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PubMed2000

Action potential backpropagation and somato-dendritic distribution of ion channels in thalamocortical neurons.

Thalamocortical (TC) neurons of the dorsal thalamus integrate sensory inputs in an attentionally relevant manner during wakefulness and exhibit complex network-driven and intrinsic oscillatory activity during sleep. Despite these complex intrinsic and network functions, little is known about the dendritic distribution of ion channels in TC neurons or the role such channel distributions may play in synaptic integration. Here we demonstrate with simultaneous somatic and dendritic recordings from TC neurons in brain slices that action potentials evoked by sensory or cortical excitatory postsynaptic potentials are initiated near the soma and backpropagate into the dendrites of TC neurons. Cell-attached recordings demonstrated that TC neuron dendrites contain a nonuniform distribution of sodium but a roughly uniform density of potassium channels across the somatodendritic area examined that corresponds to approximately half the average path length of TC neuron dendrites. Dendritic action potential backpropagation was found to be active, but compromised by dendritic branching, such that action potentials may fail to invade relatively distal dendrites. We have also observed that calcium channels are nonuniformly distributed in the dendrites of TC neurons. Low-threshold calcium channels were found to be concentrated at proximal dendritic locations, sites known to receive excitatory synaptic connections from primary afferents, suggesting that they play a key role in the amplification of sensory inputs to TC neurons.

Action Potentials↗

PubMed1999

Direct connections between dendritic terminals of tectal ganglion cells and glutamate-positive terminals of presumed optic fibres in layers 4-5 of the optic tectum of Gallus domesticus. A light- and electron microscopic study.

The principal afferent fibres of the avian optic tectum are the optic fibres of retinal origin. They terminate on the contralateral side, in the external layers (2-7) of the optic tectum (called optic layers) turning into these layers from the external surface. The terminal branchings of the optic fibres develop four densely innervated areas in layers 2, 3, 4-5 and 7. Their terminals are large and of various appearance in the different areas. In the middle third of the optic layer (in layers 4-5), thin dendritic terminal sections of tectal ganglion cells (according to Ramòn y Cajal) of layer 13 terminate into bunches. Phaseolus vulgaris lectin immunotracer corroborates these dendritic endings (further: dendritic terminals) of tectal ganglion cells. The direct connections between these dendritic terminals and the supposed optic fibres were studied under electron microscope and it was found that the large terminals of optic fibres containing round synaptic vesicles establish asymmetrical synapses with several dendritic profiles, among them Phaseolus lectin labelled dendritic terminals of ganglion cells. This result morphologically supports the former physiological observation of a direct synaptic transmission between optic fibres and ganglion cells of layer 13. In addition, on the dendritic terminals of ganglion cells, symmetrical synapses established by GABA-positive terminals were found. The optic terminals, the GABA-immunopositive terminals and the dendritic terminals of ganglion cells form complex synaptic units surrounded with glial sheath, and thus they establish glomerulus-like synaptic units. The size of the dendritic tree and the branching pattern of the dendrites of ganglion cells point to divergence and convergence in visual transmission.

Animals↗

PubMed2000

Depletion of a microtubule-associated motor protein induces the loss of dendritic identity.

Dendrites are short stout tapering processes that are rich in ribosomes and Golgi elements, whereas axons are long thin processes of uniform diameter that are deficient in these organelles. It has been hypothesized that the unique morphological and compositional features of axons and dendrites result from their distinct patterns of microtubule polarity orientation. The microtubules within axons are uniformly oriented with their plus ends distal to the cell body, whereas microtubules within dendrites are nonuniformly oriented. The minus-end-distal microtubules are thought to arise via their specific transport into dendrites by the motor protein known as CHO1/MKLP1. According to this model, CHO1/MKLP1 transports microtubules with their minus ends leading into dendrites by generating forces against the plus-end-distal microtubules, thus creating drag on the plus-end-distal microtubules. Here we show that depletion of CHO1/MKLP1 from cultured neurons causes a rapid redistribution of microtubules within dendrites such that minus-end-distal microtubules are chased back to the cell body while plus-end-distal microtubules are redistributed forward. The dendrite grows significantly longer and thinner, loses its taper, and acquires a progressively more axon-like organelle composition. These results suggest that the forces generated by CHO1/MKLP1 are necessary for maintaining the minus-end-distal microtubules in the dendrite, for antagonizing the anterograde transport of the plus-end-distal microtubules, and for sustaining a pattern of microtubule organization necessary for the maintenance of dendritic morphology and composition. Thus, we would conclude that dendritic identity is dependent on forces generated by CHO1/MKLP1.

Animals↗

PubMed2001

Maturation of human dendritic cells as sulfasalazine target.

AIM: Sulfasalazine, a nonsteroidal anti-inflammatory drug, is effective in treating some autoimmune diseases, but its mechanism of action is unclear. To determine whether dendritic cells could be a possible target of the drug, we studied the effects of sulfasalazine and its metabolites, aminosalicylate and sulfapyridine, on in vitro maturation (terminal differentiation) of human myeloid dendritic cells. METHODS: We prepared immature dendritic cells by incubating CD14-positive cells in the presence of granulocyte- macrophage colony-stimulating factor and interleukin (IL)-4. The cells were matured by addition of tumor necrosis factor (TNF)-a, IL-1 beta, and prostaglandin E2 in the presence of sulfasalazine or its metabolites -- aminosalicylate and sulfapyridine, or their combinations. We quantified the effect of drugs on the dendritic cell characteristics, such as stimulation of autologous and allogeneic pan-T cell proliferation, surface marker phenotype, IL-12 p40 subunit secretion, and activation of nuclear transcription factor (NF)-kappa B. RESULTS: Dendritic cells treated with sulfasalazine (1.25 micromol/L or 2.5 micromol/L) could not stimulate T cells (p<0.028, two-sided paired t-test). In distinction to drug-free maturing dendritic cells, 2.5 micromol/L sulfasalazine upregulated the levels of CD14 and CD68 and downregulated the levels of CD40, CD80, and CD83 (for all CD markers, p<0.03 for difference between measurements in the absence and the presence of sulfasalazine). From concentration-dependent changes in CD83 expression, we found an apparent ID50 >>1.5 micromol/L sulfasalazine. The apparent ID50 value for aminosalicylate-inhibited maturation was 4 micromol/L. Sulfapyridine had no effect. At 1.25 micromol/L, sulfasalazine largely inhibited NF-kB activation in dendritic cells. CONCLUSION: Maturing human dendritic cells are hundred-fold more sensitive to sulfasalazine than T cells and NK cells and the most sensitive human cells described so far. Thus, dendritic cell maturation is an important target of sulfasalazine. Because of the role of dendritic cells in (auto)immunity, inhibition of their maturation might provide a target for further optimization of sulfasalazine therapy.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed2002

Interplay between presynaptic and postsynaptic activities is required for dendritic plasticity and synaptogenesis in the supraoptic nucleus.

Developing oxytocin and vasopressin (OT/AVP) supraoptic nucleus (SON) neurons positively autocontrol their electrical activity via dendritic release of their respective peptide. The effects of this autocontrol are maximum during the second postnatal week (PW2), when the dendritic arbor transiently increases and glutamatergic postsynaptic potentials appear. Here, we studied the role and interaction of dendritic OT/AVP release and glutamate release in dendritic plasticity and synaptogenesis in SON. In vivo treatment with the peptides antagonists or with an NMDA antagonist suppressed the transient increase in dendritic arbor of SON neurons at the beginning of PW2. Incubation of acute slices with these compounds decreased the dendritic arbor on a short time scale (3-8 hr) in slices of postnatal day 7 (P7) to P9 rats. Conversely, application of OT/AVP or NMDA increased dendritic branches in slices of P3-P6 rats. Their effects were inhibited by blockade of electrical activity, voltage-gated Ca2+ channels, or intracellular Ca2+ mobilization. They were also interdependent because both OT/AVP and NMDA (but not AMPA) receptor activation were required for increasing the dendritic arbor. Part of this interdependence probably results from a retrograde action of the peptides facilitating glutamate release. Finally, blocking OT/AVP receptors by in vivo treatment with the peptides antagonists during development decreased spontaneous glutamatergic synaptic activity recorded in young adults. These results show that an interplay between postsynaptic dendritic peptide release and presynaptic glutamate release is involved in the transient increase in dendritic arbor of SON neurons and indicate that OT/AVP are required for normal synaptogenesis of glutamatergic inputs in SON.

Animals↗

PubMedDate not supplied

[On the function of dendritic filopodia].

INTRODUCTION: Dendritic spines were first described by Ramón y Cajal in 1888, and considered by him to be the major sites of axo dendritic apposition and therefore of synaptic input in the CNS. Although a considerable wealth of information has been gathered over the last few decades about the function of spines in the mature nervous system, much less is known about how spines first appear on the otherwise smooth dendritic shafts. DEVELOPMENT: The earliest dendritic appendages, known as filopodia, are long and thin protrusions that occur predominantly during early postnatal development of the mammalian CNS. It is tempting to consider filopodia simply as precursors to spines because at first glance their overall shape is similar to that of mature spines and because their expression during development precedes that of spines. However, the elongated shape of dendritic filopodia (reminiscent of that of axonal filopodia and filopodia in non-neuronal cells) suggests an exploratory function, so that their role may be to contact axons in order to establish early synapses, independently of the eventual formation of spines. CONCLUSIONS: Here we review the literature on dendritic filopodia in an attempt to resolve this issue regarding these two distinct (though potentially overlapping) roles of filopodia in development: spinogenesis vs synaptogenesis. We summarize what is known about the physical characteristics and developmental time course of filopodia expression, as well as the mechanisms of growth and motility of these early dendritic protrusions, both in the intact nervous system and in pathologic settings. Throughout this review we present evidence that supports two hypotheses: that filopodia and spines are two inherently different types of protrusions, and that the role of dendritic filopodia is to capture axons and make early synapses, rather than transform into spines. Finally, we also discuss the potential role of filopodia in the sculpting of the dendritic tree. We also postulate that filopodia have additional important roles in regeneration and repair, in developmental plasticity and in the elaboration of dendritic arbors. These functions may not be limited to a specific developmental period, but probably extend into adulthood. We end by discussing specific experiments that could serve to test these hypotheses.

Animals↗

PubMed2002

Immunosuppressant effect of IDS 30, a stinging nettle leaf extract, on myeloid dendritic cells in vitro.

OBJECTIVE: Dendritic cells are important antigen presenting cells that play a role in the initiation of rheumatoid arthritis (RA). The stinging nettle leaf extract IDS 30 (Hox alpha) has been recommended for adjuvant therapy of rheumatic diseases. We investigated the immunomodulating effect of IDS 30 extract on the maturation of hematopoietic dendritic cells. METHODS: Human dendritic cells were generated from peripheral blood mononuclear cells cultured in granulocyte macrophage-colony stimulating factor and interleukin 4 (IL-4). Dendritic cell maturation was induced by keyhole limped hemocyanin (KLH). Dendritic cell phenotype was characterized by flow cytometric analysis; dendritic cell cytokine production was measured by ELISA. The ability of dendritic cells to activate naive autologous T cells was evaluated by mixed leukocyte reaction. RESULTS: IDS 30 prevented the maturation of dendritic cells, but did not affect their viability. IDS 30 reduced the expression of CD83 and CD86. It increased the expression of chemokine receptor 5 and CD36 in a dose dependent manner. The secretion of tumor necrosis factor-alpha was reduced. Application of IDS 30 to dendritic cells in culture caused a high endocytosis of dextran and a low capacity to stimulate T cell proliferation. CONCLUSION: Our in vitro results showed the suppressive effect of IDS 30 on the maturation of human myeloid dendritic cells, leading to reduced induction of primary T cell responses. This may contribute to the therapeutic effect of IDS 30 on T cell mediated inflammatory diseases like RA.

Antigens, CD↗

PubMed2003

A dynamic dendritic refractory period regulates burst discharge in the electrosensory lobe of weakly electric fish.

Na+-dependent spikes initiate in the soma or axon hillock region and actively backpropagate into the dendritic arbor of many central neurons. Inward currents underlying spike discharge are offset by outward K+ currents that repolarize a spike and establish a refractory period to temporarily prevent spike discharge. We show in a sensory neuron that somatic and dendritic K+ channels differentially control burst discharge by regulating the extent to which backpropagating dendritic spikes can re-excite the soma. During repetitive discharge a progressive broadening of dendritic spikes promotes a dynamic increase in dendritic spike refractory period. A leaky integrate-and-fire model shows that spike bursts are terminated when a decreasing somatic interspike interval and an increasing dendritic spike refractory period synergistically act to block backpropagation. The time required for the somatic interspike interval to intersect with dendritic refractory period determines burst frequency, a time that is regulated by somatic and dendritic spike repolarization. Thus, K+ channels involved in spike repolarization can efficiently control the pattern of spike output by establishing a soma-dendritic interaction that invokes dynamic shifts in dendritic spike properties.

Action Potentials↗

PubMed2003

Dendritic cell-based glioma immunotherapy (review).

Despite advances in radiation and chemotherapy along with surgical resectioning, the prognosis of patients with malignant glioma is poor. Among the new treatments currently being investigated for malignant glioma, immunotherapy is theoretically very attractive, since it offers the potential for high tumor-specific cytotoxicity. There are increasing reports demonstrating that systemic immunotherapy using dendritic cells is capable of inducing an antiglioma response. Therefore, dendritic cell-based immunotherapy could be a new treatment modality for patients with glioma. In this review, we will discuss the implications of these findings for glioma therapy. A literature review of dendritic cell-based glioma immunotherapy was used to overview the dendritic cell in immunobiology, in the central nervous system and in tumor immunology, glioma-associated antigens, dendritic cell therapy in animal glioma model, dendritic cell therapy in clinical trials and future directions in dendritic cell therapy. Dendritic cell-based immunotherapy strategies appear promising as an approach to successfully induce an antitumor immune response and increase survival in patients with glioma. Dendritic cell therapy of glioma seems to be safe and without major side effects. Its efficacy should be further determined in randomized, controlled clinical trials. The development of methods for manipulating dendritic cells for the purpose of vaccination will enhance the clinical usefulness of these cells for biotherapy for malignant glioma.

Animals↗

PubMed2003

Localization of a beta-actin messenger ribonucleoprotein complex with zipcode-binding protein modulates the density of dendritic filopodia and filopodial synapses.

The dendritic transport and local translation of mRNA may be an essential mechanism to regulate synaptic growth and plasticity. We investigated the molecular mechanism and function of beta-actin mRNA localization in dendrites of cultured hippocampal neurons. Previous studies have shown that beta-actin mRNA localization to the leading edge of fibroblasts or the growth cones of developing neurites involved a specific interaction between a zipcode sequence in the 3' untranslated region and the mRNA-binding protein zipcode-binding protein-1 (ZBP1). Here, we show that ZBP1 is required for the localization of beta-actin mRNA to dendrites. Knock-down of ZBP1 using morpholino antisense oligonucleotides reduced dendritic levels of ZBP1 and beta-actin mRNA and impaired growth of dendritic filopodia in response to BDNF treatment. Transfection of an enhanced green fluorescent protein (EGFP)-beta-actin construct, which contained the zipcode, increased the density of dendritic filopodia and filopodial synapses. Transfection of an EGFP construct, also with the zipcode, resulted in recruitment of endogenous ZBP1 and beta-actin mRNA into dendrites and similarly increased the density of dendritic filopodia. However, the beta-actin zipcode did not affect filopodial length or the density of mature spines. These results reveal a novel function for an mRNA localization element and its binding protein in the regulation of dendritic morphology and synaptic growth via dendritic filopodia.

Actins↗

PubMed1975

Motoneuron dendrites: role in synaptic integration.

Dendrites constitute over 80 per cent of the receptive surface area in cat motoneurons. Calculations based on matched electrical and gemoetrical measurements in these neurons indicate that the specific resistance of dendritic membranes in resting motoneurons is at least 2,000 ohm-cm2. When the specific membrane resistance is this high, even the most distal dendritic synapses can contribute significantly to the depolarization of the soma, and hence influence the rate of action potential generation. However, dendritic membrane resistance depends strongly on the level of background synaptic activity. The conductance changes associated with excitatory synaptic activity on a dendrite can be great enough to reduce significantly both the excitatory synaptic driving potential and the effective membrane resistance on that dendrite, and thus greatly reduce the effectiveness of synapses on the dendrite. Inhibitory synaptic activity produces an even greater reduction in dendritic membrane resistance. Thus the relative effectiveness of dendritic synapses depends on the type, distribution, and intensity of background synaptic activity, as well as on dendritic geometry and resting membrane properties.

Action Potentials↗

PubMed1988

Dendritic growth and remodeling of cat retinal ganglion cells during fetal and postnatal development.

We have studied the development of retinal ganglion cell morphology in the cat's visual system from early fetal to postnatal times. In particular, we have examined the contribution of growth and remodeling to the establishment of mature retinal ganglion cell form. Ganglion cells were identified by retrograde labeling with rhodamine latex microspheres deposited in the superior colliculus and lateral geniculate nucleus between embryonic day 34 (E34; birth = E65) and adulthood. To reveal the fine morphological details of retrogradely labeled ganglion cells, 48 hr later Lucifer yellow was injected intracellularly in living retinae that had been dissected and maintained in vitro. Our results show that at E35-37 the majority of ganglion cells are very simple in morphology, with a few dendritic processes that are generally aligned in a radial direction towards or away from the optic disc. During the ensuing 2 week period, there is a progressive growth and elaboration of dendrites. By E50, some ganglion cells resembling the adult alpha, beta, and gamma classes can be identified based on comparisons of the appearance and dimensions of their dendritic trees and somata with neighboring filled cells. However, ganglion cell dendrites and axons at this age express several transient morphological features. The axons of ganglion cells give rise to delicate processes originating from the intraretinal portion of the axon, including side branches, present in about half of the cells, and occasionally bifurcations that give rise to axon collaterals. These transient axonal features are present throughout development, including the neonatal period; no axon collaterals were observed after postnatal day 15, while axonal side branches persisted even at P31 but were gone by adulthood. Ganglion cell dendrites exhibit excessive branches and exuberant somatic and dendritic spines. Quantitative analysis of these processes shows that after E45 dendritic trees increase dramatically in complexity, reaching the peak number of spines and branch points by the first week of postnatal life. The number of dendritic processes then falls abruptly to reach near-adult levels by the end of the first postnatal month. Even though dendritic morphology closely resembles that seen in the adult at this age, ganglion cell bodies and dendrites must continue to grow to reach their adult size.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1982

Impulse activity in presynaptic dendrites: analysis of mitral cells in the isolated turtle olfactory bulb.

Impulse activity has been reported in neuronal dendrites in several regions of the central nervous system, where it is believed to assist in boosting transmission of signals from remote dendritic sites to the cell body. We have studied this activity in the dendrites of mitral cells in an isolated preparation of the turtle olfactory bulb. Intracellular recordings have been obtained from mitral cells responding to single volleys in the olfactory nerves or lateral olfactory tract. In addition to the large somatic spike, a small fast prepotential (FPP) was present in nearly all cells in response to an orthodromic volley in the olfactory nerves, but it was never seen in antidromic responses from the lateral olfactory tract. Collision tests using antidromic and orthodromic volleys showed that the EPP does not propagate into the axon. Hyperpolarizing current injections caused delay and blocking of the soma spike with little effect on the FPP response. These and other tests provided evidence to localize the EPP in the dendrites and to distinguish it from injury potentials and from spikes in the axon hillock or axonal initial segment. These results suggest that one function of the impulse in mitral cell dendrites is the classical one of boosting transmission of synaptic responses from the glomerular tuft to the cell body. In addition, it si well established that mitral cell dendrites are presynaptic to the dendrites of interneurons within the bulb and that these connections provide pathways for recurrent inhibition of the mitral cells. It therefore appears that the dendritic impulse in mitral cells acts as a booster for local dendritic synaptic output. These results provide further evidence for the multiple state-dependent input-output functions of cells with presynaptic dendrites.

Action Potentials↗

PubMed1995

Relationships between dendritic fields and functional architecture in striate cortex of normal and visually deprived cats.

We examined relationships between the pattern of geniculocortical innervation and the dendritic fields of cells in layer 4 of in cat primary visual cortex. Experiments were performed on normal animals and on cats in which the geniculocortical projection was altered by monocular deprivation or by the induction of divergent squint during the critical period. Thalamic afferents providing the input from the contralateral eye were anterogradely labeled by injecting the fluorescent tracer Dil into lamina A of the lateral geniculate nucleus. Intracellular staining with Lucifer yellow in slice preparations allowed simultaneous visualization of the morphology of individual cells and the thalamic afferents. Our results demonstrate that spiny stellate cells close to the upper and lower margin of the geniculocortical input have highly asymmetric dendritic fields, and thereby confine their dendrites to the termination zone of these afferents. This effect was specific for the cell class; it was not observed in pyramidal neurons. These dendritic asymmetries perpendicular to the laminar borders of spiny stellate cells were not altered by monocular deprivation or strabismus. In contrast, visual deprivation strongly influenced the dendritic arbors of spiny stellate cells near the borders between adjacent ocular dominance columns. In normal animals, the dendrites of cells near columnar borders remained preferentially within one column. These dendritic asymmetries became much more pronounced in strabismic animals. Monocular deprivation weakened the influence of the columnar borders on dendritic fields. Spiny stellate cells within the columns of the open eye exhibited a slight tendency to confine their dendrites to these columns. Cells in the columns of the deprived eye showed the opposite effect; they extended their dendrites preferentially into the adjacent columns of the open eye. These results demonstrate that the segregation of geniculocortical afferents into ocular dominance columns and its perturbation by manipulation of the visual input plays an important role in defining the morphology of cortical target cells. Thus, activity-dependent structural changes not only occur at the level of the presynaptic terminals, but also at the level of the postsynaptic target cells, and thereby contribute to build up the functional architecture of the cortex.

Animals↗

PubMed1995

Ultrastructural and immunophenotypic differentiation of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor (GM-CSF).

The present study examined electron microscopical, immunohistochemical and morphometric changes in the development, differentiation, and maturation of dendritic cells in the culture of mouse bone marrow cells supplemented with granulocyte/macrophage colony-stimulating factor (GM-CSF). A large number of large dendritic cells were released from the aggregates of small round cells. These released cells showed morphological, immunophenotypic, and functional characteristics of typical dendritic cells. These dendritic cells possessed irregularly-shaped nuclei in abundant cytoplasm with rough endoplasmic reticulum (rER), vesicles, multivesicular bodies, and tubulovesicular system, and projected long dendritic cytoplasmic processes. The tubulovesicular system and dendritic surface projections were characteristic of interdigitating cells usually residing in the paracortical area of lymph nodes. Small cells in aggregates were round in shape, had oval nuclei in narrow cytoplasm with poorly developed intracellular organelles, and projected a few short processes. These cells were a proliferating population distinct from monocytes in both ultrastructure and immunophenotype. Morphometrical analysis of cultured cells provided evidence that the small cells differentiate into typical dendritic cells via intermediate cells. These results imply that dendritic cells differentiate from small round dendritic precursor cells and that GM-CSF is a major cytokine capable of inducing the development, differentiation, and proliferation of dendritic cells.

Animals↗

PubMed1994

Targeting and activity-related dendritic modification in mammalian retinal ganglion cells.

We have studied factors that influence the development of dendritic morphology in hamster retinal ganglion cells. By combining fluorescent retrograde tracing with in vitro Lucifer yellow injection into fixed retina, cells with appropriate and inappropriate visuotopic projections have been compared. In adult hamsters, cells with an aberrant ipsilateral projection from the nasal retina display a uniformly sparse dendritic morphology. However, following monocular enucleation at postnatal day 0 (P0), this population displays a significantly enhanced dendritic complexity in the adult. By contrast, removal of one eye at P6 or at P12 produces progressively less effect. These results suggest that dendritic complement of the adult aberrant projection can be regulated by altering the early postnatal axonal environment. The development of aberrant ganglion cells was investigated to determine the relative influences of cell death and dendritic remodeling in shaping the composition of the adult aberrant population. Aberrant cells were found to be indistinguishable from other cells in nasal retina throughout early development. After ganglion cell death (P1-P12) is over, aberrant cells still display a full range of cell types. However, at eye opening (P16) they undergo a rapid loss of dendritic complexity by remodeling. By P22, aberrant cells display a uniformly sparse dendritic morphology. When hamsters were raised in the dark between P12 (the end of ganglion cell death) and P22, this severe remodeling was blocked. This block was maintained when hamsters were dark reared to P42. Hence, both dark rearing and monocular enucleation at P0 produce similar effects on the development of visuotopically inappropriate hamster retinal ganglion cells. We speculate that the patterns of dendritic sculpting that we have observed reflect activity-mediated modulation of dendritic form via retrograde signals from the terminal arbors. This has implications for retinal ganglion cell morphological classification and, more generally, for mechanisms that influence the dendritic development of other neurons in the CNS.

Animals↗

PubMed1993

[Dendritic arborization patterns of interneurons labeled with a lectin, Vicia villosa, in rat cerebral cortex: studies by intracellular injection of lucifer yellow using aldehyde-fixed slices].

In order to characterize the dendritic field of a number of interneurons in the cerebral cortex, the labeling of extracellular sugar chains which define a subset of interneurons was combined with the subsequent intracellular filling of dyes in aldehyde-fixed tissue. Neurons whose cell body had been outlined by a lectin, Vicia villosa (VVA), which recognizes terminal N-acetylgalactosamine, were intracellularly injected with a fluorescent tracer, Lucifer yellow (LY), in the rat parietal cortex under direct visualization. After immunohistochemical detection of LY, somal morphology and the dendritic fields of injected neurons were reconstructed from serial sections and characterized in each of the layers II/III, IV, V and VI. Multipolar, flask-shaped and bitufted somata were VVA-positive. Multipolar neurons with round soma and spherical dendritic field were found in layers II/III, IV and V, while those with vertically elongated dendritic fields were found in layer VI. Cell bodies were located roughly in the center of the spherical or cylindrical dendritic fields. Neurons with apparently multipolar but flask- or pear-shaped soma were found frequently in layer IV, and much less frequently in layer II/III and VI. The majority of the dendrites originated from the neck portion of flask and formed a roughly spherical dendritic field with the cell body located more or less eccentrically. Some neurons in layer IV had an oval, somewhat vertically elongated soma and displayed a typical bitufted dendritic arborization pattern with vertically elongated dendritic fields. The overall dendritic field sizes of the cells gradually increased at deeper layers of the cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehydes↗

PubMed1997

Retrovirally transduced human dendritic cells express a normal phenotype and potent T-cell stimulatory capacity.

Dendritic cells are attractive candidates for vaccine-based immunotherapy because of their potential to function as natural adjuvants for poorly immunogenic proteins derived from tumors or microbes. In this study, we evaluated the feasibility and consequences of introducing foreign genetic material by retroviral vectors into dendritic cell progenitors. Proliferating human bone marrow and cord blood CD34+ cells were infected by retroviral vectors encoding the murine CD2 surface antigen. Mean transduction efficiency in dendritic cells was 11.5% from bone marrow and 21.2% from cord blood progenitors. Transduced or untransduced dendritic cell progeny expressed comparable levels of HLA-DR, CD83, CD1a, CD80, CD86, S100, and p55 antigens. Granulocytes, macrophages, and dendritic cells were equally represented among the transduced and mock-transduced cells, thus showing no apparent alteration in the differentiation of transduced CD34+ precursors. The T-cell stimulatory capacity of retrovirally modified and purified mCD2-positive allogeneic or nominal antigen-pulsed autologous dendritic cells was comparable with that of untransduced dendritic cells. Human CD34+ dendritic cell progenitors can therefore be efficiently transduced using retroviral vectors and can differentiate into potent immunostimulatory dendritic cells without compromising their T-cell stimulatory capacity or the expression of critical costimulatory molecules and phenotypic markers. These results support ongoing efforts to develop genetically modified dendritic cells for immunotherapy.

Antigen-Presenting Cells↗