Ultrastructural changes in the chick thymus following unilateral vagotomy

The ultrastructure of the thymus in the chick (Gallus domesticus) was studied after unilateral vagotomy at survival times of 3, 7 and 10 days. Ultrastructural changes in the ipsilateral thymus were observed in axon boutons as well as in myoid and cystic cells in the medulla, especially those situated near the corticomedullary junction. Structural changes in axon boutons ranged from granular degeneration of the axonal cytoskeleton to vacuolation of the axoplasm. Myelin figures of different sizes and configurations and clumping of small agranular vesicles were commonly observed in the axon terminals. Degeneration of myoid cells appeared to peak at 7 days post‐vagotomy. Changes ranged from oedematous appearance and intense vacuolation of the peripheral cytoplasm to disorganisation and clumping of myofibrils. In some myoid cells the sarcomeres showed granular degeneration at the I‐bands and in others, the myofibrils were completely degenerated such that amorphous material and partially degenerated organelles filled the entire cell. The majority of cystic cells at 3 days post‐vagotomy showed a uniform increase in electron density. Numerous electron dense bodies, some displaying concentric lamellation, were observed throughout the expanse of the cytoplasm. At 7 days post‐vagotomy, the cytoplasm of some cells gave a “moth‐eaten” appearance. Dying cystic cells were encountered at 10 days after vagotomy. Degeneration in the myoid and cystic cells suggests that these cellular components may be the putative targets of the vagal fibres in the chick thymus. The changes in these cells reflect a disturbance in the cell metabolism presumably brought about by the removal of vagal influence. Anat Rec 255:261–270, 1999. © 1999 Wiley‐Liss, Inc.     

Bilateral enzymic changes in rat nodose ganglia following unilateral cervical vagotomy.

Aspects of the metabolism of the nodose ganglia of the rat and their relationship to chromatolysis induced by unilateral cervical vagotomy were examined. The development of chromatolysis in the vagotomized ganglion followed a typical pattern. The changes in nucleic acid metabolism were elucidated by measurement of the activity of the pyrimidine biosynthesis specific enzyme: glutamine dependent carbamoyl phosphate synthetase. The activity of this enzyme showed a biphasic response supporting the conclusion that the first rapid increase in the rate of synthesis of ribosomal RNA may be a result of increased activity of the de novo pyrimidine biosynthetic pathway; a biphasic response also occurred in the enzyme activity in the contralateral ganglion. Lysosomal activity during the response was investigated by measuring the activity of acid phosphatase. There was also a bilateral change in the acid phosphatase activities of the two ganglia. This was more marked in the vagotomized ganglion, but followed a biphasic time response.The bilateral nature of the response observed in enzyme activities may reflect the similarities in metabolic requirements of axon regrowth in the vagotomized ganglion and axon collateral growth in the contralateral ganglion.     

Ultrastructural changes in the dorsal motor nucleus of monkey following bilateral cervical vagotomy

Summary The neurons of the dorsal motor nucleas (DMN) of the monkey (Macaca fascicularis) were of two main types: small (13 × 8 m) and medium-sized (20 × 13 m). The latter, which were the predominant form, contained a pale oval nucleus surrounded by organelle-rich cytoplasm. Between one and three long principal dendrites per section profile arose from eac¹ of the somata. Both axosomatic and axodendritic synapses were seen on these cells although the latter were more common.No structural changes were noted in the DMN 1–3 days after bilateral cervical vagotomy. Some of the dendrites of the medium-sized axotomized vagal neurons appeared darkened 5–10 days after the operation. With longer surviving intervals, i.e. 21 and 28 days after operation, darkened dendrites were more commonly seen and the cytoplasmic density of these dendrites was dramatically enhanced. Their mitochondria were pale and some of them also showed vesiculation. Both normal and degenerating axon terminals were seen to form synaptic contacts with the darkened dendrites. The degenerating axon terminals were characterized by the clumping of their round agranular vesicles. Both darkened dendrites and degenerating axon terminals were phagocytosed by hypertrophied astrocytes and activated microglial cells. Blood elements infiltrating into the DMN were a possible source for some of the neural macrophages.It was concluded from the present study that the dendrites of the vagal neurons were the first structures to degenerate in axotomy and these were subsequently removed by glial elements. Degenerating axon terminals on the darkened dendrites could represent endings of the central processes of peripheral vagal ganglion cells that had undergonetransganglionic degeneration after damage to their peripheral processes.     

Ultrastructural changes of neuromuscular receptor organs in the masseter muscles following unilateral transection of the rat infraorbital nerve

Definite ultrastructural changes of the neuromuscular receptor organs were demonstrated in the young and adult rat masseter muscles either on the operated or unoperated side following the unilateral transection of the infraorbital nerve. The grade of the degeneration was intensive but quite similar in having no relation to the age of the rat when the operation was performed, while it increased drastically with time after the operation. On this base, it may be suggested that the sensory input coming from the various kinds of sensory receptors in the snout field do rather affect bilaterally the minor reflexive movements of the jaw. In other words, it can be said that the minor reflexive movements of the jaw might have been controlled by the sensory inputs coming from the snout sensory receptor organs. The definitely degenerated changes of the neuromuscular receptor organs in the masseter muscles should be regarded as disuse atrophy following the interception of the snout sensory input.     

Transneuronal changes in the myenteric ganglia of the monkey following vagotomy

This study describes the ultrastructural changes in the myenteric ganglia at the gastro-oesophageal junction of the monkey (Macaca fascicularis) after unilateral cervical vagotomy. Degenerating vagal fibres occurred within the ganglia and they represented only a small fraction of the endings present. The most striking finding at days 1-3 after vagotomy, was that some dendrites of myenteric neurons had a distinctly increased electron density which ranged from a moderate darkening of the cytoplasm to an almost complete blackening of the profile. This regressive change was widespread; however, apparently, it did not affect more than one dendrite in any neuron. Darkened dendrites were no longer found at 5-7 days after vagotomy, and they were not present in control ganglia. It is concluded that the degeneration of vagal endings is accompanied by transneuronal regressive changes that are very rapid in onset, are short lasting and possibly fully reversible, and affect only one dendrite of the neuron. It is suggested that the process observed represents a novel form of transneuronal influence.     

Patterns of gene expression in the developing chick thymus.

Gene expression in thymic T cells during late embryogenesis and early growth in chicks was examined using cDNA microarrays. Gene expression patterns were profiled into nine clusters by using self-organizing maps (SOM) clustering analysis. The expression patterns for a set of genes confirmed current information on the development of immune response. Expression of cell surface markers (MHC class I alpha chain, MHC class II associated invariant chain, CD8 beta chain, CD18, and beta2-microglobulin), and genes involved in the innate immune response (NK lysin-like) increased with age, and these patterns were consistent with an increase in the immune responsiveness of the young chick. The expression of cytokine receptor common gamma chain (gammac), death receptor-3 (DR3), and TCR alpha chain increased up to 1 day of age and then decreased. DR3 could play a role in the apoptosis during T-cell maturation, while the differential expression of TCR genes could reflect regulation of the rearrangement of TCR genes and TCR-mediated signal transduction during T cell development. Three genes coding for previously uncharacterized proteins are included in the clusters. These gene expression profiling studies provide background information on the developing chick immune system and provide preliminary functional information on unknown proteins.     

Ultrastructural changes in the kidney following chronic exposure to low levels of halothane.

Rats were subjected to chronic exposure to low levels of halothane (10 and 500 ppm for 8 and 4 weeks, respectively). The ultrastructural changes in the kidneys were studied. Animals exposed to 10 ppm halothane demonstrated chronic degenerative changes in the proximal convoluted tublues, including proliferation and membranous whirling of the basal infoldings of some epithelial cells and membranous degeneration of the mitochondria to form membranous bodies within the cellular cytoplasm. These pathologic changes were even more extensive and exaggerated in animals exposed to 500 ppm halothane. Fusion of the membranous bodies to form large membranous plaques and coalescence of lysosomes to form irregulary shaped cytoplasmic dense bodies were frequently found. Swelling of the mitochondria and areas of focal cytoplasmic degradation were also observed. Extrustions of large cytoplasmic masses containing mitochondria. clusters of smooth endoplasmic retriculum and ribosomes into the tubular lumen were frequently observed. Accumulation of spherical microparticles within the tubular basement membranes were also a prominent finding. The present investigation clearly indicated that halothane is nephrotoxic and may be considered as an occupational hazard.     

Age-related changes in human thymus.

Thymic biopsies obtained during open heart surgery were examined for age-related involution of the parenchyma and changes in cell surface characteristics. In parallel with the parenchymal atrophy, E-rosette-forming cells continuously decreased with age and were progressively replaced by an increasing proportion of 'null' lymphoid cells. These changes appeared to be independent of each other. The significance of these findings in the context of the host's immune mechanism is discussed.     

Ultrastructural changes in odontoblasts and pulp capillaries following cavity preparation in rat molars.

Responses of odontoblasts and pulp capillaries to cavity preparation were investigated in the upper first molar teeth of rats, using light and transmission electron microscopy. At 100 days of age, the blood vessels of the pulp formed a subodontoblastic network consisting of continuous capillaries at a short distance from the odontoblast layer. Cavity preparation caused the displacement of some odontoblasts into the dentinal tubules, while others were separated from the predentin by rapid inflammatory exudation after drilling. The subodontoblastic capillary network under the injured dentin was shifted inwards together with the separated odontoblasts. The endothelium of the shifted capillaries showed a remarkable increase of pinocytotic vesicles, an event thought to be closely related to the formation of the exudative lesion. By one day after cavity preparation, most of the damaged odontoblasts had degenerated. Many cells with high nucleus/cytoplasm (N/C) ratios and prominent nucleoli accumulated around the subodontoblastic capillaries, some of which had many endothelial fenestrae facing these cells. These cells were suggestive of newly differentiating odontoblasts receiving nutritional supply from the capillaries. Three days after cavity preparation, newly differentiating odontoblasts took the place of the degenerated odontoblasts. They began to produce reparative dentin by five days after cavity preparation. Capillaries were located beneath the newly differentiating odontoblasts, but endothelial fenestrae gradually decreased in number. During the active reparative dentin formation, capillaries remained closely beneath the new odontoblast layer. Although the rate of reparative dentin deposition was not significantly lower than that in the primary dentin formation, one could not recognize an invasion of capillaries into the odontoblast layer nor a remarkable increase of endothelial fenestrae, both of which are common in active primary dentin formation. The results suggest that the function of capillaries differs between primary and reparative dentin formation.     

Ultrastructural changes in the liver in heatstroke.

The ultrastructural changes in the human liver 24 to 96 hours after an attack of heatstroke are described. The alterations are most obvious along the vascular pole of the hepatocytes. These consist of degenerative changes or desquamation of sinusoidal lining cells, ballooning or flattening of microvilli, breaks in hepatocyte outer membranes, and electron-lucent vacuoles along the sinusoidal border. Also noteworthy is the appearance, in a number of cases, of basement membranes or ill-defined electron-dense material which may be of basement membrane character. Sinusoidal elements, such as erythrocytes, are found in hepatocytes, and hepatocellular debris appears in sinusoids. The membranes of hepatocytes and sinusoidal lining cells thus seem to be the prime targets of the hepatic injury in heatstroke. Other changes in the hepatocytes include vesiculation of endoplasmic reticulum, detachment of ribosomes, and alterations of mitochondria. Morphologic evidence of intravascular coagulation of intravascular hemolysis is often encountered. A comparison between the findings described here and those in experimental hyperthermia suggests that many of the hepatic changes seen in heatstroke are due to an excessively high tissue temperature per se but that some of the alterations are probably a consequence of complicating factors such as hypoxia, intravascular hemolysis, or disseminated intravascular coagulation.     

Ultrastructural and biochemical changes in rat soleus muscle following tenotomy

This study was designed to correlate changes in the rate-limiting enzymes of glycogen synthesis (glycogen synthase) and glycogen breakdown (glycogen phosphorylase) with the ultrastructural changes which occur in the soleus muscle following tenotomy. Soleus muscles were removed at 1, 2, 3, 7, 14, 21, and 63 days after tenotomy and were prepared for electron microscopy or frozen for enzyme analysis. In the first 7 days posttenotomy, soleus muscle fibers underwent a series of degenerative changes, while both synthase and phosphorylase activities decreased. Over the next 8 weeks the histological appearance of the soleus muscle eventually returned to normal while synthase and phosphorylase activities increased. We suggest that recovery from tenotomy involves an increase in the energy demands of the muscle, resulting in the increased activity of the key rate-limiting enzymes of muscle glycogen metabolism from the drastically reduced levels observed in the period before recovery begins.     

大鼠脑缺血后突触超微结构的变化

目的：探讨脑缺血损伤对突触的影响。方法：采用大鼠，制成脑缺血模型，应用透射电镜观察大脑顶叶皮质突触的变化。结果：随着缺血时间的延长，神经毡内突触数目逐渐减少；突触结构中突触小泡、线粒体也发生改变。缺血48h，突触小泡减少，甚至消失；线粒体变性、减少乃至消失，嵴减少或消失呈空泡状。突触前后膜被破坏，典型的突触结构已不存在。结论：脑缺血后，随缺血时间延长，突触结构异常，突触密度下降。