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Selective Damage (selective + damage)
Selected AbstractsSpatial memory and the monkey hippocampus: Not all space is created equalHIPPOCAMPUS, Issue 1 2009Pamela Banta Lavenex Abstract Studies of the role of the monkey hippocampus in spatial learning and memory, however few, have reliably produced inconsistent results. Whereas the role of the hippocampus in spatial learning and memory has been clearly established in rodents, studies in nonhuman primates have made a variety of claims that range from the involvement of the hippocampus in spatial memory only at relatively longer memory delays, to no role for the hippocampus in spatial memory at all. In contrast, we have shown that selective damage restricted to the hippocampus (CA regions) prevents the learning or use of allocentric, spatial relational representations of the environment in freely behaving adult monkeys tested in an open-field arena. In this commentary, we discuss a unifying framework that explains these apparently discrepant results regarding the role of the monkey hippocampus in spatial learning and memory. We describe clear and strict criteria to interpret the findings from previous studies and guide future investigations of spatial memory in monkeys. Specifically, we affirm that, as in the rodent, the primate hippocampus is critical for spatial relational learning and memory, and in a time-independent manner. We describe how claims to the contrary are the result of experimental designs that fail to recognize, and control for, egocentric (hippocampus-independent) and allocentric (hippocampus-dependent) spatial frames of reference. Finally, we conclude that the available data demonstrate unequivocally that the central role of the hippocampus in allocentric, spatial relational learning and memory is conserved among vertebrates, including nonhuman primates. © 2008 Wiley-Liss, Inc. [source] The anatomy of language: contributions from functional neuroimagingJOURNAL OF ANATOMY, Issue 3 2000CATHY J. PRICE This article illustrates how functional neuroimaging can be used to test the validity of neurological and cognitive models of language. Three models of language are described: the 19th Century neurological model which describes both the anatomy and cognitive components of auditory and visual word processing, and 2 20th Century cognitive models that are not constrained by anatomy but emphasise 2 different routes to reading that are not present in the neurological model. A series of functional imaging studies are then presented which show that, as predicted by the 19th Century neurologists, auditory and visual word repetition engage the left posterior superior temporal and posterior inferior frontal cortices. More specifically, the roles Wernicke and Broca assigned to these regions lie respectively in the posterior superior temporal sulcus and the anterior insula. In addition, a region in the left posterior inferior temporal cortex is activated for word retrieval, thereby providing a second route to reading, as predicted by the 20th Century cognitive models. This region and its function may have been missed by the 19th Century neurologists because selective damage is rare. The angular gyrus, previously linked to the visual word form system, is shown to be part of a distributed semantic system that can be accessed by objects and faces as well as speech. Other components of the semantic system include several regions in the inferior and middle temporal lobes. From these functional imaging results, a new anatomically constrained model of word processing is proposed which reconciles the anatomical ambitions of the 19th Century neurologists and the cognitive finesse of the 20th Century cognitive models. The review focuses on single word processing and does not attempt to discuss how words are combined to generate sentences or how several languages are learned and interchanged. Progress in unravelling these and other related issues will depend on the integration of behavioural, computational and neurophysiological approaches, including neuroimaging. [source] Phototoxicity of exogenous protoporphyrin IX and ,-aminolevulinic acid in the photo hen's egg testPHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 5 2004Norbert J. Neumann Background: Oxygen, appropriate light sources, and special photosensitizers are necessary to induce photochemical damage in tumor cells via photodynamic therapy (PDT) ,-aminolevulinic acid (ALA) is increasingly used in PDT, because topical or systemic administration of ALA induces accumulation of endogenous porphyrins preferentially in neoplastic tissues. Subsequent radiation with light of approximately 630 nm leads to selective damage of tumor cells. PDT should optimally leave peritumoral tissues unaffected, but only few data are reported on the effects and the time course of ALA-induced porphyrins in tumor-free tissues. Methods: Therefore, we studied the phototoxic effects of protoporphyrin IX (PP) and ALA-induced porphyrins in a recently established photototoxic model based on tumor-free tissue, the photo hen's egg test (PHET). Results: Employing this test procedure, PP provoked strong phototoxic reactions when irradiated with Ultraviolet A immediately and up to 30 h after substance application. In contrast, ALA induced a significant phototoxic effect only if irradiated 24 h after application. Conclusion: Thus, we observed a delayed phototoxic effect of ALA in tumor-free tissue of the yolk sac (YS) blood vessel system. This delayed phototoxic response 24 h after ALA application is probably caused by endogenously synthesized porphyrins. In contrast, epithelial tumors show a maximum porphyrin accumulation 4,8 h after ALA application whereas in healthy human skin porphyrin synthesis is less intensive but prolonged with maximum levels 24,48 h after ALA application. Thus, ALA induced virtually the same delayed phototoxic effect in the tumor-free YS blood vessel tissue as in healthy human skin. These results show that the PHET is a useful model for the predictive preclinical risk assessment of exogenous or endogenous photosensitizers. [source] Acquired loss of chromatic sensitivityACTA OPHTHALMOLOGICA, Issue 2009J BARBUR Purpose A range of ophthalmic and neurological conditions cause diminished visual performance, even when the subject is often unaware of any problems and the loss of vision remains undetected in conventional perimetry and visual acuity tests. The extent to which detection of acquired colour vision loss can revealed in subclinical cases and distinguished from congenital loss has been investigated. Methods Over 400 subjects with congenital and acquired colour vision loss have been examined using conventional colour screening methods. In addition, the loss of yellow / blue and red / green chromatic sensitivity has been quantified using the CAD test (http://www.caa.co.uk/docs/33/200904.pdf). Those investigated included subjects with diseases of the retina and / or the optic nerve as well as patients with selective damage to central visual pathways. Patients with various stages of glaucoma, photoreceptor dystrophies, diabetes, optic neuritis, age-related macular degeneration as well as tobacco and alcohol toxicity have been examined. Results Algorithms developed for analysis of colour vision loss and automatic classification of congenital and / or acquired colour deficiency will be described. In acquired deficiency, the loss of chromatic sensitivity tends to affect both the rg and the yb channels. Significant differential effects have, however, been observed in relation to stimulus size, retinal location and state of light adaptation. Conclusion The findings from these studies show that in the majority of these conditions, the loss of chromatic sensitivity is the most sensitive measure of early changes in diseases of the eye. [source] | |||||||||||||