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Biomedical subjects

S S Tay

Publications and source records attributed to S S Tay.

At least 37 records · Page 2Linked to original sources

Motoneuronal death without expression of NADPH-diaphorase activity after sciatic nerve cut in 5-day-old mice.

In BALB/c mice, the number of sciatic motoneurons lost was statistically insignificant whether the nerve was cut at one (P1) or five days (P5) of age. Although the motoneurons showed intense NADPH-d staining after sciatic nerve cut at P1, they were NADPH-d negative when the nerve was cut at P5. The present study casts doubt on a neurodestructive role of NO in the sciatic motoneurons after axotomy at P1.

Age Factors↗

Macrophage and microglial cell response after common peroneal nerve cut and crush in C57BL/6J mice.

The present study using Mac-1 immunohistochemistry for the detection of macrophages and microglial cells, has investigated the signals for macrophage recruitment in the peripheral nerve fibres and dorsal root ganglia, and microglial cell activation in the dorsal and ventral horns of the spinal cord, at different periods after a right common peroneal (CP) nerve cut or crush in 86 C57BL/6J mice. Though a previous study has demonstrated a delayed regeneration of the peripheral sensory but not the motor fibres in this strain of mice, the present study could not demonstrate a corresponding delay in macrophage recruitment in the L4-L6 dorsal root ganglia and microglial cell activation in the dorsal and ventral horns of the corresponding segments of the spinal cord. In fact, macrophage recruitment and microglial cell activation appeared a short time after the nerve lesion and peaked at 5 days post-operation then subsequently declined. Microglial cells, however, became reactivated at 20-30 days after CP nerve cut, perhaps because of the presence of newly degenerated fibres. In contrast to the above observation, there was no exuberant macrophage recruitment or microglial cell reaction during the period when the majority of the regenerated fibres were detected in the distal segment of the crushed nerve.

Animals↗

Localization of insulin-like immunoreactive neurons in the rat gracile nucleus.

An insulin-like immunoreactivity (ILIR) was localized in the neuronal somata, dendrites and myelinated axons in the gracile nucleus of the male Wistar rat. In the neuronal somata, the reaction product was dispersed in the cell nucleus and cytoplasm. In the cell nucleus, the reaction product was scattered throughout the nucleoplasm, but not within the nucleolus. In the cytoplasm, the reaction product was evenly distributed, mainly in the vicinity of the cisternae of the rough endoplasmic reticulum. In labelled dendrites, the reaction product was closely associated with the parallel arrays of neurotubules and postsynaptic densities. Most of these labelled dendrites were postsynaptic to unlabelled axon terminals. A labelled dendrite often formed the central element of a synaptic glomerulus with several unlabelled axon terminals. Numerous labelled myelinated axons were also present in the neuropil. However, axon terminals appeared to be unlabelled. It is hypothesized that insulin-like substance(s) may be modulating nuclear activities as well as neurotransmission at the synapse in the gracile nucleus.

Animals↗

Localization of NADPH-diaphorase activity in the pancreatic ganglia of the young chick.

NADPH-diaphorase activity was localized in pancreatic ganglia of the young chick. At 1 day posthatching, 60% of the neurons in the pancreatic ganglia were NADPH-diaphorase positive. In each neuron, the NADPH-diaphorase labelling was localized mainly in the cytoplasm of the cell body and its proximal processes, but not in the cell nucleus. There was a gradation in the labelling for the enzyme, with some neurons being heavily labelled while others were lightly to moderately labelled. At 7 days post-hatching, 100% of the pancreatic neurons showed NADPH-diaphorase activity and the average size of the NADPH-diaphorase positive neurons had also increased. By 14 days post-hatching, all the neurons present were heavily labelled for NADPH-diaphorase activity. Some of the labelled nerve processes traversed long distances and finally terminated on other ganglia as well as on the exocrine acinar or endocrine cells. It is concluded that this increase in NADPH-diaphorase/NOS activity in the pancreatic neurons is possibly correlated to the increase in modulation of neurotransmission in the young chick.

Age Factors↗

Localization of age-related changes in NADPH-diaphorase activity in pancreatic neurons.

The distribution of NADPH-diaphorase activity in the pancreatic neurons of neonatal, adult and aging rats was investigated using histochemistry. In the neonates, only 40% of the neuronal population showed NADPH-diaphorase labelling, and there was variation in the intensity of labelling ranging from light to heavy staining. In the young and mature adults, 95% of the neurons were labelled for NADPH-diaphorase activity, with most of the neurons being heavily labelled for the enzyme in the older animals. Immediately after birth, the pancreatic neurons found were small clusters of smaller sized cells compared with those observed in the mature adults. Their number reached the adult level by the third month after birth; this was maintained throughout the mature adult phase and subsequently decreased in the aging rats.

Aging↗

Ultrastructural changes in the hypothalamic paraventricular nucleus of the streptozotocin-induced diabetic rat.

This study describes the ultrastructural and morphometric changes in the hypothalamic paraventricular nucleus (PVN) of the streptozotocin-induced diabetic rat. During the acute phase (3 days after induction of diabetes), dendrites were swollen and appeared to have a watery cytoplasm. The affected dendrites were postsynaptic to seemingly normal axon terminals. During the intermediate phase (1-9 months after induction of diabetes), the neuronal somata contained numerous vacuoles of various sizes which were probably formed from dilated rough endoplasmic reticulum. Several unidentifiable vacuolated profiles were also seen in the neuropil. During the late phase (12 months after induction of diabetes) electron-dense dendrites and axon terminals were readily encountered in the neuropil. Most of the electron-dense dendrites were postsynaptic to normal as well as electron-dense axon terminals. Some of the electron-dense axon terminals formed axosomatic synapses with seemingly normal somata. Perivascular glial cells in the neuropil were in the process of phagocytosis. At 1-12 months of diabetes, the sizes of the somata and nuclei of PVN neurons were significantly increased in comparison with age-matched control rats.

Age Factors↗

Short- and long-term effects of streptozotocin-induced diabetes on the dorsal motor nucleus of the vagus nerve in the rat.

The present study describes ultrastructural changes in the dorsal motor nucleus of the vagus nerve of male Wistar rats after induction of diabetes by streptozotocin. 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 containing short segments of dilated rough endoplasmic reticulum, swollen mitochondria and scattered ribosomes, while degenerating axon terminals were characterized by an electron-defense cytoplasm, clustering of small spherical agranular vesicles and swollen mitochondria. Some of these degenerating axon terminals formed axodendritic synapses with seemingly normal as well as degenerating dendrites. During the mid phase (1-6 months), most of the degenerating neuronal profiles had been engulfed or removed by macrophages that infiltrated the neuropil. During the late phase (9-12 months), a second wave of degeneration occurred in the dorsal motor nucleus of the vagus nerve, similar to that of the acute phase. In addition to the degenerating dendrites and axon terminals, several neuronal cell bodies with electron-dense cytoplasm were observed. Numerous macrophages containing degenerating debris were also present in the neuropil. It is concluded that the ultrastructural changes in the dorsal motor nucleus of the vagus nerve are the result of streptozotocin-induced diabetes.

Animals↗

NADPH-diaphorase is colocalized with nitric oxide synthase and vasoactive intestinal polypeptide in rat pancreatic neurons in culture.

NADPH-diaphorase activity together with nitric oxide synthase- and vasoactive intestinal polypeptide-immunoreactivities were examined in the neurons of the rat pancreas in culture. Nitric oxide synthase (NOS)- and vasoactive intestinal polypeptide (VIP)-immunoreactivities were localized in a subpopulation of neurons which were also NADPH-diaphorase positive. All neurons expressing colocalized activities for NOS/VIP and NADPH-diaphorase were solitary cells in culture. Each of these double-labelled neurons was characterized by a round or oval cell body, with short and long processes emanating from it. Some of these processes traversed several micrometres before terminating on the exocrine acinar and endocrine cells. The present study provides evidence that nitric oxide may act as a regulatory agent in the inhibitory neural control of the secretory functions in the pancreas, thereby maintaining the milieu interieur of the organism.

Amino Acid Oxidoreductases↗

Arginine vasopressin- and oxytocin-like immunoreactive neurons in the hypothalamic paraventricular and supraoptic nuclei of streptozotocin-induced diabetic rats.

This study describes ultrastructural and morphometric changes in the arginine vasopressin (AVP)-like immunoreactive and oxytocin (OT)-like immunoreactive neurons in the hypothalamic paraventricular nuclei (PVN) and supraoptic nuclei (SON) of streptozotocin-induced diabetic rats at 1-12 months post-diabetes. At 1-6 months post diabetes, both AVP-immunoreactive and OT-immunoreactive neuronal somata were hypertrophied in the PVN and SON. These neuronal somata contained highly dilated rough endoplasmic reticulum in the cytoplasm. The reaction product for AVP as well as OT localization was dispersed throughout the cytoplasm and cell nucleus, but not within the nucleolus. Moreover, the reaction product appeared to be studded onto the ribosomes on dilated cisterns of the endoplasmic reticulum. At 9-12 months post-diabetes, both AVP-immunoreactive and OT-immunoreactive dendrites contained dilated endoplasmic reticulum, autophagic vacuoles, lipid bodies, microtubules, membranous bodies and occasionally swollen mitochondria. Labelled hypertrophied axonal profiles containing neurosecretory granules, autophagic vacuoles, membranous bodies and tubulovesicular elements were also observed in the neuropil. Morphometric study showed that both AVP-immunoreactive and OT-immunoreactive neuronal somata of the PVN and SON in the diabetic rats were markedly hypertrophied at all the time intervals examined. It is concluded that the morphometric changes observed represent hyperactivity of both AVP- and OT-immunoreactive neurons, while the concurrent ultrastructural changes observed at later stages may be indicative of degeneration.

Animals↗

Colocalisation of NADPH-diaphorase with nitric oxide synthase and vasoactive intestinal polypeptide in newborn pancreatic neurons.

Numerous NADPH-diaphorase positive neurons were localised in the pancreatic ganglia cultured from newborn guinea pigs. Most of these ganglia were found in the head region of the pancreas. A majority of the labelled neurons occurred in groups, although solitary neurons were also present. NADPH-diaphorase labelling was localised mainly in the cell cytoplasm and its processes, but not within the nucleus. There were more nitric oxide synthase (NOS)-immunoreactive neurons in culture as compared with those positive for NADPH-diaphorase. NADPH-diaphorase activity has been colocalised with NOS and vasoactive intestinal polypeptide (VIP) in a subset of neurons in culture. Colocalisation of NADPH-diaphorase with NOS and VIP in cultured neurons was not restricted to the cell body but also to the proximal and distal processes. Some of these labelled processes made contacts with exocrine acinar and endocrine cells. It is concluded that neuronal nitric oxide (NO) may be influencing the secretory roles of the pancreas, thereby participating in homeostasis.

Amino Acid Oxidoreductases↗

Localization of NADPH-diaphorase positive neurons in the pancreas of the mouse, rat, chick, kitten and monkey.

In the present study, nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH-d) histochemistry has been used as a marker for nitric oxide synthase. NADPH-d positive neuronal cell bodies and fibres have been localized in the pancreas of the mouse, rat, chick, kitten and monkey. In all these species, most of the NADPH-d labelled neuronal cell bodies in the ganglia were found in the interlobular and interacinar connective tissue while some were intimately associated with pancreatic ducts and blood vessels. There was, however, a gradation of innervation amongst the species. Only in the pancreatic islets of the mouse and monkey were NADPH-d positive neuronal cell bodies and nerve fibres detected in the formation of neuro-insular complexes. Besides labelling of neuronal cell bodies, nerve fibres and endothelial cells, the islet cells of the mouse, kitten and chick pancreas also gave a light positive reaction for NADPH-d activity. The nerve fibre and the outer core of the connective tissue of the Pacinian corpuscles in the kitten pancreas were also labelled for NADPH-d activity. It is concluded that nitric oxide may play an important role in the neural regulation of both exocrine and endocrine secretion and in controlling the activity of the blood vessels and ducts of the pancreas.

Amino Acid Oxidoreductases↗

Localization of insulin-like immunoreactive neurons in the hypothalamic paraventricular and supraoptic nuclei of streptozotocin-induced diabetic rats.

Insulin-like immunoreactive (ILIR) neurons were localized in the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON) of normal as well as streptozotocin-induced diabetic rats at different time intervals ranging from 1 to 12 months post-diabetes. Insulin-like immunoreactivity was localized in the cytoplasm and nucleoplasm of the neuronal somata in the PVN and SON of control rats but the nucleolus appeared unlabelled. In the neuropil of PVN and SON, the reaction product was mainly localized in the dendrites and axonal profiles. The overall intensity of labelling was light and diffuse. In streptozotocin-induced diabetic rats, also the PVN and SON contained ILIR neuronal somata, dendrites and axonal profiles. However, these ILIR neuronal profiles displayed abnormality at all the time intervals studied. At 1-6 months post-diabetes, the ILIR somata and dendrites appeared to be hypertrophied and they contained dilated endoplasmic reticulum. Both ILIR myelinated as well as non-myelinated axons were also present in the neuropil. Numerous unlabelled axon terminals showing swollen agranular as well as dense-cored spherical vesicles were also present in the neuropil and they were presynaptic to labelled dendrites. At 9-12 months post-diabetes, some of the ILIR neuronal profiles appeared to be degenerating. The ILIR somata showed distended rER, membranous bodies and autophagic vacuoles. Highly vacuolated ILIR dendritic processes were also present in the neuropil. It is hypothesized that streptozotocin-induced diabetes produced a state of hypoinsulinemia or hyperglycemia which in turn sensitized the PVN and SON resulting in hyperactivity of the ILIR neurons and the prolonged stimulus could have possibly produced the neuronal degeneration seen at later survival periods.

Animals↗

Ultrastructural changes in the hypothalamic supraoptic nucleus of the streptozotocin-induced diabetic rat.

Ultrastructural and morphometric studies were undertaken on the hypothalamic supraoptic nucleus of streptozotocin-induced diabetic rats over a period of 1 y. At 3 d, a few dendrites showing electron-dense cytoplasm and dilated rER were dispersed in the neuropil among seemingly normal neuronal somata. At 1-6 months, the somata contained numerous vacuoles of various sizes which probably originated from fragmented and dilated rER. Numerous unidentifiable vacuolated and electron-dense neuronal profiles were also seen in the neuropil. At 9-12 months, the number of degenerating electron-dense axon terminals and dendrites was markedly increased in diabetic rats. Glial cells containing electron-dense debris in their cytoplasm were involved in phagocytosis. At all time intervals studied, the mean cross-sectional cell area and mean cross-sectional nuclear area of supraoptic nuclei neurons of diabetic rats were significantly increased in comparison with age-matched controls injected with normal saline. The causative factors for these changes are not clear. However, it is suggested that the osmotic stress caused by chronic dehydration in the diabetic animals may be partly or wholly responsible for these ultrastructural changes.

Animals↗

Ultrastructure of the cuneate nucleus in the streptozotocin-induced diabetic rat.

This study describes the ultrastructural changes in the cuneate nucleus of the streptozotocin-induced diabetic rats at 3, 6, 9, and 12 months post-induction. At 3 and 6 months, post-diabetes, a marked atrophy was observed in the myelinated axons. The atrophic axons showed delamination of myelin sheath, tightly arranged lamellar whorls, vesicular elements and degenerating debris within the electron-lucent axoplasm. At 9 and 12 months post-diabetes, a variety of dystrophic and degenerating axonal profiles and dendrites were seen in neuropil. The dystrophic axonal profiles containing tubulovesicular elements, slit-like clefts, vacuoles, swollen mitochondria, membranous and multigranular bodies appeared to be hypertrophied. The degenerating axon terminals contained swollen mitochondria and clustered spherical agranular vesicles in their electron-dense granular axoplasm. The degenerating dendrites were identified by the presence of swollen mitochondria, dilated ER in the electron-dense cytoplasm and they often formed the synaptic glomeruli with central axon terminals. Macrophages containing lipid bodies and electron-dense elements in their cytoplasm were in the process of phagocytosis. In all the time intervals studied, the somata appeared to be normal and the number of dystrophic and degenerating axonal profiles in the cuneate nucleus of diabetic rats was significantly increased in comparison with age-matched saline injected control rats.

Animals↗

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-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↗