Neurons of the claustrum projecting to the motor and somatosensory cortex in the rabbit--assessment with the method of retrograde transport of fluorescent tracers.
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Biomedical subjects
Publications and source records attributed to J Dziewiatkowski.
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Our morphometric study of 30 dogs, mongrels, from 6.5 to 26.5 years of age, shows amyloid angiopathy in cortical and leptomeningeal vessels of all dogs older than 13.2 years of age, and the increase in the numerical density of amyloid-positive vessels correlated with age. Cluster analysis distinguished the group of six dogs (25%) to be relatively less affected, a large group of 13 animals (54%) to have moderate pathology, and five dogs (21%) to have severe amyloid angiopathy. Amyloid accumulation starts in large vessels, particularly in the tunica media of large arteries. Amyloid deposition appears to be associated with smooth muscle cells. Ultrastructural studies of samples from nine dogs are in agreement with in vitro studies suggesting that smooth muscle cells are the source of soluble amyloid beta. beta-protein polymerizes in the basal lamina of the tunica media. Muscle cells in the area of amyloid-beta accumulation degenerate and die. Thioflavin-positivity of only 24% of cortical and 66% of leptomeningeal beta-protein-positive vessels suggests that thioflavin-negative deposits contain soluble, not yet fibrillized protein and/or partially degraded and depolymerized amyloid.
The morphometric analysis of some hypothalamic nuclei was performed on 20 brains of subjects of both sexes aged from 29 to 79 years. They were divided into two groups: below and above the age of 60. Supraoptic (SON), lateral tuberal (LTN) and lateral mammillary (LMN) nuclei were investigated. In the group of aged subjects a decrease in cross-section area of neuron nuclei was observed in all investigated structures, expressed most in the LTN. A considerable increase in the neuron density with age was found in the LTN. The size of neuron cell bodies and the number of neurons did not change significantly with age in any of the investigated nuclei.
The morphology of the claustrum in Galloway syndrome was investigated. Galloway syndrome is a rare autosomal recessive disease that causes microcephaly and is associated with kidney pathology. The brain examined was small, and the external surface of the hemispheres was lissencephalic, with an abnormal gyrification pattern. The whole cerebral cortex showed severe pathological changes, but the most affected area was the cortex lying on the medial aspect of the temporal lobe, especially the entorhinal cortex. In addition, the paraamygdalar and temporal parts of the claustrum were intensively changed. These results may confirm the opinion that the claustrum is a cortico-dependent structure and that the limbic cortex receives large projection from its ventral parts.
The cytoarchitectonics of the nucleus of the lateral olfactory tract (NLOT) was studied on Nissl stained sections in 6 brains of adult Wistar rats by using morphometric methods. The neuronal density of layer III (11,866 +/- 547 mm-3) is on average about three times smaller than that of layer II (30,947 +/- 1110 mm-3). The average cross-section area of neurons in layer III (254.3 +/- 3.8 microns2) is about twice as large as that of neurons in layer II (115.8 +/- 0.8 microns2). The layer II is rather homogenous in contrast to layer III which possesses neurons of various size. Other morphometric parameters of layer II and III are also different.
Cyto- and myeloarchitectonics as well as acetylcholinesterase activity of the nucleus limitans thalami--an important part of the nociceptive system--were studied in insectivora (Sorex araneus, Erinaceus europaeus, Talpa europaeus), rat, rabbit, cat, monkey and man. Our results suggest that nucleus limitans is phylogenetically a rather new structure. In insectivora and in the rat we could not find any evident group of neurons resembling nucleus limitans. In the rabbit and cat nucleus limitans is composed of few layers of elongated cells. In macaca and man it is a larger, more complicated structure possessing various types of neurons, and arranged into many layers.
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The decrease in the number of neurons free of neurofibrillary changes, neurons with neurofibrillary degeneration, and the total volume of beta-amyloid (A beta) deposits in the amygdala of people with Down syndrome and in late stages of Alzheimer disease were estimated by using morphometry and regression analysis. This model predicts that the duration of neurofibrillary changes from the pretangle stage to ghost tangles is approximately 4.7 years. The correlation between the decrease in the number of neurons and the decrease in the amount of A beta indicates that amyloid deposition is associated with neurons and that loss of neurons causes decrease in A beta deposition. The presence of neurons only with neurofibrillary tangles, and the absence of the amyloid deposits predicted by regression analysis suggest that neurons with tangles are not engaged in amyloid deposition. The disappearance of amyloid by approximately 2.2 years after loss of neurons free of neurofibrillary changes indicates that A beta deposits are degradable and removable and that even in severely atrophic amygdala, there are mechanisms of amyloid resolution. This study shows that in normal aging in the amygdala, extracellular A beta appears later than neurofibrillary changes.
Individual differences in the development of neurofibrillary changes were examined in eight cortical regions in the brains of 43 subjects with Down syndrome (DS; age range, 15-69 years) using sections stained with monoclonal antibodies (mAb) tau-1 and 3-39. Neurofibrillary pathology was found in 4 cases below 36 years of age and in all 20 cases above that age. In the 24 positive cases, numerical density of pretangles stained with tau-1 and 3-39, respectively, was 6.1/mm2 and 0/mm2; early tangles, 5.0/mm2 and 5.3/mm2; mature tangles, 4.0/mm2 and 5.0/mm2 (p < 0.01); and end-stage tangles, 0.04/mm2 and 2.5/mm2 (p < 0.001). Numerical density of pretangles stained with mAb tau-1 and tangles and plaques stained with mAb 3-39 correlates weakly with age (r = 0.43; p< 0.02), and together with the wide range of numerical densities suggested heterogeneity of the population examined. Cluster analysis based on two variables - i.e., numerical density of pretangles stained with mAb tau-1 and neurofibrillary tangles (NFTs) and plaques stained with mAB 3-39, distinguished three groups of subjects with severe, moderate and weak changes. The severely affected group of 5 subject (21%) had an average 54.6/mm2 of neurons and 13.9/mm/ plaques with neurofibrillary changes, whereas the moderately affected group (6 subjects; 25%) showed a significantly lower numerical density of neurons and plaques with neurofibrillary changes (25.7/mm2 and 8.1/mm2, respectively) as compared with the most affected group. Most of the subjects (13; 54%) belong to the third group with only 2.2/mm2 of neurons and 1.4/mm2 plaques with neurofibrillary pathology. Comparison of these three groups of Down syndrome subjects representing high, moderate, and low susceptibility to neurofibrillary changes with the general population suggests that the risk of Alzheimer disease is similar but the onset of pathological changes is earlier in DS.
BACKGROUND: Sevoflurane is one of the newest volatile anaesthetic agents. The effect of sevoflurane on ICP in conditions of intracranial pathology is essential from the clinical point of view but still not sufficiently clear. The aim of the study was to examine the effects of 1 MAC, 2 MAC, 3 MAC sevoflurane on intracranial pressure (ICP), mean arterial blood pressure (MABP) and heart rate (HR) in rabbits with experimental intracerebral haematoma (ICH). MATERIAL AND METHODS: The experiments were performed in 13 adult rabbits, 3.5-4.0 kg weight. The rabbits were randomly allocated to two different groups. In group I, (n = 7), sevoflurane was administered in stepwise increasing concentrations of 2.2 vol%, 4.4 vol% and 6.6 vol%, each for a period of 15 minutes. In group II (n = 6), intracerebral haematoma was produced and subsequently sevoflurane was administered in the same manner as in group I. Ventilation parameters, inspiratory and end-tidal sevoflurane concentration, end-tidal CO2 concentration (ETCO2), HR, MABP, ICP and body temperature, measured in the nasopharynx, were monitored throughout the experiment. RESULTS: Mean values of ETCO2 and temperature in the nasopharynx were not significantly different in both groups and remained stable in the whole observation period. In group II in all cases the evidence of intraventricular haematoma was observed. In this group mean values of ICP, MABP and HR after haematoma production were significantly higher than those in group I. Statistically significant increase of ICP was observed in 30th minute in group I, while in 35th minute in group II. In both groups a statistically significant decrease in MABP was observed from 20th minute of observation. A significant decrease in HR in both groups from 25th minute of experiment was also observed. CONCLUSION: In conclusion it should be stressed that sevoflurane, in doses not exceeding 1 MAC, shows no significant effect on ICP and cardiovascular function in the course of intracranial haematoma.