Dopamine-containing cells in rabbit nodose ganglia.
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Biomedical subjects
Publications and source records attributed to J Ochi.
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Spinal cords of the lamprey and hagfish were fluorescence histochemically and electron microscopically examined. Ventrally to the central canal of both cyclostomes, yellow fluorescence bound to small to medium sized neurons was observed. In the lamprey only, weakly blue-green fluorescent subependymal cells were seen just beneath the central canal. In the ventral floor of their spinal cord, yellow fluorescent varicosities were observed; their density was much higher in the lamprey than in the hagfish. The lateral surface of the hagfish spinal cord was marginated by a chain of yellow fluorescent varicosities. The yellow fluorescence was microspectrofluorometrically identified as fluorescence due to 5-HT. Electron microscopically, the 5-HT neurons contained many large dense-core vesicles. The 5-HT varicosities or terminals seen in the ventral zone of both cyclostomes possessed the large dense-core vesicles and small clear synaptic vesicles, which appeared as small dense-core vesicles after KMnO4 fixation. The terminal of the lamprey was nakedly situated on the ventral surface, while that of the hagfish was always covered by the superficial glial layer. This finding seems to favor the view that lamprey and hagfish should be divided into two different classes.
The identification of serotonergic input to the rat median eminence and nucleus suprachiasmaticus was carried out by fluorescence and electron microscopy. The clear differentiation of serotonin (5-HT) from catecholamine (CA) neurons was possible with an improved new filter system. 6-hydroxytryptamine (6-HT) was selectively taken up by 5-HT terminals and produced an intense yellow fluorescence. The yellow fluorescence of 5-HT disappeared 2 weeks after treatment with 5,6-dihydroxytryptamine (5,6-DHT), whereas the blue-green fluorescence of CA persisted. Combined treatment with either 6-HT and reserpine with addition to alpha-methyl-p-tyrosine, or with 6-HT and 6-hydroxydopamine, caused a marked reduction of CA and yellow fluorescence prominent only in 5-HT terminals. Under the electron microscope, 6-HT and 5,6-DHT were selectively taken up by the 5-HT terminals and produced electron-dense cores in the small vesicles with a diameter of 50 nm. The quantitative study revealed that the density of serotonin boutons marked with such dense-cored vesicles was 4.3 +/- 0.5% (mean +/- S.E.M.) in the suprachiasmatic nucleus and 4.8 +/- 0.8% in the perivascular region of the median eminence. Several studies have indicated an important functional role of 5-HT in the control of gonadotrophin secretion. The present study suggests that the serotonergic terminals exert their influence on the anterior pituitary function, not only at the level of the suprachiasmatic nucleus, but also at the level of the perivascular region of the median eminence, either through the axo-axonic synapses with the axons containing the releasing hormone or by the direct release of 5-HT into the portal vessels.
Blue-green fluorescent subependymal cells with intraventricular processes were shown by the fluorescent histochemical method to be distributed from the preoptic recess to the infundibular recess of the frog hypothalamus. Electron microscopy revealed at least two types of CSF-contacting subependymal cells, type 1 containing large dense granules (about 100-200 nm in diameter) and type 2 containing small dense core vesicles (about 60-100 nm in diameter). Subsequent to fixation in permanganate solution, the small dense core vesicles in type 2 cells reacted with the fixative and consistently showed a dense content. However, the large granules in type 1 cells were mostly pale or less dense after this fixation. Two hours after intraventricular injection of 3H-dopamine, a large number of silver grains appeared only in the cytoplasm of intraventricular processes possessing dense core vesicles (type 2 cells). A few grains were also found in the perikarya. It is concluded that type 2 cells are catecholamine-storing cells. It is suggested that type 1 cells in the infundibular recess are peptidergic neurons which may secrete some hypothalamic regulating hormones of the anterior pituitary. Most of these cells in the preoptic recess belong to the neurosecretory cells of the preoptic nucleus, while some cells probably function similarly to those in the infundibular recess.
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Portal vein aneurysm, especially that of the extrahepatic portal vein, is a very rare entity. We recently observed a case of aneurysm at the junction of the superior mesenteric vein and the splenic vein which accompanied lupoid hepatitis. Abdominal ultrasonography, color Doppler ultrasonography, abdominal computed tomography (CT), magnetic resonance imaging (MRI), and angiography revealed a portal vein aneurysm that increased in size after a period of about 10 months.
Symmetrical low density areas in the thalami at CT were found in an 11-month-old boy with measles encephalitis. The focal lesions on CT appeared to be localized inflammation, necrosis or edema. The cause of these lesions is unknown.
A boy with infantile spasms was found to have a balanced de novo translocation, 6q;14q. The karyotype was 46,XY,t(6;14)(q27;q13.3). He had mental retardation and microcephaly but no dysmorphic features. Whether or not there is a relationship between the translocation in our patient and his infantile spasms is unknown. If there is a connection, a gene or genes on chromosome 14 may be implicated in the seizure disorders that are common in patients with ring chromosome 14 syndrome or proximal partial trisomy 14 syndrome.
The immunoreactive leucine-enkephalin (IR Leu-E) content in the brains of epileptic E1 mice was determined. E1 mice are mutants from the dd strain of mice and are susceptible to convulsions. Seizures were elicited in E1 mice by repeated postural stimulations. As controls, ddY strain (nonconvulsive) mice and nonstimulated E1 mice (which had not developed convulsions) were used. IR Leu-E content was measured by radioimmuno-assay. Before the convulsion, the IR Leu-E content in the striatum of E1 mice was 60% of the content in the controls. In the hypothalamus, IR Leu-E levels were increased by 85% 45 min after a convulsion. IR Leu-E was also increased in the striatum (176% of preconvulsive state), cortex (121%), medulla oblongata + pons (132%), hypothalamus (180%), and midbrain (159%) 48 h after a convulsion.