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W C Wong

Publications and source records attributed to W C Wong.

At least 19 recordsLinked to original sources

Long-term effects of alloxan-induced diabetes on the nucleus ventralis posterolateralis in the thalamus of the rat.

The present paper describes the long-term ultrastructural changes in the nucleus ventralis posterolateralis of the thalamus of male Wistar rats after alloxan-induced diabetes. Degenerating dendrites were characterized by an electron-dense cytoplasm with scattered endoplasmic reticulum and ribosomes. Degenerating axon terminals were characterized by an electron-dense cytoplasm and clustering of small spherical agranular vesicles. Degenerating axon terminals formed axosomatic synapses with seemingly normal cell bodies and axodendritic synapses with normal as well as degenerating dendrites. Degenerating axons (both myelinated and unmyelinated) were readily encountered in the neuropil. Activated microglial and astrocytic cells in the neuropil were in the process of phagocytosis or had residua in their cytoplasm.

Animals

Insulin-like immunoreactivity in the monkey spinal cord.

Insulin-like immunoreactive neurons were localized in the cervical, thoracic, lumbar and sacral segments of the monkey spinal cord. Both dorsal and ventral horn cells were labelled. Insulin-like reaction product was localized in the cell nucleus and cytoplasm. Both inner and outer nuclear membranes were labelled. Reaction product appeared to be scattered throughout the nucleoplasm but not within the nucleolus. In the cytoplasm, labelling was mainly localized in the cisternae of rER and saccules of Golgi apparatus. Both proximal and distal dendrites were labelled, the reaction product was closely associated with the parallel arrays of neurotubules. Most of the distal dendrites were postsynaptic to non-labelled axon terminals; however, some were postsynaptic to lightly labelled axon terminals. A labelled dendrite often formed the central element of a synaptic glomerulus with several nonlabelled axon terminals. It is hypothesized that insulin-like substance(s) may be modulating nuclear activities as well as neurotransmission at the synapse.

Animals

Immunocytochemical localisation of substance P in vagal ganglion cells and pericellular arborisations in the monkey.

The quantitative cell count showed the presence of about 20,000 ganglion cells with associated satellite elements in the nodose ganglion in the monkey. Among these closely packed cells, at least one-third were substance P (SP) immunoreactive, ranging from faint or moderate to intense staining. Substance P immunoreactivity (SP-IR) was localised in the cell bodies and their long extending neurites. Ultrastructural study showed that SP-IR was not associated with any particular organelles or inclusions. A striking feature of the nodose ganglion was the occurrence of SP-positive pericellular arborisations associated with about 0.5% of the ganglion cells which were almost exclusively SP-negative. The pericellular arborisation displayed diverse morphological forms from a simple tortuous fibre to complex glomerular networks or plexuses encircling the soma of SP-negative ganglion cells. The varicose nerve fibres forming the pericellular arborisations appeared to terminate as 'boutons' contacting the soma of the ganglion cells. Electron microscopic study demonstrated the close spatial relation between the SP-IR profiles and the ganglion cell but there was no direct synaptic contact. In some instances, the SP-IR profiles containing agranular and dense-cored vesicles penetrated the cytoplasm of satellite cells, almost reaching the surface of the soma of the ganglion cell. The sources of origin of the nerve plexuses in the pericellular arborisation were either from the small and sparsely distributed jugular ganglion cells which were intensely SP-IR or from the intrinsic SP-IR nodose ganglion cells. The possibility that the efferent neurons in the dorsal motor nucleus of the vagus could also contribute to the pericellular arborisation was also considered. The function of the pericellular arborisations may be related to the modulation of the SP-deficient ganglion cells with which they associate through the release of SP and probably by way of the satellite cells.

Animals

The intraglandular submandibular ganglion of postnatal and adult rats. II. A morphometric and quantitative study.

A morphometric study was undertaken on the submandibular ganglion cells in rats of different ages. This showed a direct proportional increase with age in all the variables measured. Mean cross-sectional cell area showed the most dramatic growth, an increase of more than 5-fold between birth and young adulthood. Mean cell diameter and cell perimeter doubled over the same period. The growth of the nucleus, expressed as diameter, was slower when compared with that of the ganglion cells as a whole. The number of intraglandular ganglion cells remained relatively unchanged from birth to young adulthood, ranging from about 3000 to 5000 cells. They were mainly distributed at the hilar region of the submandibular salivary gland, contributing 1/2 to 2/3 of the total ganglion cell population. The second largest cell population was in the intralobular region, which made up about one-third of the population. The least populated region was in the connective tissue of the sublingual salivary gland, which contained only about 5-7% of the total cell number. Cell counts based on the fluorogold labelling method were generally lower than those made after haematoxylin and eosin staining. In the 2-d-old animals, counts of fluorogold-labelled cells were only about half the H & E counts. The discrepancy may be due to the thicker sections used in the fluorogold method, superimposition of cells leading to an underestimation of cell numbers. Nevertheless, the fluorogold labelling method provided rapid and reproducible results. Its main advantage is that the labelled ganglion cells emit a bright yellow fluorescence which is readily identified; the other is the simplicity of the procedure, as labelling of ganglion cells can be achieved by the intraperitoneal route.

Aging

Immunocytochemical localisation of substance P-like nerves in the cardiac ganglia of the monkey (Macaca fascicularis).

Substance P-like immunoreactive (SP-IR) nerves formed 2 types of relationships with nerve cells in the cardiac ganglia of the monkey (Macaca fascicularis). The first type consisted of varicose SP-IR nerve fibres that ramified throughout the cardiac ganglia, forming a loose network with several nerve cell bodies. The second type consisted of several nerve cell bodies enwrapped by a dense pericellular (basket-like) investment of varicose SP-IR nerve fibres. Numerous SP-IR nerve fibres formed perivascular networks around the walls of the blood vessels within the cardiac ganglia and the muscle. The cardiac muscle cells were also innervated either by an isolated single varicose SP-IR nerve fibre or by complex networks. At the ultrastructural level, the substance P reaction product appeared to be associated with the microtubules and the outer mitochondrial membranes of labelled axons. Substance P reaction product was also localised on the membranes of small agranular vesicles of the labelled axon terminals. The SP-IR axons and axon terminals were closely related to the nerve cell bodies and they occurred either singly or in small groups. Most of the axons were enwrapped by a sheath from the adjacent Schwann cells which often exhibited pseudopodia-like processes. None of the axon terminals was observed to make synaptic contact with the cell bodies. However, a few axoaxonal contacts involving SP-IR and non-SP-IR axon terminals were present, the significance of which is not understood. Several axon terminals lay close to blood vessels, and may modulate the activity of these vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Ultrastructural localization of insulin-like immunoreactivity in the rat spinal cord.

Insulin-like immunoreactive neurons were localized in the cervical, thoracic, lumbar and sacral segments of the rat spinal cord. Neurons from both the ventral and dorsal horns were labelled. The insulin-like reaction product was predominantly localized in the cell nucleus and the proximal and distal dendrites. In the labelled cell nucleus, the reaction product was scattered throughout the nucleoplasm and the inner and outer nuclear membranes but not within the nucleolus. In the labelled dendrites, the reaction product was closely associated with the parallel arrays of neurotubules. Most of the labelled distal dendrites were postsynaptic to non-labelled axon terminals. A labelled dendrite often formed the central element of a synaptic glomerulus with several non-labelled axon terminals. It is hypothesized that the insulin-like substance(s) may be modulating nuclear activities as well as neurotransmission at the synapse in the spinal cord.

Animals

Insulin-like immunoreactivity persists in the spinal cord of streptozotocin-induced diabetic rats.

In both saline-injected control and streptozotocin-induced diabetic rats, insulin-like immunoreactivity was localized in the cervical, thoracic, lumbar and sacral segments of the spinal cord. This insulin-like immunoreactivity was consistently localized in the neurons and dendrites from control rats as well as from diabetic rats ranging from 1 month to 12 months after diabetes induction. In the neuronal cell bodies, the reaction product was predominantly localized in the cell nucleus and the proximal and distal dendrites. In the labelled cell nucleus, the reaction product was scattered throughout the cell cytoplasm and nucleoplasm, but not within the nucleolus. The inner and outer nuclear membranes were also labelled. In labelled dendrites, the reaction product was closely associated with the parallel arrays of neurotubules, plasma membranes and synaptic densities. Most of the labelled distal dendrites were postsynaptic to unlabelled axon terminals. A labelled dendrite often formed the central element of a synaptic glomerulus with several unlabelled axon terminals. It is hereby hypothesized that some of the neurons in the spinal cord of the diabetic rat are capable of synthesizing insulin-like substance(s), which appears to be involved in neurotransmission and neuromodulation.

Animals

Ultrastructure of murine cardiac ganglia in experimental Chagas' disease.

Albino mice, infected with Trypanosoma cruzi (Tulahuen strain) were sacrificed on days 7, 9, 12, 14, 16, 18, 21, 32 and 39 following infection. Transmission electron microscopic examination of the cardiac ganglia revealed no ultrastructural change at day 7. At day 9 there was peri- and intraganglionic monocytic infiltration but parasites were absent. Between days 12 and 16 there was intense monocytic infiltration, with intra-ganglionic presence of parasites within fibroblasts, monocytes and macrophages. None were seen within capsular cells, endothelial cells, Schwann cells, satellite cells and ganglion cells. The Schwann cells and satellite cells, however, showed phagocytic activity. Satellite cells were also reactive with proliferative pseudopodia which encircled neuronal processes. By day 18, parasites were absent in the ganglia. But monocytes were still present up to day 39, some of them still engulfing satellite cell and neuronal processes. Satellite cells continued to be reactive and Schwann cells phagocytic. Ganglion cells remained normal throughout the experiment. The results suggest that infection of Schwann cells, satellite cells and ganglion cells may depend upon the tissue tropism of the strain of the parasite used and its concentration in the inoculum. The results are consistent with the view that any parasympathetic dysfunction in experimental Chaga's disease in the mouse may be of a transient nature.

Animals

The intraglandular submandibular ganglion of postnatal and adult rats. I. A light and electron microscope study.

The structure of the intraglandular submandibular ganglion is described in both postnatal and adult rats. The ganglion is localised mainly at the hilum where the majority of the cell bodies are observed. Ganglia are also present in the intralobular septa of both the submandibular and the sublingual glands. Often they are found along the main salivary ducts with the larger ganglia being encapsulated by connective tissue. On electron microscopy, the submandibular ganglion cells show the usual features of autonomic neurons. The cells contain a prominent round nucleus. Numerous short processes project from the soma together with a few long dendrites. The organelles are randomly distributed throughout the soma. Most of the synapses observed were on the short processes with occasional axosomatic synapses. Nonsynaptic desmosome-like contacts are a common feature among the ganglion cells. Especially noteworthy are contacts made by the dendrites which deeply invaginate the soma of an adjacent nerve cell. The ganglion cells of the postnatal and adult submandibular ganglia show minor differences. Ultrastructurally, the postnatal cells show signs of immaturity such as abundant free ribosomes, well developed Golgi complexes and disorganised rough endoplasmic reticulum. Mitotic satellite cells were observed associated with the postnatal ganglion cells. The study has confirmed that all the submandibular ganglion cells show a positive reaction for acetylcholinesterase. Enzyme activity is localised in the cisternae of rough endoplasmic reticulum, the Golgi complex, plasma membrane and nuclear envelope.

Acetylcholinesterase

Expression of major histocompatibility complex antigens and CR3 complement receptors in activated microglia following an injection of ricin into the sciatic nerve in rats.

The ventral horn motor neurons in the lower lumbar cord underwent rapid degeneration following an injection of Ricinus communis agglutinin-60 (RCA) into the sciatic nerve. The cell death which was most drastic between the fifth and seventh post-injection day elicited a significant increase in the number of microglia. The activated microglia were scattered throughout the neuropil but the dramatic feature was their close association with the somata of the degenerating neurons. Often several microglial cells were seen surrounding the soma of a degenerating neuron. Immunocytochemical study showed that both the interstitial as well as the perineuronal activated microglia were labelled with the monoclonal antibodies OX-18 and OX-42 for the detection of MHCI encoded antigen and type three complement receptors, respectively. Intense immunoreactivity was observed especially in the perineuronal microglia with OX-18. Electron microscopic study confirmed the identification of the activated microglia. Although the activated microglia closely apposed the neuronal soma, there was no sign of a direct endocytosis. The cytoplasm of the activated microglia, however, contained massive lipofuscin bodies in longer survival animals. Electron microscopic immunocytochemical study showed that the immunoreactivity of the activated microglia was localized along their plasma membrane facing the neuronal soma. Since the microglia cells on the contralateral side of the ventral horn were not marked by the antibodies used, it was postulated that the vigorous expression of MHCI antigen and CR3 receptors on the activated microglia was induced by the neuronal degeneration resulting from the application of the toxin ricin.

Animals

Gracile nucleus of streptozotocin-induced diabetic rats.

This study reports ultrastructural changes in the gracile nucleus of male Wistar rats after streptozotocin-induced diabetes. During the acute phase (3-7 days) degenerating electron-dense dendrites and axon terminals were dispersed in the neuropil. Degenerating dendrites were characterized by an electron-dense cytoplasm, swollen mitochondria, dilated endoplasmic reticulum and scattered ribosomes. Degenerating axon terminals were characterized by an electron-dense cytoplasm and clustering of small spherical agranular vesicles. Degenerating axon terminals may form part of a synaptic glomerulus with a central electron-dense dendrite, or they may form the central element of a synaptic glomerulus. These degenerating profiles were absent in the gracile nucleus of the 3 and 7 days insulin-treated post-streptozotocin rats. Macrophages were present in the neuropil and were in the process of engulfing neuronal elements. During the medium phase (1-6 months), most of the degenerating dendrites and axon terminals had been engulfed or removed by macrophages. During the late phase (9-12 months) a second wave of degeneration occurred in the gracile nucleus, similar to the acute phase. During the medium and late phases, dystrophic axonal profiles were also significantly increased in the rats after streptozotocin treatment. It is concluded that the ultrastructural changes observed in the gracile nucleus in the present study were the result of streptozotocin-induced diabetes rather than a toxic effect of streptozotocin, even in the acute phase.

Animals

The cardiac ganglia in streptozotocin-induced diabetic rats.

The ultrastructure of the cardiac ganglia of streptozotocin-induced diabetic rats was studied at survival times of 3 and 7 days, 1, 3, 6, 9 and 12 months. At 3-7 days post-induction, some intracardiac neurons showed an overall increase in electron density, with the dendrites darkening first. Some of the affected dendrites appeared jet black and their intracytoplasmic organelles were hardly distinguishable except for some swollen mitochondria. Both electron dense and lucent types of degenerating axon terminals were observed in the interstitial spaces. Several myelinated and unmyelinated axons also showed early signs of degeneration. At 1-6 months post-induction, numerous myelinated and unmyelinated axons were shown to be degenerated. The majority of the intracardiac neurons appeared to be normal. Numerous macrophages containing phagosomes were found in the interstitial spaces. At 9-12 months post-induction, macrophages containing engulfed debris were still commonly observed amongst the neuronal profiles, which appeared to be morphologically normal. It is concluded that degenerative changes occur in the cardiac ganglia of streptozotocin-induced diabetic rats and that these changes appear to be both progressive and prolonged.

Animals

Expression of major histocompatibility complex and leukocyte common antigens in amoeboid microglia in postnatal rats.

The expression of major histocompatibility complex (MHC) antigen and leukocyte common antigen (LCA) was observed in the amoeboid microglial cells in postnatal rat brain. Considerable MHC class I surface antigen was detected at the plasma membrane and its tubular invaginations in the amoeboid microglia in the corpus callosum using the monoclonal antibody OX-18. In early postnatal (2 and 5 day) rats, the OX-18 positive cells were mostly round but a few possessed stout processes. With increasing age (9 and 15 days) the OX-18 positive amoeboid microglia assumed an oval or elongated form. By the time of weaning (21 days) and in older animals, the immunoreactivity was extremely weak and was detectable only on some branched microglia bearing fine processes. The presence of MHC class Ia antigens with OX-3 and OX-6 was hardly detectable except for a few weakly stained cells in the corpus callosum and cavum septum pellucidum in early postnatal rats. The expression of LCA was observed in amoeboid microglial using the monoclonal antibody OX-1 and this followed a similar temporal pattern to that with OX-18. The additional phenotypic features of amoeboid microglial cells in the present study support their monocytic origin. These cells are endowed with MHC class I antigens which may serve as the restriction elements for T lymphocytes, at least in the early postnatal brain.

Animals

Ultrastructural changes in the gracile nucleus of the spontaneously diabetic BB rat.

The present study describes the structural changes in the gracile nucleus of the spontaneously diabetic BB rat. At 3-7 days post-diabetes, axons, axon terminals and dendrites showed electron-dense degeneration. Degenerating axons were characterized by swollen mitochondria, vacuolation, accumulation of glycogen granules, tubulovesicular elements, neurofilaments and dense lamellar bodies. Degenerating axon terminals consisted of an electron-dense cytoplasm containing swollen mitochondria, vacuoles and clustering of synaptic vesicles. These axon terminals made synaptic contacts with cell somata, dendrites and other axon terminals. Degenerating dendrites were postsynaptic to normal as well as degenerating axon terminals. At 1-3 months post-diabetes, degenerating electron-dense axons, axon terminals and dendrites were widely scattered in the neuropil. Macrophages containing degenerating electron-dense debris were also present. At 6 months post-diabetes, the freshly degenerating neuronal elements encountered were similar to those observed at 3-7 days. However, there were more degenerating profiles at 6 months post-diabetes compared to the earlier time intervals. Terminally degenerating axons were vacuolated and their axoplasm appeared amorphous. It is concluded that degenerative changes occur in the gracile nucleus of the spontaneously diabetic BB rat.

Animals

Ultrastructural changes of the nodose ganglion cells following an intraneural injection of Ricinus communis agglutinin-60 into the vagus nerve in hamsters.

Virtually all the ganglion cells in the nodose ganglion in hamsters underwent rapid degeneration following an intraneural injection of RCA-60 into the vagus nerve in the cervical region. The earliest signs of neuronal degeneration were evident in animals which survived 5 days after the ricin application. A remarkable feature was the appearance of a variable number of granular dense bodies measuring 1-4 microns in diameter in the cytoplasm. They were composed of closely stacked cisternae which were continuous at the periphery with those of the rough endoplasmic reticulum. Associated with the membranous cisternae were large accumulations of glycogen. With longer survival time, these glycogen-membrane complexes appeared to disintegrate. Numerous vacuoles and neurofilaments accumulated in their vicinity. Satellite cells were activated between the 7th and 10th postoperative days. These penetrated deeply into the degenerating neurons dividing them into numerous fragments by their extensive cytoplasmic prolongations. The cytoplasmic fragments of the RCA-poisoned neurons eventually became necrotic and disintegrated in the satellite cells, suggesting a rapid mode of neuronophagia. The biosynthesis of acetylcholinesterase was inhibited by the ricin injected as shown by the drastic reduction of the enzyme activity in the rough endoplasmic reticulum and nuclear envelope. Some isolated ganglion cells apparently survived the RCA injection as shown by their occurrence in long surviving animals (30-90 days). A few of them displayed an enhanced density of their cytoplasm and neurites. It is postulated that this was induced by the RCA released from the RCA-poisoned neurons.

Animals

Immunocytochemical localization of CR3 complement receptors with OX-42 in amoeboid microglia in postnatal rats.

The present study described the labelling of amoeboid microglial cells in the postnatal rat brain with OX-42, an antibody that recognizes type 3 complement receptors CR3 in mononuclear phagocytes. Of the diverse morphological forms of amoeboid microglia present in the corpus callosum in early postnatal (2-5 days) rats, cells with a round regular outline, or showing short stout processes, were the most intensely stained. When traced from the main cell colony into the borderline zone with the cortex, the immunoreactivity of amoeboid microglia that assumed a ramified form was drastically reduced. Examination of materials from the late postnatal (8-12 days) age group showed that the majority of the OX-42 positive cells in the corpus callosum became oval, elongated and ramified. Immunoelectron microscopy confirmed the above observations, and also showed that the immunoreactivity in the round amoeboid microglia was localized in their plasma membrane, surface projections and invaginations, as well as in some of the subsurface vacuoles. The immunoreactivity was reduced in the oval cells, and diminished in the elongated or ramified form. It is proposed that the presence of CR3 membrane receptors in amoeboid microglial cells is related to their active role in endocytosis. These, however, diminish with the growth of the brain.

Animals

Synaptic junctions between sympathetic axon terminals and pinealocytes in the monkey Macaca fascicularis.

The distribution of axon terminals in the pineal gland of monkeys was studied by electron microscopy. Numerous terminals bearing small pleomorphic agranular and dense-cored vesicles were localized in the perivascular space and among the pinealocytes in the parenchyma in normal monkeys. Following bilateral superior cervical ganglionectomy, they underwent degenerative changes, including the accumulation of glycogen masses, appearance of dense residual bodies and the displacement of synaptic vesicles. Some of these degenerating terminals showed synaptic contacts with the cell bodies of pinealocytes. At the synaptic junction the postsynaptic membrane was thickened asymmetrically. Examples of synaptic contacts were most frequently observed in 5 and 7 days postoperative animals. In the longer surviving (30 days) monkey, most of the axon terminals showed round agranular vesicles, and they were mainly presynaptic to the intrapineal ganglion cells with some of the pinealocytes. They remained structurally unchanged following the resection of both the superior cervical ganglia. A few axon terminals containing small dense-cored vesicles appeared to have survived the initial insult, but some of their vesicles appeared swollen 30 days after the operation. It is concluded from this study that some of the pinealocytes are under the influence by the postganglionic neurons in the superior cervical ganglia through direct synaptic contacts. The intrapineal ganglion cells are postsynaptic to fibres originating exclusively from the central nervous system. Some of these fibres, however, may be presynaptic directly to pinealocytes.

Animals

Degenerative changes of neurons in the superior cervical ganglion following an injection of Ricinus communis agglutinin-60 into the vagus nerve in hamsters.

The present study describes neuronal changes in the superior cervical ganglion of hamsters following injection of Ricinus communis agglutinin-60 (RCA-60) into the ipsilateral vagus nerve in the cervical region. There were no noticeable structural changes in the ganglion 1 day after injection. Between 3 and 15 days after injection, a small number of neurons located in the caudal part of the ganglion underwent degenerative changes including disappearance of rough endoplasmic reticulum and cytoplasmic vacuolation. The structural alterations were most acute 7 days after the injection when some neurons showed signs of total vacuolation and lysis. A second phase of neuronal change occurred after longer survival periods extending from 60 to 120 days after injection. The most striking feature of such neurons was darkening of their dendrites associated with abnormally high density cytoplasm that contained mitochondria with disrupted cristae. As distinct from the early phase in which cell necrosis was observed, there was no evidence of cell death of neurons bearing darkened dendrites. Since examples of exfoliation of the affected dendrites and their phagocytosis by satellite cells were extremely rare, it is postulated that these structural alterations are probably reversible but over an extended period. The significance of the two phases of degenerative change is discussed in connection with the acute and possible chronic effects of the toxic lectin. The present study also confirms the presence of postganglionic sympathetic axons in the cervical vagus nerve.

Animals