Electron microscopic observations on the postaganglionic sympathetic fibers in the guinea pig cochlea.
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Biomedical subjects
Publications and source records attributed to Y Terayama.
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To clarify the incidence, age relationships and pathogenesis of white matter lesions of unknown origin (leuko-araiosis) detected by neuroimaging among normal elderly volunteers, we measured the severity of leuko-araiosis using computerized tomographic (CT) densitometry among 42 healthy self-supporting men and women of different ages, all with normal neurological and cognitive test performance. Results were correlated with local cerebral perfusion using xenon-contrasted CT. The 42 volunteers, who are followed in this laboratory for studies of normal aging, were divided into two groups in order to determine aging effects by an extremes design. One group consisted of 19 adults below age 60 (M = 53.3, SD = 6.0). The index group comprised 23 individuals all over the age of 60 (M = 71.6, SD = 8.7). Leuko-araiosis around the anterior horns of the lateral ventricles (frontal leuko-araiosis) was more severe (p < .01) among the older group, however, occipital leuko-araiosis did not significantly differ between older and younger groups. Cerebral perfusion in frontal, temporal, and parietal cortex was decreased among older compared with younger volunteers (ps < .001, .01, and .05, respectively). Multiple regression analyses disclosed significant and direct relationships between severity of frontal leuko-araiosis and (a) frontal cortical atrophy and (b) reductions of cerebral perfusion within frontal white matter and caudate nucleus. We conclude that cortical atrophy with hypoperfusion and ischemia of frontal white matter play a part in the pathogenesis of frontal leuko-araiosis associated with normal aging and this may be a predictor for later cognitive declines.
The organ of Corti in the five-month human fetus was studied by transmission and scanning electronmicroscopy. Differentiation of the surface organization of the organ of Corti into a single row of inner and three to four rows of outer hair cells was complete at this stage except at the apical end. The morphological aspects of the hair bundles changed with maturation of the sensory cells; the inner hair cells preceded the outer hair cells in cytodifferentiation at a given location.
Guinea pigs were inoculated with a Sendai virus into the scala tympani and subsequent pathological changes of the cochleas were investigated by electron microscopy. Replication of the virus was indicated by buddings at the endolymphatic surface and by the intracytoplasmic occurrence of filamentous substances, ie, nucleocapsids. Budding viruses or free virus particles observed in a series of our experiments were identified as Sendai viruses by means of the immunological labeling with ferritin. Viral lesions, which were defined as the pathological changes of the cells associated with virus multiplication, were found in eight cochleas out of 20. This study revealed that the early lesions of the cochleas infected by Sendai viruses were primarily confined to Reissner's membrane and the stria vascularis, but the sensory cells were not affected.
Many authors report alterations of cephalic (both intracranial and extracranial) blood flow and vascular responsiveness in patients with migraine. In the majority of reports, rCBF has been decreased during the prodromal phase and increased during and immediately after the headache phase of migraine attacks. Abnormal vascular responsiveness has been demonstrated, not only during each attack, but also between attacks. Pharmacological and therapeutic evidence that many vasoactive agents induce, prevent or abolish attacks of migraine headache are consonant with the close relationships that exist between vascular abnormalities and the pathogenesis of migraine with aura. This is particularly true of the marked therapeutic effectiveness of calcium entry blockers, which are effective in the prophylaxis of migraine, and sumatriptan, which has direct vasoconstrictive effects, with relief of the headache, which lends strong support to a vascular hypothesis.
3-137 days after disruption of the guinea pig organ of Corti by perilymphatic perfusion with 20% streptomycin (SM), ultrastructural changes of the nerve fibers in the organ were observed. Most of nerve fibers began to degenerate after a latent period of 4 days. On the other hand, a number of fibers survived reactively enlarged and later developed into myelinated and unmyelinated fibers by becoming enclosed in Schwann cells which entered the organ of Corti through the habenula perforata. Regeneration and sprouting of the surviving nerve fibers also occurred. The fibers became mature, but atrophied after 60 days and then gradually disappeared. The regenerating fibers were mainly of the myelinated and unmyelinated efferent type. Retrograde degeneration occurred in both afferent and efferent fibers. In the less damaged organ of Corti perfused with 2% SM or Ringer's solution, Schwann cell invasion was not found.
Ultrastructural changes of the extrasensory epithelium in the scala media of guinea pig cochleae were observed from 3 to 137 days after perilymphatic perfusion with 20% streptomycin. The degeneration started in the organ of Corti, progressed to the interdental cells and roots of the outer sulcus cells and finally involved other epithelial cells such as Claudius and the inner and outer sulcus cells. In the final stage, except for the stria vascularis and Reissner's membrane, all epithelial cells which lined the cochlear duct were replaced by a single-cell layer membrane which originated medianly from the epithelial cells of Reissner's membrane and laterally from the superficial outer sulcus cells.