Stellate cells as phagocytes of the anuran pars distalis

When the stellate cells (nongranulated cells) from dissociated-cell preparations of the anuran pars distalis were examined, they were seen to contain debris within phagocytic vacuoles (phagosomes). These phagosomes were variable; some contained granules from secretory cells while others were similar to lipid-like bodies and myelin figures. In situ partes distales from frogs were examined at the breeding season. The tissues were divided into lobules that were bounded by processes of stellate cells located between the secretory cells. Processes of stellate cells in the interior of a lobule interdigitate with processes extending inward from the stellate cells forming the border of the lobule. When these processes come together, a small cavity is formed. In many of the intact frogs the spaces between the stellate and secretory cells were greatly enlarged. At this particular time the processes of the stellate cells were attenuated and enclosed secretory granules that were also present as debris in these dilated, intercellular spaces. Within the cytoplasm of these stellate cells were not only phagosomes containing secretory granules but also organelles that appeared to be lipid bodies and lysosomes. Thus, the stellate cells of the pars distalis function in vivo, as well as in vitro, as phagocytes. In addition, macrophage-like cells moving from the blood may form another component of this system of phagocytes.     

Configuration of the medial and lateral segments of duck (Anas platyrhynchos) salt glands

Salt glands of the domestic duck Anas platyrhynchos differ from those of the herring gull Larus argentatus and other birds. In ducks, each salt gland consists of distinct medial and lateral segments. Centrally located drainage ducts that extend along the entire length of these medial and lateral segments collect hypertonic fluid secreted by an array of lobules. Each lobule is formed by a single mass of branched tubules in which the direction of capillary blood flow is opposite to that of the secreted fluid. This fluid drains from the medial segment through an external duct that opens into the nasal cavity at the base of the vestibular fold. A duct from the lateral segment loops and opens onto the surface of the nasal septum. The structure and function of the secretory cells is reviewed briefly within the context of our study of the configuration of duck nasal salt glands.     

Peripheral Glia Have a Pivotal Role in the Initial Response to Axon Degeneration of Peripheral Sensory Neurons in Zebrafish

Axon degeneration is a feature of many peripheral neuropathies. Understanding the organismal response to this degeneration may aid in identifying new therapeutic targets for treatment. Using a transgenic zebrafish line expressing a bacterial nitroreductase (Ntr)/mCherry fusion protein in the peripheral sensory neurons of the V, VII, IX, and X cranial nerves, we were able to induce and visualize the pathology of axon degeneration in vivo. Exposure of 4 days post fertilization Ntr larvae to the prodrug metronidazole (Met), which Ntr metabolizes into cytotoxic metabolites, resulted in dose-dependent cell death and axon degeneration. This was limited to the Ntr-expressing sensory neurons, as neighboring glia and motor axons were unaffected. Cell death was rapid, becoming apparent 3–4 hours after Met treatment, and was followed by phagocytosis of soma and axon debris by cells within the nerves and ganglia beginning at 4–5 hours of exposure. Although neutrophils appear to be activated in response to the degenerating neurons, they did not accumulate at the sites of degeneration. In contrast, macrophages were found to be attracted to the sites of the degenerating axons, where they phagocytosed debris. We demonstrated that peripheral glia are critical for both the phagocytosis and inflammatory response to degenerating neurons: mutants that lack all peripheral glia (foxD3^−/−; Ntr) exhibit a much reduced reaction to axonal degeneration, resulting in a dramatic decrease in the clearance of debris, and impaired macrophage recruitment. Overall, these results show that this zebrafish model of peripheral sensory axon degeneration exhibits many aspects common to peripheral neuropathies and that peripheral glia play an important role in the initial response to this process.     

Engulfment of Axon Debris by Microglia Requires p38 MAPK Activity

The clearance of debris after injuries to the nervous system is a critical step for restoration of the injured neural network. Microglia are thought to be involved in elimination of degenerating neurons and axons in the central nervous system (CNS), presumably restoring a favorable environment after CNS injuries. However, the mechanism underlying debris clearance remains elusive. Here, we establish an in vitro assay system to estimate phagocytosis of axon debris. We employed a Wallerian degeneration model by cutting axons of the cortical explants. The cortical explants were co-cultured with primary microglia or the MG5 microglial cell line. The cortical neurites were then transected. MG5 cells efficiently phagocytosed the debris, whereas primary microglia showed phagocytic activity only when they were activated by lipopolysaccharide or interferon-β. When MG5 cells or primary microglia were co-cultured with degenerated axons, p38 mitogen-activated protein kinase (MAPK) was activated in these cells. Engulfment of axon debris was blocked by the p38 MAPK inhibitor SB203580, indicating that p38 MAPK is required for phagocytic activity. Receptors that recognize dying cells appeared not to be involved in the process of phagocytosis of the axon debris. In addition, the axons undergoing Wallerian degeneration did not release lactate dehydrogenase, suggesting that degeneration of the severed axons and apoptosis may represent two distinct self-destruction programs. We observed regrowth of the severed neurites after axon debris was removed. This finding suggests that axon debris, in addition to myelin debris, is an inhibitory factor for axon regeneration.Axon degeneration is an active, tightly controlled, and versatile process of axon segment self-destruction. The lesion-induced degeneration process was first described by Waller (1) and has since been known as Wallerian degeneration (2, 3). This degeneration involves rapid blebbing and fragmentation of an entire axonal stretch into short segments, which are then removed by locally activated phagocytic cells. Phagocytic removal of damaged axons and their myelin sheaths distal to the injury is important for creating a favorable environment for axonal regeneration in the nervous system. Although the debris of degenerated axons and myelin is cleared by phagocytes in the peripheral nervous system (PNS), the debris is removed very slowly in the central nervous system (CNS)³ (4, 5). This is considered to be one of the obstacles for regeneration of the injured axons in the CNS.Apoptotic neurons are also engulfed by activated phagocytic cells. Apoptosis is very well documented in the CNS where a significant proportion of neurons undergo programmed cell death (6). To prevent the diffusion of damaging degradation products into surrounding tissues, dying neurons are phagocytosed. In the brain, apoptotic cells are engulfed mainly by the resident population of phagocytes known as microglia. Microglia are generally considered to be immune cells of the CNS (7). They respond to any kind of pathology with a reaction termed “microglial activation.” After injuries to the CNS, microglia react within a few hours with a migratory response toward the lesion site.Although insight into the mechanism of phagocytosis of dying cells by microglia has improved, little is known about the mechanism of clearance of degenerated axons and myelin debris by microglia after axonal injury in the CNS. Interestingly, the axons undergoing Wallerian degeneration do not seem to possess detectable activation of the caspase family (8), suggesting that Wallerian degeneration and apoptosis may represent two distinct self-destruction programs. Thus, the mechanism of microglial phagocytosis of dying cells might be different from that of axon/myelin debris. We aimed to elucidate the mechanism of debris clearance by microglia after an axonal injury. We established an in vitro assay system to estimate phagocytosis of degenerated axon debris. We found that p38 mitogen-activated protein kinase (MAPK) was critical for the phagocytic activity of microglia. Treatment with lipopolysaccharide (LPS) or interferon-β (IFN-β) was necessary for the primary microglia to become phagocytic. In addition, clearance of degenerated axon debris allowed axonal growth from the severed neurites, suggesting that removal of the axon debris provides a favorable environment for axonal regeneration.     

Glial cells phagocytose neuronal debris during the metamorphosis of the central nervous system in Drosophila melanogaster

 Using electron microscopy we demonstrate that degenerating neurons and cellular debris resulting from neuronal reorganization are phagocytosed by glial cells in the brain and nerve cord of the fruitfly Drosophila melanogaster during the first few hours following pupariation. At this stage several classes of glial cells appear to be engaged in intense phagocytosis. In the cell body rind, neuronal cell bodies are engulfed and phagocytosed by the same glial cells that enwrap healthy neurons in this region. In the neuropil, cellular debris in tracts and synaptic centres resulting from metamorphic re-differentiation of larval neurons is phagocytosed by neuropil-associated glial cells. Phagocytic glial cells are hypertrophied, produce large amounts of lysosome-like bodies and contain a large number of mitochondria, condensed chromatin bodies, membranes and other remains from neuronal degeneration in phagosomes. Received: 23 January 1996 / Accepted in revised form: 21 May 1996     

Cytological identification of cell types in the testis of Esox lucius and E. niger

Summary Testes of Esox lucius and Esox niger were investigated histologically, cytochemically, and ultrastructurally in reproductive fish. Intralobular Sertoli cells possessed numerous lipid droplets in Esox lucius, but not in Esox niger. In both species, interlobular cell types included myoid cells and lipid-negative Leydig cells within the extravascular space. Evidence is presented for a contractile network of myoid cells within the testes of these teleosts. The presence of Leydig cells and myoid boundary cells in the testis of Esox lucius refutes the reported homology between lobule boundary cells and Leydig cells in this species.     

Sperm development in the teleost Oryzias latipes

Summary In Oryzias latipes the processes of spermatogenesis and spermiogenesis occur within testicular or germinal cysts which are delimited by a single layer of lobule boundary cells. These cells, in addition to comprising the structural component of the cyst wall, ingest residual bodies cast off by developing spermatids. Therefore, they are deemed to be the homologue of mammalian Sertoli cells. The germ cells within a cyst develop synchronously owing to the presence of intercellular bridges connecting adjacent cells. Since bridges also connect spermatogonia, it seems probable that all of the germ cells within a cyst may form a single syncytium and do not exist as individual cells until the completion of spermiogenesis when the residual bodies are cast off. Significant differences between spermiogenesis in O. latipes and in the related poeciliid teleosts are discussed.     

Degenerative regression of the digestive tract in the colonial ascidian Botryllus schlossen (Pallas)

Summary Degenerative changes in the digestive tract of zooids of Botryllus schlosseri were studied by light and electron microscopy. Three main processes occurred in the tissues: contraction, involution and phagocytosis. The contraction of epidermis and peribranchial epithelium in which cytoplasmic microfilaments probably participate, seemed to have a special role in compressing the underlying organs. During contraction most of the body cavities collapsed, the branchial walls disintegrated and the fragments were rapidly taken up by large phagocytes. The gut epithelium retained its apparent continuity longer, though isolated phagocytes infiltrated it to eliminate single cells. Cell degeneration came about chiefly either through swelling and lysis of cells or through loss of water and condensation of cytoplasm and nucleus.The fate of all regressed tissues was to be engulfed and digested by wandering phagocytes. However, it was also observed that numerous cells of different epithelia could act as fixed phagocytes by engulfing cell debris and entire cells into heterophagic vacuoles.     

Buccal glands of adults of the lamprey Mordacia mordax,including comparisons with other species

Mordacia mordax is one of the two anadromous parasitic lamprey species of the southern hemisphere family Mordaciidae. Its adults possess two lateral buccal glands and one central buccal gland. When the tongue-like piston is retracted, the buccal glands occupy much of the opening of the oral cavity at the rear of the buccal cavity. The glands contain numerous tube-like, ductless secretory units, which discharge directly into the buccal cavity. Their secretory epithelial cells contain numerous granules, some of which are zymogen-like, while others have a beaded, spiralled appearance. The similarity of the latter to mast cell granules suggests that they may likewise produce an anticoagulant, which would be valuable to a presumed blood feeder such as M. mordax. The mucus produced by these cells could act as a carrier for the secretions and as an adhesive for promoting retention of t he secretions on the host's surface. When the young adults is transferred to salt water, the buccal glands increase their production and discharge of secretions. Since the glands are not enclosed in musculature, their secretions are probably discharged by mechanical pressure applied by the forward movement of the head of the tooth-bearing piston into the buccal cavity. An account is given of the way in which the location, number, glandular organization, secretory granules, and type of secretion of the buccal glands of M. mordax, and thus presumably also their mode of function, differ markedly from those of members of the other lamprey family found in the southern hemisphere, and of all holarrctic lampreys. © 1995 Wiley-Liss, Inc.     

Schistosoma mansoni: Drug induced changes in the cell population of the vitelline gland

Using the electron microscope four stages in the development of the mature vitelline cell in normal Schistosoma mansoni have been defined precisely and the percentage of their contribution to the cell population of the vitelline lobule has been determined. The effects of Astiban, Lucanthone, and Hycanthone on this cell population were examined and compared with the composition of the normal vitelline lobule. Astiban damaged mature cells and those stages exhibiting protein synthesis. Undifferentiated, nonsynthetic cells did not exhibit morphological damage and rapidly developed and replenished the vitelline lobule so that a normal population was attained within a few days after cessation of drug treatment. In contrast, Lucanthone and Hycanthone appeared to inhibit the division of these undifferentiated cells so that they gradually disappeared from the lobule. The various developmental stages and mature cells which had arisen from these undifferentiated cells accumulated in the lobule, but were eventually damaged. With both these drugs, the lobule population eventually came to consist largely of mature cells. In the case of Hycanthone, it is suggested that the retention of these stages within the lobule was due to interference with the neuromuscular system so that the cells were not passed down the vitelline duct. Withdrawal of Lucanthone and Hycanthone did not result in the replenishment of the vitelline lobule. With all drugs used, cell death was associated with vacuolation, the appearance of myelin configuration, disruption of vitelline droplets, an increase in the lipid content of cells, and an increase in the density of the cytoplasm. The experiments indicate that these three drugs produced a differential cell death in the vitelline lobule, the precise changes in the cell population being dependant on the particular drug being used.     

A study of the source of virus in the Pholem exudate appearing on leaves of Amscinckia infected with the beet curly top virus

Abstract Leaves of Amsinckia douglasiana discharging phloem exudate after infection with the beet curly top virus (BCTV) were studied with the electron microscope. Infected tissue differed from the noninfected in having much hyperplastic phloem characterized by abnormally high proportion of sieve elements, scarcity of companion cells, degenerating parenchyma cells, and some unusually large intercellular spaces. Many spaces contained amorphous debris. Particles resembling BCTV were discernible within the debris. Such particles were encountered also in the debris trapped between stomatal guard cells. Since the phloem exudate excreted from leaves of BCTV-infected plants contains virus particles, and since the virus is found extremely rarely in sieve elements, we suggest (1) that most of BCTV particles apparently released into intercellular spaces are derived from degenerating parenchyma cells in which the virus had multiplied; (2) that the exudate is derived from sieve elements of the hyper-plastic phloem in which the normal functional control by companion cells is lacking; (3) that the exudate leaks from the nontransporting sieve elements through cell walls into intercellular spaces and carries the virus to the outside. Initially, stomata may serve as exits for the infectious exudate, but subsequently ruptures in the epidermis are involved.     

Ultrastructural analysis of nematocyte removal in Hydra

A consecutive series of ultrathin sections through the distal one-third of a Hydra tentacle has revealed at least four categories of nematocytes: (1) normal, mounted nematocytes, in specific arrangements within the battery cells; (2) degenerating nematocytes, within the battery cells; (3) mature nematocytes, enclosed within endodermal cells; (4) a mature nematocyte, in the enteric cavity. The degenerating nematocytes within the battery cells and the nematocytes in the endoderm and enteric cavity appeared to be aging nematocytes undergoing death and removal. The results provide the first ultrastructural evidence for nematocyte degeneration within battery cells and also suggest phagocytosis of mature nematocytes by endodermal cells.     

DEVELOPMENT OF THE PERITHECIUM IN GNOMONIA COMARI (DIAPORTHACEAE)

Perithecia of Gnomonia comari (Ascomycetes) mature within 14 days on cornmeal agar under continuous fluorescent light at 25 C. The perithecium is initiated by a coiled, multicellular ascogonium. Branches from somatic hyphae surround the ascogonium. This hyphal envelope early differentiates into two regions: a centrum of pseudoparenchymatous cells and a peripheral wall of more elongated, flattened cells. The wall produces a long, ostiolate beak by eruption of a column of hyphae from the inner layers at the apex; the cells gradually become thick-walled and brown from the peripheral layers inward. Proliferations from the ascogonial cells near the center of the perithecium form a bowl-shaped mass of ascogenous hyphae which expands centrifugally until it appears in section as a crescentic layer across the middle of the centrum. The centrum pseudoparenchyma above this incipient hymenium disintegrates, and short abortive paraphyses extend upward from the subhymenial pseudoparenchyma into the resulting cavity. The paraphyses disintegrate as the asci develop among them. The hymenium gradually pushes downward into the disintegrating subhymenial pseudoparenchyma until it rests on the perithecial wall. Maturing asci become detached from the hymenium, fill the perithecial cavity, and pass through the ostiole. At the tip of the beak they discharge their ascospores forcibly. Diaporthaceae with abortive paraphyses may occupy an intermediate position in a series leading from forms (Gaeumannomyces graminis) with long delicate paraphyses resembling those in the Sordariaceae to forms (Stegophora ulmea) in which the centrum is entirely pseudoparenchymatous.     

Invasion of microglia/macrophages and granulocytes into the Mauthner axon myelin sheath following spinal cord injury of the adult goldfish,Carassius auratus

Rapid activation of resident glia occurs after spinal cord injury. Somewhat later, innate and adaptive immune responses occur with the invasion of peripheral immune cells into the wound site. The activation of resident and peripheral immune cells has been postulated to play harmful as well as beneficial roles in the regenerative process. Mauthner cells, large identifiable neurons located in the hindbrain of most fish and amphibians, provided the opportunity to study the morphological relationship between reactive cells and Mauthner axons (M-axons) severed by spinal cord crush or by selective axotomy. After crossing in the hindbrain, the M-axons of adult goldfish, Carassius auratus, extend the length of the spinal cord. Following injury, the M-axon undergoes retrograde degeneration within its myelin sheath creating an axon-free zone (proximal dieback zone). Reactive cells invade the wound site, enter the axon-free dieback zone and are observed in the vicinity of the retracted M-axon tip as early as 3 hr postinjury. Transmission electron microscopy allowed the detection of microglia/macrophages and granulocytes, some of which appear to be neutrophil-like, at each of these locations. We believe that this is the first report of the invasion of such cells within the myelin sheath of an identifiable axon in the vertebrate central nervous system (CNS). We speculate that microglia/macrophages and granulocytes that are attracted within a few hours to the damaged M-axon are part of an inflammatory response that allows phagocytosis of debris and plays a role in the regenerative process. Our results provide the baseline from which to utilize immunohistochemical and genetic approaches to elucidate the role of non-neuronal cells in the regenerative process of a single axon in the vertebrate CNS.     

Terminal degeneration in the mediodorsal cerebral cortex of the lizard Agama agama: Light and electron microscopy

The degeneration of axon terminals in the small-celled part of the mediodorsal cortex (sMDC) of the lizard Agama agama has been studied after lesions in the dorsal cortex at various survival periods. The Fink-Heimer stain was used to map and demonstrate terminal degeneration with the light and electron microscope. Electron microscopy was used to identify and describe degenerating boutons ultrastructurally. One sham-operated and three unoperated animals served as controls. Between 6 and 21 days postsurgically, degenerating terminals can be seen through 80% of the superficial plexiform layer, the zone adjacent to the cellular layer remaining free of degeneration. Swelling of dendrites in the outer part of the superficial plexiform layer and increased numbers of vacuolar invaginations, both present at short (24 hr–6 days; peak at 48–54 hr) survival periods, can be regarded as reaction to the surgical trauma. Degeneration of axon terminals takes three forms, all of the electron-dense type: gray boutons, degenerating bouton-dendritic spine complexes surrounded or engulfed by glia, and degeneration debris inside glial processes. Several forms of terminal degeneration occur concomitantly at any short (3–12 days) survival time. At longer survival times (15–21 days) only debris is present. From 6 days on, considerable numbers of degenerating structures are present, but the majority of degenerating boutons and debris are associated with reactive glia rather than with dendrites. From these observations it is concluded that in this lizard application of the combined degeneration-Golgi-EM technique would probably lead to little success. Electron microscopy of Fink-Heimer-stained sections suggests that degenerating bouton-dendritic spine complexes and degeneration debris accumulate silver particles, whereas gray boutons do not.     

Autophagy,neuron-specific degradation and neurodegeneration

Degradation of membrane compartments, organelles and other debris through macroautophagy (hereafter referred to as autophagy) is thought to occur in most, maybe all, cells. We recently reported the discovery of a neuron-specific endomembrane degradation mechanism that depends on the vesicle SNARE neuronal Synaptobrevin (n-Syb) and the vesicle ATPase component V100 (the V₀a1 subunit). Loss of n-Syb causes degeneration of adult photoreceptor neurons in Drosophila, reminiscent of adult-onset degeneration in neurons with defective autophagy. Here we explore the potential importance of this newly discovered neuron-specific degradation mechanism in comparison with ubiquitous autophagy machinery for adult-onset neurodegeneration.     

Fine structure of the silk gland in the mite Ornithocheyletia sp. (Prostigmata,Cheyletidae)

Silk spinning is widely-spread in trombidiform mites, yet scarse information is available on the morphology of their silk glands. Thus this study describes the fine structure of the prosomal silk glands in a small parasitic mite, Ornithocheyletia sp. (Cheyletidae). These are paired acinous glands incorporated into the podocephalic system, as typical of the order. Combined secretion of the coxal and silk glands is released at the tip of the gnathosoma. Data obtained show Ornithocheyletia silk gland belonging to the class 3 arthropod exocrine gland. Each gland is composed of seven pyramidal secretory cells and one ring-folded intercalary cell, rich in microtubules. The fine structure of the secretory cells points to intensive protein synthesis resulted in the presence of abundant uniform secretory granules. Fibrous content of the granules is always subdivided into several zones of two electron densities. The granules periodically discharge into the acinar cavity by means of exocytosis. The intercalary cell extends from the base of the excretory duct and contributes the wall of the acinar cavity encircling the apical margins of the secretory cells. The distal apical surface of the intercalary cell is covered with a thin cuticle resembling that of the corresponding cells in some acarine and myriapod glands. Axon endings form regular synaptic structures on the body of the intercalary cell implying nerve regulation of the gland activity.     

Identification of phagocytic glial cells after lesion-induced anterograde degeneration using double-fluorescence labeling: combination of axonal tracing and lectin or immunostaining

 Retrograde and anterograde degeneration have been reported to be sufficient stimuli to activate glial cells, which, in turn, are involved in phagocytosis of degenerating material. Here we describe a double-fluorescence technique which allows for direct and simultaneous visualization of both labeled incorporated axonal debris and incorporating glial cells in the course of anterograde degeneration. Stereotaxic application of small crystals of biotinylated and tetramethylrhodamine (TRITC)-conjugated dextran amine Mini Ruby into the medial entorhinal cortex resulted in a stable rhodamine fluorescence confined to fibers and terminals in the middle molecular layer of the dentate gyrus, the stratum lacunosum-moleculare, and the crossed temporo-hippocampal pathway. Subsequent stereotaxic lesion of the entorhinal cortex induced transformation of rhodamine-fluorescent fibers and terminals into small granules. Incorporation of these granules by microglial cells [labeled by fluorescein isothiocyanate (FITC)-coupled Bandeiraea simplicifolia isolectin B₄] or astrocytes (labeled by FITC-coupled glial fibrillary acidic protein antibodies) resulted in phagocytosis-dependent labeling of these non-neuronal cells, which could be identified by double-fluorescence microscopy. Electron microscopical analysis revealed that, following lesion, the tracer remained confined to entorhinal axons which were found to be incorporated by glial cells. Our data show that TRITC- and biotin-conjugated dextran amines are versatile tracers leading to Phaseolus vulgaris leucoagglutinin-like axonal staining. Lesion-induced phagocytosis of anterogradely degenerating axons by immunocytochemically identified glial cells can be directly observed by this technique on the light and electron microscopical levels. Accepted: 8 January 1997     

Phagocytic Cells in the Taste Buds of Rat Circumvallate Papillae after Denervation

Phagocytic cells in the taste buds of rat circumvallate papillaeafter the sectioning of bilateral glossopharyngeal nerves wereexamined by electron microscopy and immunohistochemistry. Electronmicrographs taken 1 day after denervation revealed that flat-shapedcells were present just beneath the taste buds and that theircellular processes extended toward the debris from the degeneratingtaste buds. At 2–6 days after denervation, long and thinprocesses of the flat cells surrounded the debris and appearedto have taken them up into the cytoplasm as small vesicles.Evidence for phagocytosis by the flat cells was seen up to 9days after denervation and again at 24 and 40 days, in correlationto the degeneration and regeneration of the taste buds. Pre-embeddingimmunohistochemistry using anti-vimentin antibody showed thatflat cells strongly reacted with vimentin. Light microscopicimmunohistochemistry using anti-macrophage antibodies (ED1,ED2) showed that throughout the post-operative days macrophageswere not present underneath or within the taste buds. Most ofthe ED2-immunoreactive resident macrophages were located inthe deep layer of connective tissue, and a few were found inthe nerve bundle. ED1-immunoreactive cells were seen in theduct cells of von Ebner's glands and a few were in the trenchwall of circumvallate papillae; however, they were also immunoreactivefor anti-OX62 antibody, which recognizes dendritic cells. Theresults indicate that the phagocytic cells of the taste budsare fibroblasts, not macrophages. Moreover, resident macrophagesparticipate in phagocytosis of degenerated nerves together withSchwann cells. Chem. Senses. 21: 467–476, 1996.     

Ultrastructure of the Accessory Glands in Female Genitalia of Pholcus phalangioides(Fuesslin, 1775) (Pholcidae; Araneae)

Pholcus phalangioidesdoes not possess receptacular seminis. The uterus externus (genital cavity) itself functions as a sperm storage structure. Two accessory glands are situated in the dorsal part of the uterus externus; they discharge their secretory product into the genital cavity. The secretion is considered to serve primarily as a matrix for sperm storage, i.e. to keep the spermatozoa in a fixed position. The accessory glands consist of numerous glandular units, each being composed of four cells: two secretory cells are always joined and surrounded twice by an inner and an outer envelope cell. Both envelope cells take part in forming a cuticular ductule that leads from the secretory cells to the pore plates of the uterus externus. The inner envelope cell produces the proximal part of the canal close to the microvilli of the secretory cells, whereas the outer envelope cell produces the distal part of the canal leading to the pore plate. Close to the pore the latter exhibits prominent microvilli that might indicate additional secretory activity.