[Rehabilitation in brain injuries--the objective is a reorganization of brain function].
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With the purpose of mapping those anatomical structures participating in the processing and analysis of form, colour and disparity information, we have measured, with positron emission tomography and [15O]butanol, regional cerebral blood flow (rCBF) as an indicator of regional cerebral metabolic activity in 13 right-handed male volunteers during visual discrimination of colour, form and disparity information. The brain images were anatomically standardized using a computerized brain atlas and statistically significant changes were localized by cluster analysis. The changes in rCBF between specific activation and reference states were measured and the volumes of changes were determined, as were the loci and volumes of areas commonly activated by two or three different tasks. Each of the tasks activated over a dozen distinct and separate fields in the cortex--in the occipital, parietal, temporal and frontal lobes as well as the cerebellum. A number of overlapping fields were commonly activated in two tasks (four in the form and colour tasks, five in the form and disparity tasks, and eleven in the colour and disparity tasks), and two field overlaps were present in all three tasks (in the right superior frontal and left lingual gyri). These findings indicate that, in a visual discrimination task, the processing and analysis of single visual submodalities take place in a number of cortical fields in the human brain. As the same visual submodality is processed and analysed by numerous fields and the same field may participate in the processing of different submodalities, a divergence-convergence pattern of information processing is present in the human brain. This observation supports a hypothesis based on earlier studies in primates, namely that information processing in the visual system requires the concerted activation of a relatively large number of fields of functional networks in the brain.
Diabetes mellitus is associated with moderate cognitive deficits and neurophysiological and structural changes in the brain, a condition that may be referred to as diabetic encephalopathy. Diabetes increases the risk of dementia, particularly in the elderly. The emerging view is that the diabetic brain features many symptoms that are best described as "accelerated brain ageing." The clinical characteristics of diabetic encephalopathy are discussed, as well as behavioural (e.g. spatial learning) and neurophysiological (e.g. hippocampal synaptic plasticity) findings in animal models. Animal models can make a substantial contribution to our understanding of the pathogenesis, which shares many features with the mechanisms underlying brain ageing. By unravelling the pathogenesis, targets for pharmacotherapy can be identified. This may allow treatment or prevention of this diabetic complication in the future. We discuss changes in glutamate receptor subtypes, in second-messenger systems and in protein kinases that may account for the alterations in synaptic plasticity. In addition, the possible role of cerebrovascular changes, oxidative stress, nonenzymatic protein glycation, insulin and alterations in neuronal calcium homeostasis are addressed.
Sulfatide synthesis and its subcellular distribution kinetics was followed in the myelinating brain of 17-day-old mice. Pulse-labeling-chasing conditions were achieved by an intraperitoneal injection of (35S)sulfate followed 2 h later by a second injection of a high dose of unlabeled sulfate. At 1, 2, 3, 4, and 6 h after the (35S)sulfate injection, the brains were removed, homogenized, and subcellular fractions were obtained by differential and discontinuous sucrose gradient centrifugation (Eichberg, J., Whittaker, V. P., and Dawson, R. M. (1964) Biochem. J. 92, 91-100). The microsomal membranes were further subfractionated (Siegrist, H. P., Burkart, T., Wiesmann, U. N., Herschkowitz, N. N., and Spycher, M. A. (1979) J. Neurochem. 33, 497-504) into light myelin, plasma membranes, Golgi vesicles, endoplasmic reticulum membranes, and heavy vesicles associated with acid hydrolase activities. The [35S]sulfatide-labeling kinetics was measured in all subcellular fractions. The results indicate that sulfatides are synthesized in the Golgi-endoplasmic reticulum complex and transferred in vesicles at least partially associated with lysosomes to the myelin membranes. The association of sulfatides with lysosomes could explain the existence of the previously described labile pool of newly synthesized sulfatides (Burkart, T., Hofmann, K., Siegrist, H. P., Herschkowitz, N. N., and Wiesmann, U. N. (1981) Dev. Biol. 83, 42-48) and also could be a form of vesicular transport to the myelin.
A computerized topographic technique that maps brain electrical activity is applied to the investigation of neurophysiological abnormalities in medicated and drug-free schizophrenic patients. This topographic approach uses EEG and evoked potentials to provide functional measures of electrophysiological abnormalities. Neurophysiological differences between schizophrenic patients and controls are delineated which add further evidence that frontal lobe dysfunction may be relevant to our understanding of schizophrenia. An initial investigation employs computed tomography to examine the relationship of structural anatomical pathology in schizophrenia with the functional abnormalities that may be defined using brain electrical activity mapping. When schizophrenic patients with and without frontal cortical atrophy were compared, electrophysiological differences were delineated that overlay frontal cortical regions. This preliminary work suggests that in schizophrenia, abnormal electrophysiological function is associated with definable gross morphological abnormalities of the brain.
Dietary n-6 or n-3 fatty acid deficiencies result in changes in brain and retinal phospholipid composition that can affect cell membrane and organ function. An n-3 fatty acid deficiency has been associated with altered electroretinograms and reduced visual acuity in animals. Other promising methods for assessing the effects of fatty acid deficiencies on brain and retinal maturation include visual-evoked potential acuity, sleep-wake cycle, auditory brain stem-evoked response, somatosensory-evoked potential measurements, and the Fagan and forced-choice preferential looking acuity tests. Preterm infants fed a formula low in alpha-linolenic acid (18:3n-3) had significant electroretinographic changes at discharge from the nursery, indicating a delay in rod photoreceptor maturation. However, infants fed human milk or supplementary n-3 fatty acids as marine oil had electroretinogram indexes like those of infants of comparable age tested soon after birth. Visual cortex function, measured by pattern reversal visual-evoked potential and forced-choice preferential looking visual acuity response, was also better in infants fed human milk or marine oil-supplemented formula than in infants fed formulas without docosahexaenoic acid (22:6n-3). Studies of term infants suggest that visual acuity is more mature in breast-fed than in formula-fed infants [corrected] at 4 months and 3 years of age.
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(1) The blood-brain barrier (BBB) is formed by brain capillary endothelial cells (ECs). There are various cell types, in particular astrocytes, but also pericytes and neurons, located in close vicinity to the capillary ECs which may influence formation and function of the BBB. Based on this consideration, this paper discusses various aspects of the influence of the surrounding cells on brain capillary ECs with special focus on the role of astrocytes. (2) Based on the morphology of the BBB, important aspects of brain EC functions are summarized, such as transport functions and maintenance of low paracellular permeability. Moreover, various facets are discussed with respect to the influence of astrocytes, pericytes, microglia, and neurons on the BBB. Data on the role of glial cells in the ontogenesis of the BBB are presented subsequently. The knowledge on this subject is far from being complete, however, these data imply that the neural/neuronal environment rather than glial cells may be of importance in the maturation of the barrier. (3) The role of glial cells in the induction and maintenance of the BBB is discussed under physiological as well as pathological conditions. Although the literature presents manifold evidence for a great variety of effects induced by astroglia, there are also many controversies, which may result from different cellular models and experimental conditions used in the respective studies. Numerous factors secreted by astrocytes have been shown to induce a BBB phenotype. On the molecular level, increased expression of barrier-relevant proteins (e.g., tight junction proteins) is documented in the presence of astrocyte-derived factors, and many studies demonstrate the improvement of physiological parameters, such as increased transendothelial resistance and decreased paracellular permeability, in different in vitro models of the BBB. Moreover, one has to take into account that the interaction of brain ECs and astrocytes is bi-directional, and that the other cell types surrounding the brain microvasculature also contribute to BBB function or dysfunction, respectively. (4) In conclusion, it is expected that the present and future research focused on molecular mechanisms and signaling pathways will produce new and exciting insights into the complex network of BBB regulation: the cornerstone is laid.
UNLABELLED: The aim of this work was to study cerebral function in vertically infected children with human immunodeficiency virus 1 (HIV-1). METHODS: PET with 18F-labeled fluorodeoxyglucose (FDG) was performed in eight children (2.5-5.5 yr): three with severe neurological symptoms and five without. Quantitative analysis was based on gray matter cortical and subcortical regions of interest for which glucose utilization was measured. RESULTS: Diffuse hypometabolism and subcortical hypermetabolism were found in the three children with severe neurological signs; the five other children had temporo-occipital cortical hypometabolism, mainly on the right side. CONCLUSION: Functional cerebral abnormalities seem to precede clinical symptoms in HIV-1infection of the brain in children.
This article takes an information processing perspective to review current understanding of brain mechanisms of human voluntary timing. Theoretical accounts of timing of the production of isochronous tapping and rhythms and of bimanual responding repetitive responding are reviewed. The mapping of higher level temporal parameter setting and memory processes and of lower level motor implementation process onto cortical and subcortical brain structures is discussed in relation to evidence from selective lesions in a range of neurological motor disorders. Brain activation studies that have helped identify key brain structures involved in the control of timing are reviewed.
It is well known that neonatal exposure to estrogen induces masculinization or defeminization of the brain. In this study, the effects of neonatal treatment with two kinds of soybean isoflavone aglycone, genistein (GS) and daidzein (DZ), on the estrous cycle and lordosis behavior were investigated. Female rats were injected subcutaneously with 1 mg GS, 1 mg DZ, 100 microg estradiol (E2), or oil daily for 5 days from birth. As a result, vaginal opening was advanced in GS- or E2-treated females. A vaginal smear check indicated that oil- or DZ-treated females showed a constant 4- or 5-day estrous cycle, whereas GS- or E2-treated rats showed a persistent or prolonged estrus. Ovariectomy was performed in all females at 60 days of age. The ovaries in the GS- or E2-treated groups were smaller than those in the oil- and DZ-treated groups and contained no corpora lutea. In the DZ group, although corpora lutea were seen, ovaries were smaller than that of control females. Behavioral tests were carried out after implantation of E2-tubes. All of the oil- or DZ-treated females showed lordosis with a high lordosis quotient (LQ). On the other hand, as male rats, LQs were extremely low in the E2-treated group, when compared to the oil-treated group. In the GS-treated group, the mean LQ was lower than that in the oil-treated group, but higher than those in the E2-treated female or male groups. These results suggest that genistein acts as an estrogen in the sexual differentiation of the brain and causes defeminization of the brain in regulating lordosis and the estrous cycle in rats. In addition, neonatal daidzein also has some influence on ovarian function.
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In recent years researchers have begun to investigate lateralisation of behaviour in amphibians. Given the mounting evidence of lateralisation in birds and mammals, and even reptiles, over the past two or more decades, it is not surprising that amphibians have attracted attention in this context. In particular, the evidence for lateralisation in fish has provided a strong basis for this research. This paper summarises the currently available information on lateralisation in anuran amphibians and discusses it in comparison to lateralisation in other vertebrate species, beginning with examples of motor lateralisation and then discussing functional asymmetries that occur between the left and right sides of the brain. The latter are manifested as side biases in responding to different stimuli or, in a number of non-amphibian species, revealed by monocular testing. Most of the examples discussed refer to lateralisation present at the level of the forebrain hemispheres, and so represent hemispheric specialisation. Lateralisation usually refers to examples in which there is a population bias for the majority of individuals in a population to be lateralised in the same direction. In other words, there is a significant skew in the frequency distribution. Such population biases in lateralisation are now known to be widespread among the vertebrates and, as shown, there are some surprisingly similar patterns of lateralisation in those species of fish, amphibians, reptiles, birds, and mammals that have been studied so far. It is also noted that, despite their ubiquity in vertebrates, far from all forms of lateralisation develop solely, or even largely, according to genetic determinants. In fact, the clear and powerful influences of environmental stimulation on development of some kinds of lateralisation in birds provide a basis for similar investigations in anurans.