[Results of local irradiation of inoperable tumors of the diencephalon and basal ganglia by stereotaxic implantation of iridium-192].
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To find out whether ventricular enlargement in schizophrenia, as demonstrated by neuroradiological methods, is caused by an atrophy of ventricle surrounding diencephalic structures, volume measurements and linear measurements of the whole thalamus, all large thalamic subnuclei and some extrathalamic brain parts were carried out on serial sections of post mortem brains belonging to the Vogt collection. The only significantly diminished parameter of this study was the thickness of the periventricular grey matter surrounding the third ventricle, while the volume and linear measurements of the whole thalamus and all large thalamic subnuclei were not significantly changed. The findings are discussed with respect to current hypotheses of diencephalic dysfunction in schizophrenia.
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During their jamming avoidance response (JAR), weakly electric fish of the genus Eigenmannia shift their electric organ discharge (EOD) frequency away from a similar EOD frequency of a neighboring fish. The behavioral rules and neural substrates for stimulus recognition and motor control of the JAR have been extensively studied (see review by Heiligenberg 1986). The diencephalic nucleus electrosensorius (nE) links sensory processing within the torus semicircularis and optic tectum with the mesencephalic prepacemaker nucleus which, in turn, modulates the medullary pacemaker nucleus and hence the EOD frequency. Two separate areas within the nE responsible for JAR-related EOD frequency rises and frequency falls, respectively, were identified by iontophoresis of the excitatory amino acid L-glutamate. Bilateral lesion of the areas causing EOD frequency rises resulted in elimination of JAR-related frequency rises above a baseline frequency obtained in the absence of a jamming stimulus. Similarly, bilateral lesion of the areas causing frequency falls resulted in a loss of JAR-related frequency falls below the baseline frequency. Whether these areas are also responsible for non-JAR-related frequency shifts is not known. The strength of response and spatial extent of the areas causing frequency shifts varied among fish and also varied in individual fish, reflecting the strength of JAR-related frequency shifts and the balance of activities in frequency-rise and frequency-fall areas. Local application of bicuculline-methiodide or GABA demonstrated a tonic inhibitory input to each area and suggests a reciprocal inhibitory interaction between the two ipsilateral areas, possibly accounting for much of the individual plasticity. The nE thus is a site for neuronal transformation from distributed, topographically organized processing within the laminated structures of the torus and tectum to discrete cell clusters which control antagonistic motor responses.
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Mapping of striatal and diencephalic plaque distribution was conducted in 25 cases of dementia of the Alzheimer type. This analysis was carried out by fluorescence microscopy of paraffin-embedded tissue sections treated with Thioflavine S as fluorochrome. Consistent differences in plaque morphology and density between nuclei and fiber tracts were observed. Striatal and pallidal distribution was uneven, with plaque aggregation near and within certain fiber tracts: capsules, medullary laminae, and radial fasciculi. Diencephalic plaques showed also preferred aggregation near and within fiber tracts and within the intralaminar nuclei. The different subcortical plaque morphologies observed according to the nuclear or fiber tract location of the amyloid plaque, indicates that the peripheral ("halo") portion of the plaque is determined by the neurophil response to the primary event: the amyloid deposit. No correlation was observed between the distribution of plaques and any particular neurotransmitter system. In that respect, plaques were present within the nucleus basalis. Neurofibrillary tangle distribution was also seen to be dissociated from plaque distribution.
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Macrophage-like cells have been previously shown within the suboptic necrotic centres of chick embryos during the period just previous to, and coinciding with, growth of the earliest optic axons through suboptic necrotic centres. In this paper, light and electron microscopy observations of chick embryos suggest that these macrophage-like cells originate from blood cells. Immunocytochemical techniques in chick-quail yolk sac chemeras, constituted of a chick embryo and a quail yolk sac, revealed that the macrophage-like cells within the suboptic necrotic centres are labelled with anti-MB1 antibody, which is specific for quail haemopoietic and endothelial cell lineage. These findings demonstrate that these phagocytic cells are of blood cell lineage, and originate in the extraembryonic tissues of the yolk sac. Diffuse staining around some suboptic necrotic centre macrophage-like cells suggests that they release MB1 antigens which may play a role in the growth of the optic axons through the suboptic necrotic centres.
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