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Specific ultrastructural markers of human pinealomas. A study of four cases.

An ultrastructural study of four pinealomas was carried out to precise eventual specific markers. Dark and clear cells joined with zonulae adherents, extensive and pleiomorphous processes, a complex vacuolar system, and characteristic organelles (lysosome-like structures, clear and dense-core vesicles, vesicle-crowned rodlets and related structures, microtubular sheaves and centriolar derivatives, membranous whorls, fibrous bodies, microtubules, heterogeneous cytoplasmic inclusions) offered a typical pattern. No correlation could be made between the histological and ultrastructural features. The authors stress the ultrastructural similarities between the human tumor cells and the mammalian pineal cells. Pinealomas appeared as a morphological entity distinct from neuronal and astrocytic tumors.

Adolescent↗

Sural nerve biopsies from workers with a history of chronic exposure to organic solvents and from normal control cases. Morphometric and ultrastructural studies.

An ultrastructural and morphometric study was performed on sural nerve biopsies of four industrial spray painters (35-59 years) and 11 controls (6-64 years). No difference could be shown in spray painters and age-matched controls as to the number of myelinated nerve fibres per area, their size distribution, variation of internodal length along single nerve fibres or the ratio between the number of myelin lamellae and the axon circumference. There was marked scattering of the two latter parameters in older exposed and and control individuals. The distribution of NADH2-tetrazolium reductase activity was similar in exposed and control cases. The general ultrastructural appearance of nodal-paranodal regions in controls conformed with that noted in experimental animals. The overall ultrastructural organization and age-related changes of nerves of exposed cases were similar to those of control cases except for a presence of paranodal axonal mitochondria which contained glycogen-like particles in exposed cases. In one exposed case abundant dispersed or clustered glycogen-like particles were seen in the paranodal axoplasm. These findings are suggested to be an effect of chronic exposure to organic solvent vapours. Ageing seems, however, to have a much greater impact on the morphology of the sural nerve fibre than occupational exposure to organic solvent.

Adult↗

Reappraisal of neurofibrillary tangles. Immunohistochemical, ultrastructural, and immunoelectron microscopical studies.

We have studied the immunohistochemical reactivity and ultrastructure of both neurofibrillary tangles (NFTs) occurring with severe neurofibrillary diseases, and Pick bodies (PBs) associated with Pick's disease. The NFTs and PBs did not react immunohistochemically with the anti-nonphosphorylated neurofilament monoclonal antibody irrespective of whether they were pretreated with alkaline phosphatase. In granular neurons of the dentate fascia of Ammon's horn in cases of dementia of the Alzheimer type (DAT), NFTs either resembled PB-like inclusion bodies (Horoupian's inclusion bodies) in form, or had a perinuclear structure. Immunohistochemically and ultrastructurally, the NFTs in the dentate fascia in cases of DAT, including Horoupian's inclusion bodies, were similar to the NFTs in the pyramidal neurons of Ammon's horn, which are found most frequently in association with severe neurofibrillary diseases. Under a light microscope, Horoupian's inclusion bodies and PBs could not be differentiated and appeared to be argyrophilic round cytoplasmic inclusions in granular neurons of the dentate fascia. There were, however, ultrastructural differences. Horoupian's inclusion bodies consisted of bundles made up of straight tubules (STs), each about 15 nm in diameter. These bundles were intermixed with a few paired helical filaments which occurred at intervals of about 80 nm. On the other hand, PBs were composed of randomly distributed 15-nm-wide STs, intermixed with a very few fibrillary structures. These fibrils had a periodicity of about 160 nm, and ranged in width from about 15 nm to 30 nm. Horoupian's inclusion bodies associated with DAT and PBs associated with Pick's disease are different in this neuropathological aspect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Ultrastructural and ionic studies in global ischemic dog brain.

A time course of tissue ionic changes, and their relation to ultrastructural findings during reperfusion following a 15-min global ischemic brain insult was studied in a dog model. Parietal cortex was analyzed for Ca, Na, K, Mg and Fe in controls and after 10 min, 2, 4, and 8 h of reperfusion. After 8 h of reperfusion, the mean values (mumol/g tissue wet wt.) for Ca (control = 1.43, 8 h = 2.76) and Na (control 60.4, 8 h = 107.4) doubled and K (control = 90.4, 8 h = 48.5) decreased to half that of the control. Ultrastructural studies and subcellular localization of calcium in parietal cortex of in situ-fixed brains after 8 h showed cortical neurons with clumping of nuclear chromatin, dilatation of endoplasmic reticulum and disruption of plasma membranes. Large amounts of electron-dense precipitates of calcium were present within dilated astrocytic processes, synaptic vesicles, cytoplasm of edematous dendrites and mitochondria. Cortical neurons from postischemic dogs without reperfusion showed only slight chromatin clumping and edema of astrocytic processes, but no calcium accumulation. The large ionic shifts noted between 4 and 8 h of reperfusion, indicate a progressive inability of the cells to maintain normal transmembrane gradients of these ions and may reflect a membrane destructive process, as demonstrated ultrastructurally at 8 h. Enhanced calcium entry into the neuron during reperfusion appears to be a part of the cytotoxic mechanism leading to neuronal necrosis.

Animals↗

Acute ultrastructural response of hypoxic hypoxia with relative ischemia in the isolated brain.

The acute cortical response to surgical brain isolation and subsequent extracorporal normoxic or 30 min hypoxic (PaO2 = 20 mm Hg) perfusions (hypoxic hypoxia with relative ischemia) was evaluated. Cerebral blood flow, arterial pH and CO2 were maintained constant during both perfusions; only the arterial oxygen content was changed. The isolated brain model used in this and previous investigations produces no qualitative ultrastructural changes in the neocortex following brain isolation and normoxic perfusion. However, the acute cortical structural response to 30 min of hypoxic hypoxia with relative ischemia demonstrated a number of important observations. Hypoxic hypoxia produced ultrastructural responses common to cerebral ischemia such as nuclear chromatin clumping, nucleolar condensation and cytoskeletal breakdown. Although neuronal abnormalities seen after 30 min of hypoxic hypoxia were similar to those acute neuronal changes observed following complete cerebral ischemia without recirculation, they differed three ways: (a) mitochondrial swelling and microvacuolation were observed in many cortical pyramidal neurons. (b) Glycogen particles within astroglial processes were observed even after a 30-min period of hypoxic hypoxia. (c) Perivascular astroglial swelling was minimal despite considerable perineuronal swelling. In contrast, incomplete cerebral ischemia produces mitochondrial changes similar to those in hypoxic hypoxia but also causes the depletion of tissue glycogen and perivascular glial swelling. Thus, hypoxic hypoxia with relative ischemia produces a unique acute ultrastructural response compared to either complete or incomplete cerebral ischemia.

Animals↗

Ultrastructural analysis of human proximal tubules and cortical interstitium in chronic renal disease (hydronephrosis).

A systematic ultrastructural analysis of proximal tubule atrophy and cortical interstitial changes was carried out in human chronic nephropathy. The investigation was based on human hydronephrotic kidneys, which had been surgically removed and subsequently perfusion-fixed for light and electron microscopy. Normal kidney tissue, which was derived from nephrectomy specimens with pathological changes confined to part of the kidney or to the renal pelvis, was used for control material. A slight degree of proximal tubule atrophy was characterized by reduction of mitochondria and basolateral membranes, enlargement of large endocytic vacuoles and increased numbers of lysosomes containing lamellar material. In moderate atrophy these changes were further accentuated, and in addition there was an increasing loss of microvilli and a reduction of endocytic invaginations and small endocytic vacuoles. In severe atrophy all types of organelles were sparse and the architecture of the tubule cells greatly simplified. A distinctive feature of atrophic tubules was the presence in the tubule cells of large bundles of actin-like filaments, which were often associated with outpouchings of basal cell parts and basement membrane. The reduction of mitochondria and basolateral cell membranes and the changes of endocytic vacuoles and lysosomes indicate that proximal tubule atrophy also in early stages may be associated with impairment of tubular transport processes. Comparisons with previous observations in various types of experimentally induced tubule cell degeneration and with the ultrastructure of regenerating proximal tubule cells provide some evidence that degenerative changes as well as imperfect regeneration of tubule cells may contribute to the alterations of ultrastructure in tubular atrophy. It is suggested that changes of the cortical interstitium may be of pathogenic importance for the progression of tubular atrophy by altering the spatial relationships between tubules and capillaries.

Adult↗

Immunocytochemical and ultrastructural studies of eosinophilic granular bodies in astrocytic tumors.

Eosinophilic granular bodies (EGBs) are studied immunocytochemically and ultrastructurally in a case of low-grade and a case of high-grade astrocytoma. EGBs are recognized as brightly eosinophilic round bodies of variable size in hematoxylin and eosin-stained sections. Immunocytochemically some EGBs are positive for antibodies raised against alpha B-crystallin, ubiquitin and glial fibrillary acidic protein with the staining patterns for each being different from one another. Ultrastructurally EGBs consist of membrane-bound round body of various diameter ranging from 50 nm to 20 microns. Small EGBs contain electron-dense homogeneous material with occasional myelin figures, while electron-dense homogeneous material or loose granular profiles. Our studies demonstrate (1) ultrastructural variety of EGB; (2) and alpha B-crystallin epitope in EGB; and (3) the presence of EGB in high-grade as well as low-grade astrocytoma.

Adult↗

Small cell neuroendocrine carcinoma of the urinary bladder. An immunohistochemical and ultrastructural evaluation of 3 cases with a review of the literature.

Small cell carcinoma with the histological appearance of pulmonary small cell carcinoma is a rare tumour in the urinary bladder. In previous case reports the neuroendocrine nature of small cell bladder carcinoma has been accepted, but on review the evidence for true neuroendocrine differentiation appears unsatisfactory. In this study the histological, immunohistochemical and ultrastructural characteristics of three cases of small cell carcinoma of the urinary bladder are described. Ultrastructurally, the cytoplasm of all three tumours contained neurosecretory-type granules and each of the tumours demonstrated positive immunoreaction for two or more neuroendocrine markers, from a panel including neuron-specific enolase, chromogranin A, Leu-7, bombesin and synaptophysin. Although the combination of ultrastructural and immunohistochemical examination obviously offers the strongest evidence in establishing neuroendocrine differentiation, it is argued that immunohistochemistry alone may also yield important information in demonstrating a neuroendocrine nature, provided that at least neuron-specific enolase and synaptophysin are included as markers. The clinical relevance of identifying neuroendocrine differentiation in small cell bladder carcinoma is suggested by the favourable response to combination chemotherapy in two of our cases.

Aged↗

Ultrastructural demonstration of endothelial glycocalyx disruption in the reperfused rat heart. Involvement of oxygen free radicals.

To determine the effect of post-ischaemic reperfusion on the ultrastructure of the endothelial glycocalyx and the role of oxygen free radicals, isolated working rat hearts were subjected to 20 min ischaemia followed by 3 or 30 min of reperfusion. Ruthenium red and lanthanum chloride were used to delineate the endothelial glycocalyx, and histochemical manganese/diaminobenzidine (Mn+2/DAB) or iron/diaminobenzidine (Fe+2/DAB) techniques were applied to visualize superoxide and hydrogen peroxide in myocardial capillaries. We found that ischaemia alone led to only a slightly flocculent appearance of the glycocalyx and its disruption was not observed until the onset of reperfusion. Prolongation of reperfusion to 30 min had no further effect on the ultrastructure of the glycocalyx. The ultrastructure of endothelial cells was normal. The disruption of the glycocalyx correlated in time and place with the appearance of Mn+2/DAB and Fe+2/DAB reaction products on the luminal surface of endothelial cells. Treatment with 5 mM N-(2-mercaptopropionyl)-glycine (MPG), an .OH radical scavenger, starting before ischaemia prevented the disruption of the glycocalyx, while 100 mM 3-morpholinosydnonimine (SIN-1), capable of generating both NO and -O2 simultaneously when applied at the time of reperfusion, increased the mean density of capillaries positively stained with Mn+2/DAB and Fe+2/DAB, and caused substantial disruption of the glycocalyx and damage to endothelial cells, which was not prevented by MPG. Our results suggest that the onset of reperfusion is critical for injury to the endothelial glycocalyx. Most probably the hydroxyl radical derived from the Fenton reaction is responsible for this injury. Peroxynitrite and/or nitric dioxide, if present upon reperfusion, may also account for damage of the endothelial glycocalyx.

Animals↗

Use of light microscopic immunotechniques in selecting preparation conditions and immunoprobes for ultrastructural immunolabelling of lactoferrin.

Successful postembedding immunolabelling for electron microscopy is sometimes difficult to achieve. We propose that light microscopy can be used (1) to detect quickly processing steps which have an adverse effect on the tissue antigenicity and (2) to check the specific reactivity of the immunogold detecting system normally employed at the ultrastructural level. The individual steps of fixation, dehydration and embedding were tested for their ability to preserve antigenicity by light microscopic peroxidase--anti-peroxidase cytochemistry. Steps that severely reduced antigenicity were replaced by less destructive alternatives compatible with reasonable ultrastructural preservation. The specific reactivity of the immunogold detecting system was assessed by using the light microscopic immunogold-silver staining method. We studied the antigen lactoferrin in human neutrophilic granulocytes from patients with chronic myeloid leukaemia. We obtained strong immunolabelling of specific granules and good ultrastructural preservation using routine methods at room temperature. For lactoferrin the method of choice was to fix in 3% paraformaldehyde/0.1% glutaraldehyde followed by 1% OsO4, dehydrate in 70% ethanol, embed in LR White resin and polymerize at 40 degrees C for 40 h. These conditions may not be suitable for all antigens and we emphasize that for each new antigen a similar study should be carried out.

Fixatives↗

Ultrastructure of streptozotocin-induced renal tumours in mice.

Streptozotocin-induced tumours in the kidneys of experimental animals have been shown to be histologically similar to human renal cell carcinoma. We report the ultrastructural features of renal tumours induced in 15 mice by a single intravenous bolus of 2.5% streptozotocin administered in a dose of 250 mg streptozotocin/kg mouse body weight. Animals were sacrificed 232-361 days after the administration of streptozotocin. On examination both kidneys from each animal contained 1-4 dysplastic tubules and 1-3 discrete tumours per kidney. Twelve dysplastic proximal convoluted tubules showing varying degrees of epithelial atypia and nine tumours exhibiting either a papillary or solid architecture were examined. Dysplastic epithelial cells and tumours of papillary and solid type exhibited complex cell borders with well-developed junctional complexes. The majority of cells contained surface microvilli, and in some cells microvilli-lined intracytoplasmic lumina were observed. Occasional dysplastic epithelial cells and tumour cells contained double-membrane vesicles 120-200 nm in diameter. These were similar to the intracytoplasmic vesicles characteristic of human chromophobe renal cell carcinoma. Intracytoplasmic collections of glycogen granules and flocculant protein were identified in both dysplastic and neoplastic cells, and where prominent they resulted in compression of cytoplasmic organelles. Coated vesicles were commonly observed. These were free within the cytoplasm and were also seen budding from strands of rough endoplasmic reticulum. The distribution of these vesicles suggested a role in protein transport from the rough endoplasmic reticulum. It is concluded that while streptozotocin-induced renal tumours have some ultrastructural features in common with human chromophobe renal cell carcinoma, the overall ultrastructural morphology differs significantly from that described for the various histological types of human renal cell carcinoma.

Animals↗

Ultrastructural localization of carbonic anhydrase in gastric parietal cells with the immunoglobulin-enzyme bridge method.

Ultrastructural immunostaining of carbonic anhydrase in gastric parietal cells was accomplished with the immunoglobulin-peroxidase bridge procedure applied to cryostat sections of fixed guinea-pig stomach prior to dehydration and embedment. Of a variety of fixatives tested, only freshly prepared paraformaldehyde buffered with calcium acetate provided both immunostaining and adequate preservation of ultrastructural morphology. Delipidization or exposure of specimens to detergent prior to staining enhanced the intensity of the immunostaining and increased the sensitivity of the method. Increased diaminobenzidine concentration in the peroxidase substrate appeared also to intensify the densification at the reactive site. Carbonic anhydrase was localized ultrastructurally with this pre-embedment immunobridge procedure in the hyaloplasm of gastric parietal cells and less consistently in the superficial surface epithelium. The basal portion of the parietal cells stained more intensely than the apical region and immunoreactivity appeared concentrated at the plasmalemma and around mitochondria.

3,3'-Diaminobenzidine↗

Collagen-associated sulphated proteoglycans. Ultrastructure after formaldehyde-cetylpyridinium chloride fixation.

In the course of an ultrastructural cytochemical study of intracellular sulphated proteoglycans involving the addition of cetylpyridinium chloride in the primary aldehyde fixative, a remarkable ultrastructural preservation of the collagen-associated sulphated proteoglycans was observed. Together with the preservation of their localization among the collagen fibrils (with, for some of them, a 50 nm periodic association with d-bands) and of their native elongated shape, previously observed under similar technical conditions, these stick-shaped and chondroitinase ABC-sensitive proteoglycans exhibited a typical pattern with several dense longitudinal parallel tracks (periodicity: 3-4 nm) not described as yet. Readily observable without high iron diamine-staining, the morphology of these cetylpyridinium chloride-precipitated and collagen-associated polyanions was particularly enhanced after incubation in the diamine solution which ascertained their sulphate content. Such a common ultrastructural organization with parallel tracks for both intracellular (i.e., in eosinophilic polymorphonuclear cells and Kurloff cells) and extracellular CPC-precipitated sulphated proteoglycans could correspond to intrinsic properties of the complexed molecules and could be related to 'double track' proteoglycans observed under other technical conditions in basement membranes.

Animals↗

Ultrastructural study of Cryptococcus neoformans by quick-freezing and deep-etching method.

The three-dimensional ultrastructure of Cryptococcus neoformans was studied by quick-freezing and deep-etching (QF-DE) method. C. neoformans, strain CDC551, was cultured on agar. The viable yeast cells (10(7) cells) were inoculated into each mouse from the tail vein. Three weeks after the inoculation, the brains of the mice were perfused with fixatives, quickly frozen, freeze-fractured, deeply etched and rotary shadowed with platinum and carbon. In addition, the viable cells of C. neoformans on agar were picked up and quickly frozen, and replica membranes were prepared as described above. The ultrastructure of C. neoformans was three-dimensionally demonstrated by the QF-DE method. The capsule was composed of fine meshworks of microfibrils (10-13 nm in diameter), which were directly attached to the cell walls. The capsule of the in vivo yeasts (yeast cells in the brain lesion) was thicker than that of the in vitro yeasts (yeast cells on agar culture). At the outer part of the cell wall, a particle-accumulating layer was observed. This layer in vivo was thicker than that in vitro. Occasionally, the yeast cells were ingested by phagocytes in the mouse brain. Although the cytoplasm of such yeast cells was destroyed, the capsular meshworks were well preserved. The ultrastructure of the capsule was the same both in cultured and phagocytized yeasts in the cystic lesions of the brains. This lack of morphological changes of the capsular meshworks suggests that they are resistant to the digestion by phagocytes. This stability of capsular structures may provide one of the important pathogenic factors in cystic lesions by C. neoformans.

Animals↗

The ultrastructure and synaptic architecture of phrenic motor neurons in the spinal cord of the adult rat.

Although light microscopic studies have analysed phrenic motor neurons in several different species, there has never been an ultrastructural investigation of identified phrenic motor neurons. In addition, electrophysiological studies have raised questions relating to the function of phrenic motor neurons which may be answered only by direct electron microscopic investigation. Thus, the present study was carried out to provide a detailed ultrastructural analysis of identified phrenic motor neurons. Phrenic motor neurons in the spinal cord of the rat were labelled by retrogradely transported horseradish peroxidase (HRP) after transecting the phrenic nerve in the neck and applying the enzyme directly to the central stump of the transected nerve. The results showed that the general ultrastructural characteristics of phrenic motor neurons were similar to those previously reported for other spinal motor neurons. However, phrenic primary dendrites appeared to be isolated from all other dendritic profiles in the neuropil. Primary dendrites were not fasciculated. Fasciculation occurred only among the more distal secondary and tertiary phrenic dendritic branches. Direct dendrodendritic or dendrosomatic apposition was rarely seen; gap junctions between directly apposing phrenic neuronal membranes were not observed. The membranes of adjacent phrenic neuronal profiles were most frequently separated by intervening sheaths of astroglial processes. Myelinated phrenic axons and a phrenic axon collateral were identified. The initial portion of the phrenic axon collateral was cone-shaped, lacked myelin, and thus resembled a miniature axon hillock. In one instance, a large accumulation of polyribosomes was observed within the hillock-like structure of a phrenic axon collateral. Eight morphological types of synaptic boutons, M, P, NFs, S, NFf, F, G and C were classified according to criteria used by previous investigators. Most of these endings (M, NFs, NFf, S and F) made synaptic contact with profiles of labelled phrenic somata and dendrites. F, NFf, and S boutons also terminated on phrenic axon hillocks. C and G boutons contacted exclusively phrenic somata and small calibre dendrites, respectively. P boutons established axo-axonic synaptic contacts with the M and NFs bouton. The morphological findings of the present study provide new data that may be related to phrenic synchronized output and presynaptic inhibition of primary afferents terminating on phrenic motor neurons.

Animals↗

Ultrastructure of neurons of the sensorimotor cortex in progeny of rats receiving alcohol during pregnancy.

We have studied the dynamics of ultrastructural changes in the neurons of the sensorimotor cortex on days 21, 30, and 60 of life in offspring of rats given 20% alcohol (2 g/kg) during pregnancy. Moderate antenatal alcoholization leads to certain disturbances in the ultrastructure of the cortical neurons and their dendrites. This is manifested as the presence of signs of retardation in the maturation of nervous cell populations as dystrophic changes in the neurons and their dendrites, and as display of the repair character with their own dynamics in the postnatal period of ontogenesis. The first two categories of the ultrastructural changes in the cortical neurons become more manifest at early stages of postnatal development of the offspring, and the repair processes at the age of two months. Despite the presence of the repair shifts, the dystrophic changes in the neurons of a hypoxic nature are present up to the period of sexual maturation. This shows that the antenatal alcoholic intoxication in the offspring is manifested in postnatal ontogenesis for a long period.

Animals↗

Ultrastructural and immunohistochemical analysis of axonal regrowth and myelination in membranes which form over lesion sites in the rat visual system.

Glial-connective tissue membranes which form bridges over lesion cavities in the brachial and pretectal region of the rat visual system contain regenerated myelinated and unmyelinated axons. The lesions were made between 10 and 16 days postnatal--a time at which neonatal regeneration would not be expected. A detailed ultrastructural study of these membrane bridges has been undertaken in order to describe the cellular and extracellular conditions that are associated with the regeneration, myelination and continued survival of identified retinal and other axons. The lesion-induced membrane bridges possessed a limiting surface of fibroblasts and were composed of glial cells, macrophages, endothelial cells, pericytes and collagen. There was some variability in the ultrastructural appearance of the glial cells; the majority of criteria indicate that they were astrocytes. These astrocytes formed 'glia limitans'-like surfaces beneath the fibroblasts. They contained numerous filaments and extended fine, electron-dense cytoplasmic processes, often arranged into lamellated stacks. Basal lamina was present on the outer surfaces of the astrocytes. Astrocytic processes isolated clusters of myelinated and unmyelinated axons in lacunae which may have served as conduits for axonal elongation. This suggests a role for these astrocytes in the regeneration and maintenance process which appears to recapitulate events which occur during normal development. Interestingly, regrowing retinal axons were never found adjacent to astrocytic surfaces possessing a basal lamina. We did not detect evidence of Schwann cell invasion into the lesion. By ultrastructural criteria the myelin ensheathment which occurred on the larger axons in the membrane bridge was of central rather than peripheral type. The cytoplasmic domain external to the sheath was limited to a small tongue; no basal lamina invested the fibre; and the periodicity of the myelin was equivalent to that of other CNS structures. Similarly, the CNS character of the myelin was demonstrated by intense immunostaining of myelin sheaths for myelin basic protein and proteolipid [corrected] protein and lack of staining for the PNS component PO. The oligodendrocytes responsible for this myelination may either have extended cytoplasmic processes from the adjacent neuropil, or may have differentiated from precursor cells within the membrane bridge.

Animals↗

Ultrastructure of the macaque ciliary ganglion.

The primate ciliary ganglion is an obligatory relay in the pathways that control the lens and pupil for the near response and the light reflex, two functions which have been the target of increasing inquiry in behavioural physiology paradigms. This investigation provides a comprehensive description of the ultrastructure of the ciliary ganglion in the rhesus monkey (Macaca mulatta). The results indicate that the ciliary ganglion contains a heterogeneous population of neurons in terms of somatic size, cytoplasmic contents and somatodendritic distribution of terminals. Variations in the clear and dense-cored vesicle content of the synaptic profiles present in the ganglion suggest that the synaptic inputs are also heterogeneous and may mediate separate functions. Several characteristic ultrastructural features of the macaque ciliary ganglion are noteworthy. Despite the large size of the neuronal somata, most cells do not exhibit contacts directly onto the somatic membrane. However, the few somata that do receive direct input often display several axosomatic contacts. The vast majority of synaptic interactions occur in the perisomatic neuropil, where the postsynaptic elements consist of simple and complex somatic appendages, as well as dendrites with their appendages. There is little neuropil independent of these immediately perisomatic regions. In some cases, axonal terminals form the central element of complex glomeruli, in which they are presynaptic to numerous spine-like profiles. In other cases, axon terminals and their postsynaptic targets are found within shallow depressions in the somatic membrane or, occasionally, deeply embedded within the borders of the postganglionic neuron. The somata and all the non-myelinated neuronal elements are surrounded by interdigitating, electron-dense processes of satellite cells. These glial cells are sometimes found in shallow recesses, or deeply embedded within the borders of the neuronal somata. The complexity of the ultrastructure of the ciliary ganglion in the macaque suggests that this ganglion may not be a simple relay in the parasympathetic outflow to the eye, but may instead be the site of neuronal processing of the preganglionic input.

Animals↗