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Dendro-dendritic synapses in substantia nigra: descriptions based on analysis of serial sections.

Dendro-dendritic synapses were studied in serial sections of rat substantia nigra in subjects pretreated with intraventricularly administered 5-hydroxydopamine, a monoaminergic synaptic label. These synapses had symmetrical membrane thickenings and small clusters of heavily labeled pleomorphic vesicles in the presynaptic dendrites, which were assumed to extend from the dopaminergic cells of pars compacta. Dendro-dendritic synapses were seen in the pars compacta of the substantia nigra, but were not found in blocks trimmed to include only the nondopaminergic pars reticulata. The presynaptic dendrites did not receive other synapses near the sites of dendro-dendritic synapses. These dendrites were frequently apposed to other dendrites for long distances with no intervening glial processes. In many cases, several adjacent dendro-dendritic contacts were made by a single presynaptic dendrite onto several different postsynaptic dendrites. Presynaptic dendrites did not participate in reciprocal synapses, serial synapses, or dendro-axonic synapses. Presynaptic and postsynaptic dendrites engaged in dendro-dendritic synaptic contact were of similar appearance and both had cross-sectional diameters of 0.23-1.9 microns. In several cases, label could also be detected in the postsynaptic dendrite in cisternae of smooth endoplasmic reticulum, providing evidence for dendro-dendritic synapses between dopaminergic neurons. Release of dopamine from dopaminergic dendrites and their role in the control of neuronal activity in substantial nigra are discussed.

Animals↗

Morphology of dendrite bundles in the cervical spinal cord of the rat: a light microscopic study.

Histological staining techniques and Golgi-Cox impregnation revealed three discrete dendrite bundles in the ventral horn of the rat cervical spinal cord. A midline dendrite bundle (MDB) traversed the ventromedial gray matter (C3-6), a central dendrite bundle (CDB) coursed the medial aspect of the ventral horn (C3-5), and a lateral dendrite bundle (LDB) traveled in the ventrolateral gray matter (C2-4). At the light microscopic level, the three dendrite bundles were composed of longitudinally oriented intertwined dendrites that coursed in close apposition among motoneuron perikarya, neuroglia, and capillaries. A gradient of packing density of dendrites in the bundles existed, the MDB displaying the greatest packing density and the LDB forming the most loosely interwoven dendritic plexus. Dendrites contributing to the bundles originated from several different motoneuron pools. Smaller transverse dendrite bundles radiated from the longitudinal dendrite bundles at right angles and appeared to interconnect the MDB, CDB, and LDB. Transverse dendrite bundles also exited the MDB and LDB to course into the anterior and lateral funiculi, respectively. The presence of dendrite bundles among fields of motoneurons suggests that dendrite bundles may provide an anatomical substrate for the synchronization of neuronal activity for coordination of muscle groups involved in particular movements. Dendrite bundles also would provide a means whereby functionally similar motoneurons can receive and integrate similar synaptic inputs, and thus allow these inputs to modulate and coordinate groups of neurons that act as a functional unit. The presence of transverse dendrite bundles interconnecting the longitudinal bundles may permit the fine tuning of motoneuron activity for better coordination of movements involving synergistic and antagonistic muscle groups.

Animals↗

Dendritic plasticity of CA1 pyramidal neurons after transient global ischemia.

Dendrites and spines undergo dynamic changes in physiological conditions, such as learning and memory, and in pathological conditions, such as Alzheimer's disease and epilepsy. Long-term dendritic plasticity has also been reported after ischemia/hypoxia, which might be compensatory effects of surviving neurons for the functional recovery after the insults. However, the dendritic changes shortly after ischemia, which might be associated with the pathogenesis of ischemic cell death, remain largely unknown. To reveal the morphological changes of ischemia-vulnerable neurons after ischemia, the present study investigated the alteration of dendritic arborization of CA1 pyramidal neurons in rats after transient cerebral ischemia using intracellular staining technique in vivo. The general appearance of dendritic arborization of CA1 neurons within 48 h after ischemia was similar to that of control neurons. However, a dramatic increase of dendritic disorientation was observed after ischemia with many basal dendrites coursed into the territory of apical dendrites and apical dendrites branched into the region of basal dendrites. In addition, a significant increase of apical dendritic length was found 24 h after ischemia. The increase of dendritic length after ischemia was mainly due to the dendritic sprouting rather than the extension of individual dendrites, which mainly occurred in the middle segment of the apical dendrites. These results reveal a plasticity change in dendritic arborization of CA1 neurons shortly after cerebral ischemia.

Animals↗

Dendrites of cat's spinal motoneurones: relationship between stem diameter and predicted input conductance.

1. The electroanatomy of motoneuronal dendrites was analysed using data from fifty-two dendritic trees of four completely reconstructed cat spinal motoneurones that had been labelled with intracellularly injected horseradish peroxidase. The cells belonged to m. triceps surae, and their physiological properties covered much of the known range for this muscle. 2. For each dendritic tree, the input conductance, as seen from the soma, was calculated by the method of Rall (1959), using anatomical measurements of the length and diameter of all branches and different assumed values for dendritic membrane resistivity. 3. There was a strong positive correlation between dendritic stem diameter and the calculated dendritic input conductance. Dendritic input conductance was approximately equal to a constant x (stem diameter)3/2 x (dendritic membrane resistivity)-0.76. 4. The relationship between dendritic stem diameter and computed input conductance was equal to that of Rall's equivalent-cylinder model of a dendritic tree. However, from a number of other points of view, the properties of the reconstructed dendrites differed from those of the model: (a) at branch points, the sum sigma(daughter diameters 3/2) was, on average, 19% greater than the 3/2 power of the parent diameter; (b) dendritic branches often showed a significant amount of tapering, and the mean overall degree of diameter decrease per branch was about 12%; (c) the termination of dendritic branches occurred at widely different distances from the soma within single dendritic trees (true for anatomical as well as for computed electrotonic distances). 5. When used in conjunction with previously published measurements of motoneuronal input resistance and proximal anatomy (Kernell & Zwaagstra, 1981), the present results gave further support to the conclusion that differences in membrane resistivity are of great importance for differences in motoneuronal input resistance. Furthermore, this conclusion was also confirmed by direct observation of the properties of the present four motoneurones: irrespective of the assumed ratio between somatic and dendritic membrane resistivity, there was a statistically significant positive correlation between the measured neuronal input resistance and the required membrane resistivity of soma and dendrites.

Animals↗

Axotomy induces retraction of the dendritic arbor of adult rat rubrospinal neurons.

The effect of distal axonal injury on the soma-dendritic morphology of intrinsic central neurons was examined using adult rat lumbar spinal cord-projecting rubrospinal neurons as a model. The soma-dendritic morphology was revealed using an improved Golgi-aldehyde method. Impregnated neurons were reconstructed in the two-dimensional plane for analysis. Four weeks after axotomy, neurons had reduced soma sizes and remained multipolar in shape. Some dendrites were found to end not far from their cell bodies. In addition, no long dendrite was identified following axotomy. Sholl's analysis [The Organization of the Cerebral Cortex. London, Methuen, [1956] revealed that axotomized neurons had fewer dendritic branches than control neurons. Total dendritic length was also reduced. Subsequent analyses showed that the average number of dendritic trunks was not altered however the mean number of terminal branches per dendritic trunk was reduced. The dendritic membrane of the normal neurons was usually smooth with occasional short protuberances on the proximal dendrites and spines on the distal dendrites, which did not change after axotomy. In control neurons, we identified an elaborate type of dendritic structure named dendritic appendage aggregates. These aggregates were located preferentially on terminal dendrites and were classified into three categories according to their complexity. The incidence of occurrence for these aggregates decreased following distal axotomy. These phenomena indicate that rat lumbar spinal cord-projecting rubrospinal neurons retract their distal dendrites in response to distal axotomy. The observed anatomic restructuring following axonal injury is likely to be accompanied by an alteration of afferents which normally synapse on distal dendrites.

Animals↗

Apical dendrites of the neocortex: correlation between sodium- and calcium-dependent spiking and pyramidal cell morphology.

Apical dendrites and somata of layer V pyramidal neurons were recorded with tight-seal patch electrodes in a slice preparation of rat somatosensory cortex. Recording sites were confirmed by measurements of the electrode location and by staining with biocytin. Dendritic recordings were made along the main trunk of the apical dendrite, usually within layer IV, at distances from 100 to 500 microns from the soma. Most cells recorded through the dendrite had a distinct enlargement of the apical trunk around the presumed recording site. The electrical properties of apical dendrites were readily distinguishable from those of somata. Dendrites generated two types of response when injected with depolarizing current. Group I responses were relatively small and broad Na(+)-dependent action potentials whose amplitude and rate-of-rise were negatively correlated with recording distance from the soma. Group II responses were complex, clustered firing patterns of Na(+)-dependent spikes together with higher-threshold slow spikes or plateaus; in these dendrites spike parameters were not correlated with distance from the soma. These two response groups were correlated with dendritic morphology: group I had significantly fewer oblique branches on the apical dendrite (5.5 vs 12.0) and a thinner apical trunk (2.0 vs 2.5 microns) than group II. TTX (1-2 microM) selectively blocked fast dendritic spikes, but not slow spikes and plateaus. Blocking Ca2+ currents reduced complex firing patterns and suppressed high-threshold slow spikes. Physiological and pharmacological studies imply that slow spikes and plateau potentials were primarily generated by high-threshold Ca2+ channels in the apical dendrite. Stimulating axons of layer I elicited EPSPs on distal apical dendrites of layer V cells. Recordings from both groups of apical dendrites revealed that EPSPs triggered a variety of distally generated, all-or-nothing depolarizations. The results show that voltage-dependent Na+ and Ca2+ currents are present in distal apical dendrites, in variable densities. These currents significantly modify distal synaptic events. The prevalence and character of active dendritic spiking (and presumably of Na+ and Ca2+ channel densities) correlate with the morphology of the apical dendritic tree.

Action Potentials↗

Ultrastructural evidence for association of vascular dendritic cells with T-lymphocytes and with B-cells in human atherosclerosis.

It has been previously demonstrated that dendritic cells are involved in human atherogenesis and immunohistochemical analysis indicated that S100+/CD1a+ vascular dendritic cells co-localize with lymphocytes in atherosclerotic lesions. Despite the high frequency of co-localization of vascular dendritic cells and lymphocytes in cell-rich areas, different type intimal cells were often intermingled and very closely apposed, which precluded determining whether vascular dendritic cells and lymphocytes specifically contacted each other or were simply densely packed together. Therefore, we undertook the present electronmicroscopical examination to see if vascular dendritic cells form direct contacts with lymphocytes in human atherosclerotic lesions. Serial sectioning of lymphocyte-rich areas of the human atherosclerotic aortas showed that vascular dendritic cells exhibiting a well developed tubulovesicular apparatus were located amongst T-lymphocytes and that through their processes, vascular dendritic cells formed multiple contacts with T-lymphocytes. In these contacts, vascular dendritic cell processes exhibited hypertrophied cisterns of the tubulovesicular system, which suggests the activation of vascular dendritic cells. From our observations we speculate that vascular dendritic cells may be responsible for the survival and activation of T-lymphocytes since a large number of T-lymphocytes which did not form contacts with vascular dendritic cells were found to have undergone destruction in atherosclerotic lesions. B-cells (plasma cells) were rarely seen in atherosclerotic lesions but vascular dendritic cells were found to form direct contacts with them. That vascular dendritic cells contact with both the T- and B-cells suggests that these vascular dendritic cells differ from other dendritic cells, subtypes of which are associated with T-cells (Langerhans cells, interdigitating cells) or with B-cells (follicular dendritic cells).

Adolescent↗

A quantitative light microscopic study of the dendrites of cat spinal gamma -motoneurons after intracellular staining with horseradish peroxidase.

By use of intracellular staining with horseradish peroxidase (HRP), the dendritic systems of spinal gamma-motoneurons of the adult cat were studied with a light microscope. The dendrites extended in various directions up to 1.5 mm from the cell body. The dendritic branching was sparse and even unbranched dendrites were occasionally seen. The number and combined diameter of the first-order dendrites increased in parallel with the mean cell body diameter. The number of dendritic end branches, the combined dendritic length, the membrane surface area, and the volume of the entire dendrite correlated positively with the diameter of the parent first-order dendrite. In comparison with the alpha -motoneurons (Ulfhake and Kellerth, '81) the gamma -motoneurons had smaller values for mean cell body diameter and mean diameter of the first-order dendrites and they also had a smaller number of first-order dendrites. The dendrites of the gamma-motoneurons were also found to have fewer branching points and larger values for combined dendritic length. The relation between the diameter of the first-order dendrite and the surface area of the entire dendrite was almost identical for the two types of motoneurons.

Animals↗

Dendritic maturation of displaced putative cholinergic amacrine cells in the rabbit retina.

The dendritic trees of Cb, cholinergic, amacrine cells in the ganglion cell layer of the developing rabbit retina are revealed by intracellular injection with Lucifer yellow to have the adult dendritic branching pattern at birth. It is demonstrated that these cells maintain a constant number of dendritic branches throughout postnatal development and that their dendritic trees increase in size by the growth and subsequent elongation of all branches. Proximal and distal dendrites increase in length by almost the same proportions between birth and adulthood. Although the adult pattern of dendritic branching of Cb amacrine cells is established by birth, dendrites in the young possess numerous short appendages (1-5 microns in length) resembling the "dendritic spines" of immature cat retinal ganglion cells. Some of these structures remain on the dendrites of adult cells but the majority are lost at the end of the third postnatal week. As dendritic spines disappear, the dendrites of Cb amacrine cells, especially the distal portion of the tree, acquire numerous varicosities. At each stage after P10, the gain in the number of varicosities greatly exceeds the loss in spines; this is not consistent with the hypothesis that all varicosities are retracted dendritic spines. The rapid increase in the number of varicosities on distal dendrites of Cb amacrine cells during the first 3 postnatal weeks coincides with the maturation of amacrine cell physiological responses. There is no distinct centroperipheral gradient in the postnatal dendritic maturation (acquisition of varicosities, loss of spines, attainment of the adult number of branches) of Cb amacrine cells from the visual streak to the peripheral retina. However, the area of their dendritic tree increases relatively more in the retinal periphery compared to that in the visual streak.

Aging↗

Synapses on motoneuron dendrites in the brachial section of the frog spinal cord: a computer-aided electron microscopic study of cobalt-filled cells.

Cobalt-labelled motoneuron dendrites of the frog spinal cord at the level of the second spinal nerve were photographed in the electron microscope from long series of ultrathin sections. Three-dimensional computer reconstructions of 120 dendrite segments were analysed. The samples were taken from two locations: proximal to cell body and distal, as defined in a transverse plane of the spinal cord. The dendrites showed highly irregular outlines with many 1-2 microns-long 'thorns' (on average 8.5 thorns per 100 microns 2 of dendritic area). Taken together, the reconstructed dendrite segments from the proximal sites had a total length of about 250 microns; those from the distal locations, 180 microns. On all segments together there were 699 synapses. Nine percent of the synapses were on thorns, and many more close to their base on the dendritic shaft. The synapses were classified in four groups. One third of the synapses were asymmetric with spherical vesicles; one half were symmetric with spherical vesicles; and one tenth were symmetric with flattened vesicles. A fourth, small class of asymmetric synapses had dense-core vesicles. The area of the active zones was large for the asymmetric synapses (median value 0.20 microns 2), and small for the symmetric ones (median value 0.10 microns 2), and the difference was significant. On average, the areas of the active zones of the synapses on thin dendrites were larger than those of synapses on large calibre dendrites. About every 4 microns 2 of dendritic area received one contact. There was a significant difference between the areas of the active zones of the synapses at the two locations. Moreover, the number per unit dendritic length was correlated with dendrite calibre. On average, the active zones covered more than 4% of the dendritic area; this value for thin dendrites was about twice as large as that of large calibre dendrites. We suggest that the larger active zones and the larger synaptic coverage of the thin dendrites compensate for the longer electrotonic distance of these synapses from the soma.

Animals↗

Distribution of glutamate-, glycine- and GABA-immunoreactive nerve terminals on dendrites in the cat spinal motor nucleus.

The dendritic tree constitutes more than 93% of the receptive membrane area of a spinal motoneuron, yet little is known about its synaptic inputs. In this study we examined the distribution of glutamate-, GABA- and glycine-like immunoreactivity in boutons apposing dendrites in the L7 spinal cord motor nucleus, by use of postembedding immunohistochemistry on serial sections. We examined 799 boutons apposing 401 cross-sectioned dendrites of different calibre (range 0.2-15 microm), and 14 first-order (stem) dendrites. Thirty-five percent (35%) of the boutons were immunopositive for glutamate and 59% for GABA and/or glycine. Among the latter, 30% showed glycine immunoreactivity only and 24% were immunoreactive for both GABA and glycine. Very few were immunoreactive only for GABA (5%). As few as 6% of the boutons were judged as not enriched for any amino acid analysed. The fine structural characteristics of the boutons were in accordance with previous descriptions. The sample of dendrites was arranged in calibre bins in order to facilitate distribution analysis. Stem dendrites differed from the other bins, with a high total bouton covering (61%) and a high bouton density. Sixty-nine percent of the membrane covering was by glycine- and/or GABA-immunoreactive boutons, whereas 18% was covered by boutons enriched in glutamate. For non-stem dendrites, bouton covering fell from 33% to 12% with decreasing calibre. However, bouton apposition length decreased in parallel, yielding a fairly uniform bouton density among dendrites of different calibre. The lack of correlation between packing density and dendrite calibre was also evident when the sample of dendrites was broken down into subsamples based on content of amino acid immunoreactivity. The latter analysis also revealed that both the relative covering and density of boutons containing inhibitory amino acids (57%; glycine and/or GABA) and glutamate (38%), respectively, did not vary systematically with dendrite calibre. Combined, the data indicate that in non-stem dendrites the proportion of excitatory and inhibition inputs does not change systematically throughout the dendritic arborizations of spinal alpha-motoneurons. Thus, spinal motoneurons can, with respect to the general synaptic architecture, be divided into two main compartments, i.e. the proximal soma-juxtasomatic compartment (including stem dendrites) and the distal dendritic compartment. The proximal domain is under a powerful glycine and/or GABA influence. Finally, based on the data presented here and previously published data, it was calculated that spinal alpha-motoneurons receive in the range of 50-140 x 10(3) synaptic boutons.

Animals↗

The integrative properties of spiny distal dendrites.

The dendritic spines of many central neurons are generally thought to modulate the ability of individual synaptic conductances to depolarize the dendritic shaft. A compartmental analysis using typical spine dimensions shows that spine neck resistances are probably far too low to support such a function, because low conductance synapses act as time-varying current sources. However, the collective presence of all spines on a dendrite significantly modifies the electrical properties of the branch in ways which have previously been overlooked. In particular, they lower its input impedance and length constant, reducing the amplitude of the unitary excitatory postsynaptic potential as well as the strength of spatial summation. This enables a dendrite to integrate large numbers of synaptic inputs while occupying minimal volume. In this way, dendritic spines are analogous to axonal myelin, which also alters transcellular impedance in order to maximize neurite function and minimize volume. Unlike membrane resistance changes, spines have little effect on the membrane time-constant so they maintain a long window for temporal summation. Though spine shape and neck resistance do not significantly affect dendritic potentials, spine area does. Therefore, while changes in spine morphology probably do not directly potentiate the strength of individual synapses, changes in spine density can regulate the synaptic excitability of an entire dendrite. The shortened length-constant of the spiny dendrite requires excitable membranes to be located in distal dendrites. These, in turn, eliminate many of the electrotonic nonlinearities associated with summation in long, thin processes, and make all distal synapses equipotent. The short length-constant also enhances the sensitivity of dendritic spikes to local impedance changes while decreasing the sensitivity to distant impedance changes. This would enable a neuron to effectively use inhibitory synapses or branch points to regulate propagation through its spiny dendritic tree. A model neuron is developed in which dendritic spines, excitable membranes, and dendritic branching combine to form a two-stage filter, which serves as a synaptic input coincidence detector with adjustable gain. Gain is regulated by potassium conductances which modulate branch point safety factor. The model is consistent with the notion of functional independence of distal dendrites and demonstrates that certain aspects of dendritic spiking which have previously been thought to require membrane hot-spots can also result from geometrical properties. It is suggested that the activation of spiny neurons may depend as much on the density as on the number of active synapses, and that spiny neurons may tend to have discrete output states whereas nonspiny neurons may be more continuous.

Animals↗

Age-dependence in the homeostatic upregulation of hippocampal dendritic spine number during blocked synaptic transmission.

Homeostatic regulation of spine number in mature hippocampal neurons results in more dendritic spines when synaptic transmission is blocked, providing a mechanism to compensate for diminished synaptic input. It is unsettled whether blockade of synaptic transmission also elevates spine number during development. To address this question, synaptic transmission was blocked in rat hippocampal slices during critical developmental stages of spine formation at postnatal days (P) 6-P22 and compared to adults. CA1 pyramidal cells were labeled with DiI and maintained for 5 h in one of three conditions, control artificial cerebrospinal fluid (ACSF), block media containing synaptic transmission antagonists in ACSF, or block media containing synaptic transmission antagonists in a nominally calcium-free ACSF with high magnesium. Slices were fixed in mixed aldehydes, sectioned, and the lateral dendrites were imaged in stratum radiatum with confocal microscopy. Dendritic spine density was quantified per unit length of dendrite. At P6-7 there were only a few protrusions emerging from the dendrites, which were predominantly filopodia-like in appearance. At both P11-12 and P15-16 there was a mixture of dendritic spines and filopodia-like structures. By P20-22 dendritic spines predominated and spine density was about 82% of the adult level. Dendritic spine density increased during blocked synaptic transmission at P20-22 as in adults, but was unchanged during blockade at younger ages. When extracellular calcium was nominally zero, dendritic spine density further increased on P20-22 dendrites as in adults. In contrast, spine density decreased along P11-12 dendrites under the nominally zero calcium condition. Under control conditions, dendritic protrusions were longer at P6-7 than at all other ages, which did not differ from one another. When synaptic transmission was blocked, dendritic protrusions further elongated at P6-7 only. Under the nominally zero calcium condition with blocked synaptic transmission, dendritic protrusions shortened at P11-12 only. These findings reveal age-dependent changes in the manifestation of homeostatic control of dendritic spines that could be mediated by maturational changes in mechanisms regulating postsynaptic calcium.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

Expression of maturation-/migration-related molecules on human dendritic cells from blood and skin.

Progress in dendritic cell research has been overwhelming in the past few years. This was made possible by the recent development of simple methods to generate large numbers of dendritic cells. These methods use as starting populations for culture either CD34+ progenitor cells from cord blood or bone marrow, or monocytes from peripheral blood. The latter approach is critically dependent on the combination of GM-CSF and interleukin 4. Such "priming cultures" yield populations of immature dendritic cells (CD83-/CD86 +/- /CD115+/antigen uptake high/antigen processing high/T cell sensitization low). In order to generate mature dendritic cells a subsequent "differentiation culture" has to be added whereby monocyte-conditioned medium appears to be the optimal stimulus for maturation. This results in terminally mature dendritic cells (CD83+/CD86++/CD115-/antigen uptake low/antigen processing low/T cell sensitization high). We investigated the expression of some molecules involved in maturation and migration on human monocyte-derived dendritic cells from blood in comparison with dermal dendritic cells and epidermal Langerhans cells. We present a method to highly enrich epidermal Langerhans cells. Survival of purified Langerhans cells in culture is dependent on the presence of GM-CSF and TNF-alpha. During maturation a substantial part of the Langerhans cells loses expression of the cutaneous lymphocyte antigen (CLA); mature dendritic cells from the dermis are completely devoid of CLA. Similarly, CLA as well as CD15s (Sialyl Lewis x) and CD31 (PECAM-1) that can be readily detected on immature monocyte-derived dendritic cells are down-regulated upon maturation. CD68 expression is very low in cutaneous dendritic cells; in monocyte-derived dendritic cells this molecule is abundantly present. Subsets of monocyte-derived dendritic cells express E-cadherin; CD87 (urokinase plasminogen activator receptor) is weakly expressed on both immature and mature monocyte-derived dendritic cells. Taken together, these data suggest that the phenotype of monocyte-derived dendritic cells (E-cadherin low to negative, CD68++) is not indicative for a cutaneous destiny. Furthermore, the downregulation upon maturation of molecules involved in migration through vessel walls (CD31, CLA, CD15s) indicates that the entry of mature dendritic cells into lymphatic vessels may not be as rigidly regulated by adhesion molecules as the process of extravasation from blood vessels.

Antigens, CD↗

Evaluation of phagocytic activity in human monocyte-derived dendritic cells.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-à-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Cells, Cultured↗

Developmental biology of the dendritic cell system.

AIM: To determine whether an imbalance of dendritic cell subsets might contribute to diminished adaptive host responses observed in newborn infants. It was hypothesized that the proportion of lymphoid dendritic cells would be greater than that of myeloid dendritic cells in cord blood. METHODS: To investigate this, dendritic cell subsets were evaluated in whole cord blood by flow cytometry. Circulating dendritic cells were also isolated from cord blood based on CD1c and BDCA-2 expression. Myeloid dendritic cells were also obtained by culturing cord and adult blood monocytes. Surface phenotypes of these cells were determined by flow cytometry using monoclonal antibodies directed against lineage, major histocompatibility, adhesion, co-stimulation and cytokine receptor molecules. Antigen-presenting functions of dendritic cell subsets were determined by mixed leukocyte reactions. RESULTS: Circulating myeloid dendritic cells were higher in cord blood than previously reported in adult blood, whereas lymphoid dendritic cell numbers were similar between cord and adult blood. Expression of CD11c, CD45RA and CD45RO did not accurately differentiate between dendritic cell subsets circulating in cord blood. Fresh and culture-derived cord blood myeloid dendritic cells stimulated adult allogeneic leukocyte proliferation, while lymphoid dendritic cells were less effective inducers of an adult allogeneic leukocyte response. Culture-derived dendritic cells induced modest autologous cord blood leukocyte proliferation, but freshly isolated myeloid and lymphoid dendritic cells did not stimulated autologous leukocytes. CONCLUSION: Contrary to the hypothesis, an imbalance in the ratio of circulating myeloid to lymphoid dendritic cell subsets does not exist and, therefore, does not contribute to diminished adaptive immune responses in newborn infants.

Adaptation, Physiological↗

The activation and distribution of GABA and L-glutamate receptors on goldfish Mauthner neurones: an analysis of dendritic remote inhibition.

1. The sensitivity of the membrane of the cell-body and lateral dendrite of the Mauthner neurone to iontophoretically applied GABA and L-glutamic acid has been investigated in goldfish. The cells were afterwards examined histologically. The results, taken together with physiological observations, help to explain some functional properties of dendritic synapses.2. GABA inhibits by increasing the membrane conductance, and has little effect on resting potential. L-Glutamate depolarizes, and its effects could sum with subthreshold excitatory post-synaptic potentials (e.p.s.p.s) to cause impulse firing. Neither substance was effective when released intracellularly, but only when applied to the outside of the membrane.3. Using a roving double-barrelled micropipette to apply brief iontophoretic pulses very close to the cell, and recording from the cell-body, the sensitivity to GABA was found to be uniform over a region extending from the axon-hillock to about half-way along the lateral dendrite; it then appeared to fall progressively as the drug was pipetted further and further out on the dendrite. The sensitivity to L-glutamate however seemed relatively unaffected by varying the site of application.4. In contrast to this, when the recording electrode was inserted into the same region of the cell where the drugs were applied, then the sensitivity to GABA, like that to L-glutamate, was found to be similar everywhere, including the distal part of the lateral dendrite.5. The antidromic spike, which does not actively invade the lateral dendrite, was used as a convenient test signal for detecting electrotonic decrement as well as changes in membrane conductance. The conductance changes due to small doses of GABA applied to the dendrite could be detected only over relatively short distances (tens of microns). But over these same distances very little decrement of potential change took place.6. The concept of dendritic remote inhibition has been put on a firm experimental basis. It occurs in the Mauthner cell, and is shown to be capable of providing a high spatial selectivity of action. The e.p.s.p.s most affected by it are those generated out on the same dendrite, and it follows that many of the e.p.s.p.s produced far out on other dendrites could well be influenced by it, though to a lesser extent. Least affected are large e.p.s.p.s generated in the cell-body and axon-hillock regions. The synaptic grouping provided by the distal parts of dendrites and their associated nerve endings is discussed.7. The results of a theoretical treatment (Appendix) of the effects of a localized membrane resistance change on electrotonic potentials recorded nearer to the source have been applied to results obtained on the Mauthner cell. The experimentally observed properties of the ;remote inhibition' caused by localized GABA application to the lateral dendrite, accord well with those predicted both for an infinitely long uniform cable and for a cable having a closed end at the region of the conductance change. The possible implications of these results for other central neurones are considered.8. Evidence is adduced showing that the synapses responsible for collateral inhibition in the Mauthner cell include at least part of the group of small nerve endings found on the axon-hillock, cell-body, proximal and distal lateral dendrite. (The latter distally-located endings cause dendritic remote inhibition.) All these regions, some of which certainly have excitatory synapses, thus receive an inhibitory input as well, and are sensitive to both GABA and L-glutamate.9. E.p.s.p.s recorded in the cell-body were reduced by about the same amount as was the antidromic spike when GABA was applied there, but considerably more than the spike when the GABA application was to the lateral dendrite near the origin of the e.p.s.p. Even when the recording was made from the affected region of the dendrite, the e.p.s.p. seemed more sensitive to GABA than was the electrotonically conducted spike. This, and other observations, suggests that GABA may act presynaptically on the excitatory endings as well as post-synaptically.10. The detection of effects, and the recognition of site of action, of drugs applied iontophoretically in the central nervous system is discussed on the basis of the present findings.

Action Potentials↗

Dendritic calcium transients evoked by single back-propagating action potentials in rat neocortical pyramidal neurons.

1. Dendrites of rat neocortical layer V pyramidal neurons were loaded with the Ca2+ indicator dye Calcium Green-1 (CG-1) or fluo-3, and the mechanisms which govern action potential (AP)-evoked transient changes in dendritic cytosolic Ca2+ concentration ([Ca2+]i) were examined. APs were initiated either by synaptic stimulation or by depolarizing the soma or dendrite by current injection, and changes in fluorescence of the indicator dye were measured in the proximal 170 microns of the apical dendrite. 2. Simultaneous two-pipette recordings of APs from the soma and apical dendrite, and dendritic fluorescence imaging indicated that a single AP propagating from the soma into the apical dendrite evokes a rapid transient increase in fluorescence indicating a transient increase in [Ca2+]i. At 35-37 degrees C the decay time constant of the fluorescence transient following an AP was around 80 ms. 3. Voltage-activated Ca2+ channels (VACCs) of several subtypes mediated the AP-evoked fluorescence transient in the proximal (100-170 microns) apical dendrite. The AP-evoked fluorescence transient resulted from Ca2+ entry through L-type (nifedipine sensitive; 25%), N-type (omega-conotoxin GVIA sensitive; 28%) and P-type (omega-agatoxin IVA sensitive; 10%) Ca2+ channels and through Ca2+ channels (R-type) not sensitive to L-, N- and P-type Ca2+ channel blockers (cadmium ion sensitive; 37%). 4. The decay time course of the dendritic fluorescence transient was prolonged by the blockers of endoplasmic reticulum (ER) Ca(2+)-ATPase, cyclopiazonic acid and thapsigargin, suggesting that uptake of Ca2+ into the ER in dendrites governs clearance of dendritic Ca2+. 5. The decay time course of the fluorescence transient was slightly prolonged by benzamil, a blocker of plasma membrane Na(+)-Ca2+ exchange and by calmidazolium, a blocker of the calmodulin-dependent plasma membrane Ca(2+)-ATPase, suggesting that these pathways are less important for dendrite Ca2+ clearance following a single AP. Neither the mitochondrial uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP) nor the blocker of Ca2+ uptake into mitochondria, Ruthenium Red, had any measurable effect on the decay time course of the fluorescence transient. 6. Dendritic fluorescence transients measured during trains of dendritic APs began to summate at impulse frequencies of 5 APs s-1. At higher frequencies APs caused a concerted and maintained elevation of dendritic fluorescence during the train.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗