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S S Tay

Publications and source records attributed to S S Tay.

49 records · Page 3Linked to original sources

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↗

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.

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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.

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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 in the gracile nucleus of alloxan-induced diabetic rats.

The present study reports ultrastructural changes in the gracile nucleus of male Wistar rats after alloxan-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 randomized ribosomes. Degenerating axon terminals were characterized by an electron-dense cytoplasm and clustering of small spherical agranular vesicles. Degenerating axon terminals may form the central element or part of a synaptic glomerulus. Macrophages were present in the neuropil and 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.

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Effects of bilateral vagotomy on the ultrastructure of the cardiac ganglia in the monkey (Macaca fascicularis).

This study describes the effects of bilateral vagotomy on the ultrastructure of the cardiac ganglia of the monkey (Macaca fascicularis). One to three days after bilateral vagotomy there is widespread glycogen accumulation in the cytoplasm of the principal cardiac neurons. This is associated with distension of the granular endoplasmic reticulum and the loss of ribosomes from the cisternae. Between five and ten days after operation, about 10% of the neuronal profiles show an overall increase in electron density and intense darkening of the dendrites. From twenty one to twenty eight days postoperatively, the majority of the neuronal profiles have pale cytoplasm with reduction in granular endoplasmic reticulum and polyribosomes. The plasma membrane of the neuron is ruffled over the major portion of its surface. The satellite cells, which are reactive throughout the course of the experiments, exhibit a phagocytic capacity at this stage by removing portions of the neuronal cytoplasm. Vacuolation of the neuronal cytoplasm to a variable degree occurs in a small number of profiles between five to twenty eight days. The results suggest that bilateral vagotomy causes a widespread disturbance in the metabolic activity of the cardiac neurons. This is followed by transneuronal degenerative changes that are of a prolonged nature.

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Transneuronal degeneration in the heart and gastro-oesophageal junction in the monkey (Macaca fascicularis) following unilateral vagotomy.

This study describes, at the ultrastructural level, the transneuronal degeneration that occurs in the atrial and gastro-oesophageal ganglia of the monkey following unilateral vagotomy. One day after unilateral vagotomy, some postganglionic neurons showed an overall increase in electron density, with the dendrites darkening first. Three days after the operation, the dendrites appeared jet black and their intracytoplasmic organelles were hardly distinguishable except for some pale mitochondria. The perikarya of the affected neurons showed a slight increase in electron density. Five and seven days after the operation, satellite cells and macrophages with engulfed dendritic processes were commonly observed. The majority of the postganglionic neurons appeared normal, except for the presence of numerous macrophages in their vicinities. The results of the study suggest that transneuronal degeneration occurs very rapidly in the heart and gastro-oesophageal junction of the monkey, Macaca fascicularis, and that most of the affected neurons have recovered one week after the operation.

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An ultrastructural study of the effects of right cervical sympathectomy on the sinuatrial and atrioventricular nodes in the heart of the monkey (Macaca fascicularis).

This study describes the ultrastructural changes in the sinuatrial and atrioventricular nodes of the heart of the monkey (Macaca fascicularis) after right cervical sympathectomy. Obvious changes in the nodal cells were seen one day after operation. Numerous glycogen particles grouped together to form electron-dense patches containing vacuoles in the cytoplasm. At three days after operation, intracellular organelles exhibited fragmentation and dissolution. By five and seven days after operation, the affected cells were vacuolated and some were swollen and appeared to have degenerated. Simultaneously, there was massive infiltration of macrophages were present nodal tissues. Axon profiles and terminals showing various degrees of degeneration were present in the vicinity of the nodal cells throughout the period of study. It is concluded that right cervical sympathectomy resulted in a rapid degeneration in some of the cells in the sinuatrial and atrioventricular nodes.

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An ultrastructural study of the neuronal changes in the cardiac ganglia of the monkey (Macaca fascicularis) following unilateral vagotomy.

This study describes at the ultrastructural level the neuronal changes in the intracardiac ganglia of the monkey (Macaca fascicularis) following unilateral vagotomy. One day after unilateral vagotomy, some intracardiac neurons showed an overall increase in electron density, with the dendrites darkening first. At three days after operation the dendrites appeared jet black and their intracytoplasmic organelles were hardly distinguishable except for some pale mitochondria. The perikarya of the affected neurons showed a slight increase in electron density. By five and seven days after operation, satellite cells and macrophages with engulfed dendritic processes and degenerated axons were commonly observed. The majority of the intracardiac neurons appeared normal, except for the presence of numerous macrophage (containing several phagosomes) in their vicinities. It is suggested that transneuronal degeneration occurred very rapidly in the heart of the primate, Macaca fascicularis, and that most of the affected neurons appeared to have 'recovered' one week after unilateral vagotomy.

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An ultrastructural study of the non-neuronal cells in the cardiac ganglia of the monkey (Macaca fascicularis) following unilateral vagotomy.

Non-neuronal cells in the intracardiac ganglia of the monkey (Macaca fascicularis) showed rapid responses to neuronal damage following unilateral vagotomy. Most of the satellite cells appeared normal at one day after operation. However, from three to seven days after operation they were transformed into phagocytic cells, thereby engulfing the transneuronally affected dendrites of the neurons. By seven days after operation, most of the affected dendrites from the neuronal soma were engulfed by the satellite cells. Few macrophages were seen amongst the neurons of the intracardiac ganglia at one day. In monkeys at three to seven days after operation there was a massive infiltration of macrophages into the vicinity of the affected neurons. Several of these macrophages were filled with numerous phagosomes containing partially digested debris. Macrophages also accumulated perivascularly and some intravascular monocytes lay in conformations suggesting that they were undergoing diapedesis. Therefore, perivascular macrophages are probably derived from the circulating monocytes, though the possibility of them being transformed fibroblasts should not be excluded. Schwann cells appeared to be the main scavengers in removing the degenerating myelinated and unmyelinated axons in the intracardiac ganglia after unilateral vagotomy.

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Preganglionic neurons projecting to the first thoracic sympathetic ganglion in the terrapin (Trionyx sinensis).

After injection of HRP into the first right thoracic sympathetic ganglion of the terrapin, labeled cells are found in the central autonomic area, intercalated area, intermediolateral cell column, dorsal horn, ventrolateral edge of the dorsal column, dorsolateral edge of the ventral white column, and the ventral and ventromedial border of the ventral horn. They form one discontinuous column in the portion of the spinal cord marking the attachments of the tenth or eleventh to the fourteenth spinal nerves. The preganglionic neurons consist of small (8-9 micron), medium-sized (10-16 micron) and large (18-20 micron) cells. The number of labeled neurons in individual animals varies between 154 and 541. They are found ipsilateral to the injected ganglia in all animals. In a few cases 1-2 labeled neurons are contralateral. The results are compared with previous work in birds and mammals.

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Neurotensin immunoreactivity in the central nucleus of the rat amygdala: an ultrastructural approach.

Neurotensin (NT) was demonstrated in the central nucleus of the rat amygdala (CNA) using a modification of the avidin-biotin complex immunohistochemical technique. Electron-dense reaction product (particles were 15-25 nm in diameter) was localized in perikarya, dendrites, axons, and axon terminals. It was found also associated with profiles of rough endoplasmic reticulum, mitochondria, microtubules, and small agranular as well as large granular vesicles. In distal dendrites, the reaction product was associated with microtubules, vesicles, and postsynaptic densities. Axon terminals of three types formed synaptic contracts with NT-immunoreactive neurons in the CNA: one was characterized by numerous round or oval agranular vesicles, the second by numerous pleomorphic vesicles, and the third by agranular vesicles that were loosely distributed and pleomorphic. All three types formed symmetric axosomatic and asymmetric axodendritic contacts. NT-immunoreactive axon terminals containing small round agranular vesicles stood out clearly from the intermingling profiles of immunonegative structures. We found numerous glomeruli, each consisting of a central NT-immunoreactive dendrite surrounded by all three types of axon terminals. We observed that some NT-immunoreactive terminals formed symmetric axoaxonal contacts with each other, providing evidence for the presence of local NT-to-NT circuits, whereas many others synapsed with axon terminals devoid of NT immunoreactivity.

Amygdala↗