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  • 1
    ISSN: 1432-0568
    Keywords: Key words Intrinsic laryngeal motoneurons ; Cholera toxin HRP ; Ultrastructure ; Swallowing ; Respiration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The laryngeal motoneurons innervating the cricothyroid muscle (CT) are located in the semicompact formation just ventral to the rostral part of the compact formation of the nucleus ambiguus. The motoneurons innervating the posterior cricoarytenoid muscle (PCA) are located in the loose formation. We retrogradely labeled the CT and the PCA motoneurons using cholera toxin subunit B-conjugated horseradish peroxidase, and determined the ultrastructure and synaptic organization of these neurons. The CT and the PCA motoneurons had the appearance of α-motoneurons, i.e., large, oval or polygonal cells containing well-developed organelles and a prominent spherical nucleus. Two kinds of neurons were recognized among the PCA motoneurons. The one (PCA-A) was significantly smaller than the other (PCA-B). The average number of axosomatic terminals in a section was significantly largest in the PCA-B (56.6), smaller in the PCA-A (36.0), and smallest in the CT (32.3) neurons. Most of the axosomatic terminals (64.7%) contained pleomorphic vesicles and made symmetric synaptic contacts (Gray’s type II) with the PCA-A neurons, while more than 60% contained round vesicles with asymmetric synaptic contacts (Gray’s type I) in the CT (69.5%) and the PCA-B (60.6%) neurons. A few terminals associated with subsurface cisterns were present on all laryngeal motoneurons. These results indicated that the CT motoneurons may receive mostly excitatory terminals, whereas the PCA muscle may be regulated by neurons having many inhibitory terminals, and neurons having many excitatory terminals.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Anatomy and embryology 177 (1988), S. 485-493 
    ISSN: 1432-0568
    Keywords: Ventral tegmental nucleus of Gudden ; Dorsal tegmental nucleus of Gudden ; Quantitative morphometric study ; Synaptic organization ; Electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The fine structure of neuronal somata and axosomatic synapses in each subnucleus of Gudden's tegmental nuclei was studied by use of electron microscopy. The pars principalis of the ventral tegmental nucleus of Gudden (TVP) is composed of oblong or triangular, medium sized neurons (11.8x22.6 μm, 211.4 μm2) containing many mitochondria, lysosomes, Golgi apparatus, and rough endoplasmic reticulum composing Nissl bodies. The light oval nucleus with a prominent nucleolus is centrally situated, and indentations of its nuclear envelope are recognized in all neurons. The neuron in the pars ventralis of the dorsal tegmental nucleus of Gudden (TDV) is similar to that in the TVP, but its average size is significantly smaller (10.0x18.8 μm, 151.4 μm2), and its organelles are also less well developed. The pars dorsalis of the dorsal tegmental nucleus of Gudden (TDD) is composed of spindle shaped, small neurons (6.9x16.2 μm, 85.1 μm2) characterized by their irregular shaped nucleus with its invaginated envelope. These neurons have a thin rim of cytoplasm, poorly developed organelles and no Nissl bodies. The average number of axosomatic terminals in a sectional plane is 9.9 in the TVP, 9.6 in the TDV and 2.6 in the TDD, and the bouton covering ratio is 24.3% in the TVP, 26.5% in the TDV and 7.4% in the TDD. The respective percentages of round, flat and pleomorphic type axosomatic terminals were estimated, and the flat type terminals were found to be dominant in the TVP, the pleomorphic type terminals in the TDV, and the round type terminals in the TDD.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Delayed neuronal death ; Gerbil ; Hippocampus ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ultrastructural damage leading to delayed neuronal death was investigated in the mid-CA1 region of the hippocampus from the stratum (str.) moleculare to oriens after transient bilateral forebrain ischemia in Mongolian gerbils. After ischemia for 5 min without recirculation, mild swelling of the peripheral part of the apical and basal dendrites was already apparent in the str. moleculare and str. oriens. Mitochondria in the dendrites were also swollen in the same area. During recirculation for 12 h to 3 days, swelling of the dendritic cytoplasm persisted with formation of microvacuoles, but swelling of mitochondria receded. Microvacuolation and loss of microtubules were also observed in the proximal part of the dendrites during this period, and swelling and disruption of internal cristae were observed in mitochondria after recirculation for 3 days. The dendrites became severely degenerated after recirculation for 4 days. In the pyramidal cell bodies, no abnormality was observed at the end of ischemia for 5 min, but disaggregation of polyribosomes and swelling of the endoplasmic reticulum were observed 12 h after recirculation. Proliferation of the endoplasmic reticulum in parallel arrays occurred after recirculation for 1 day and persisted. Severe degeneration of the pyramidal cell bodies was obvious after recirculation for 4 days. The findings observed in the present investigation suggested that the neuronal structure most vulnerable to ischemia was the peripheral part of the dendrites and postischemic neuronal damage occurred early in this part of the dendrites.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 68 (1985), S. 87-92 
    ISSN: 1432-0533
    Keywords: Pituitary neoplasm ; Anterior pituitary hormone ; Amyloid ; Electron microscopy ; Bromocriptine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The accumulation of amyloid in pituitary adenomas was examined in relation to the types of adenoma and the effect of bromocriptine treatment. Amyloid had accumulated in 34 of 48 adenomas (71%). The occurrence in prolactin-secreting adenomas and growth hormone-secreting adenomas was 79%, respectively, while that in non-functioning adenomas was 50%. Treatment with bromocriptine enhanced the occurrence and extent of the amyloid accumulation in prolactin- or growth hormone-secreting adenomas. Electron microscopy revealed the initial appearance of the amyloid fibrils in the smooth endoplasmic reticulum and a possible sequential process of their release from the cells. The presence of secretory granules in vesicles containing amyloid fibrils and their simultaneous release with amyloid fibrils suggested that degradation of secretory granules was involved in the formation of amyloid.
    Type of Medium: Electronic Resource
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