, neurite-promoting factor, synthesize merosin in vivo and in vitro as shown by protein and mRNA analysis. The results suggest that merosin, which is the more abundant basement membrane protein in the laminin family, has properties very similar to laminin despite differences in the structure of the heavy chain. Furthermore, merosin may be identical to or a component of the neurite-promoting factors previously reported from heart, muscle, and Schwann cells.

Base Sequence↗
PubMed1987

Neurofascin: a novel chick cell-surface glycoprotein involved in neurite-neurite interactions.

We have identified neurofascin, a novel chick cell-surface glycoprotein involved in neurite-neurite interactions. Neurofascin is defined by its reactivity with monoclonal antibody (MAb) F6, which detects two polypeptides (160 and 185 kd) in immunotransfers of brain plasma membrane proteins. Immunoaffinity chromatography using immobilized MAb F6 yields major molecular mass bands at 185, 160, 135-110, and 92 kd. Fingerprint analyses show that these polypeptides are related. Neurofascin is expressed primarily in fiber-rich areas of embryonic cerebellum, spinal cord, and retina. Fab fragments of polyclonal antibodies to neurofascin interfere with the outgrowth of retinal and sympathetic axons in two different in vitro bioassays. Neurofascin is immunologically distinct from other known neurite-associated surface glycoproteins.

Animals↗
PubMed1992

Adriamycin promotes neurite outgrowth in the "neurite-minus" N1A-103 mouse neuroblastoma cell line.

Adriamycin, an anticancer agent acting on topoisomerase II, promotes the arrest of cell division and neurite extension in a "neurite-minus" murine neuroblastoma cell line, N1A-103. This morphological differentiation is accompanied by a blockade in the S phase of the cell cycle, modification of the amount of peripherin, and appearance of the beta 7-tubulin isoform. Yet, adriamycin-induced N1A-103 cells fail to express other neuronal markers, such as long-lasting Ca2+ channels, synaptophysin, and the shift in the proportion of the beta'1 tubulin isoform to the beta'2 isoform, whose appearance parallels the terminal differentiation of the wild type neuroblastoma cell line N1E-115. Hence, a comparison of the behavior of these two cell lines leads to the proposal that there are two programs of neuroblastoma differentiation: one where expression is triggered by the arrest of cell division and which is observed in adriamycin-induced N1A-103 variant cells, and the other, presumably occurring further downstream, which would involve further changes in morphogenesis and acquisition of new electrophysiological properties.

Animals↗
PubMed1990

Extracellular matrix allows PC12 neurite elongation in the absence of microtubules.

Several groups have shown that PC12 will extend microtubule-containing neurites on extracellular matrix (ECM) with no lag period in the absence of nerve growth factor. This is in contrast to nerve growth factor (NGF)-induced neurite outgrowth that occurs with a lag period of several days. During this lag period, increased synthesis or activation of assembly-promoting microtubule-associated proteins (MAPs) occurs and is apparently required for neurite extension. We investigated the growth and microtubule (MT) content of PC12 neurites grown on ECM in the presence or absence of inhibitors of neurite outgrowth. On ECM, neurites of cells with or without prior exposure to NGF contain a normal density of MTs, but frequently contain unusual loops of MTs in their termini that may indicate increased MT assembly. On ECM, neurites extend from PC12 cells in the presence of 10 microM LiCl at significantly higher frequency than on polylysine. On other substrates, LiCl inhibits neurite outgrowth, apparently by inhibiting phosphorylation of particular MAPs (Burstein, D. E., P. J. Seeley, and L. A. Greene. 1985. J. Cell Biol. 101:862-870). Although 35-45% of 60 Li(+)-neurites examined were found to contain a normal array of MTs, 25-30% were found to have a MT density approximately 15% of normal. The remaining 30% of these neurites were found to be nearly devoid of MTs, containing only occasional, ambiguous, short tubular elements. We also found that neurites would extend on ECM in the presence of the microtubule depolymerizing drug, nocodazole. At 0.1 micrograms/ml nocodazole, cells on ECM produce neurites that contain a normal density of MTs. This is in contrast to the lack of neurite outgrowth and retraction of extant neurites that this dose produces in cells grown on polylysine. At 0.2 microgram/ml nocodazole, neurites again grew out in substantial number and four of five neurites examined ultrastructurally were found to be completely devoid of microtubules. We interpret these results by postulating that growth on ECM relieves the need for MTs to serve as compressive supports for neurite tension (Dennerll, T. J., H. C. Joshi, U. L. Steel, R. E. Buxbaum, and S. R. Heidemann. 1988. J. Cell Biol. 107:665). Because compression destabilizes MTs and favors disassembly, this would tend to increase MT assembly relative to other conditions, as we found. Additionally, if MTs are not needed as compressive supports, neurites could grow out in their absence, as we also observed.

Adrenal Gland Neoplasms↗