von Tanja Martens-Mantai
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| [1.] Tmm/Fragment 040 03 - Diskussion Zuletzt bearbeitet: 2014-04-28 18:29:35 Schumann | BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Wernsmann et al 2006 |
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| Untersuchte Arbeit: Seite: 40, Zeilen: 3-20, 23-28 |
Quelle: Wernsmann et al 2006 Seite(n): 1108, 1109, Zeilen: 1108: r.col: last 5 lines; 1109: l.col: 1-22 |
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| The entorhinal cortex, a palaeocortical area, receives projections from secondary and higher associative areas of the neocortex. Regions of both ipsilateral frontal and temporal lobes are found to contribute afferents to this region of the brain. The association areas from the primary sensory modalities of vision, audition, and somesthesis project to multimodal convergence areas in the frontal and parietal lobes (Pandya & Kuypers, 1969). Both multimodal regions project in turn to the cingulate gyrus on the medial surface of the hemisphere, which contributes a heavy supply of afferents to the presubiculum and entorhinal cortex (Jones & Powell, 1970). Therefore, the entorhinal cortex is a final cortical link between the sensory systems of the neocortex and the hippocampus of the limbic system and plays a role as a filter between these two structures. From the entorhinal inputs, the hippocampus receives highly complex and differentiated signals, coding information about the properties of the applied stimuli. The entorhinal cortical neurons constitute the direct perforant path and the crossed temporoammonic path to the hippocampus. They terminate on dendritic branches of CA1–CA3 and the dentate fascia neurons (Van Hoesen et al., 1972). Transient sensory cortical dysfunction induced by abortive SD enhanced hippocampal activity (Wernsmann et al., 2006). This suggests an inhibitory tone mediated through neocortical influence on hippocampal plasticity. In our study, application of GABAA blocker inhibited propagation of SD to the hippocampus via the entorhinal cortex. This may related to the manipulation of this inhibitory inputs of the entorhinal cortex to the hippocampus. Our conclusion is supported by recent evidence indicating that elimination of cortical input resulted in increased reactivity and complete disappearance of habituation, with prolongation of tonic responses in the hippocampus (Vinogradova, 2001). Lesions of the entorhinal cortex in adolescent rats also resulted in enhancement of spontaneous locomotor activities, an effect possibly mediated by postsynaptic hypersensitivity (Sumiyoshi et al., 2004). | The entorhinal cortex, a palaeocortical area, receives projections from secondary and higher associative areas of the neocortex. Regions of both ipsilateral frontal and temporal lobes are found to contribute afferents to this region of the brain. The association areas from the primary sensory modalities of vision, audition and somesthesis project
[page 1109] to multimodal convergence areas in the frontal and parietal lobes (Pandya & Kuypers, 1969). Both multimodal regions project in turn to the cingulate gyrus on the medial surface of the hemisphere, which contributes a heavy supply of afferents to the presubiculum and entorhinal cortex (Jones & Powell, 1970). Thus, the entorhinal cortex is a final cortical link between the sensory systems of the neocortex and the hippocampus of the limbic system. From the entorhinal input, the hippocampus receives highly complex and differentiated signals, coding information about the properties of the applied stimuli. The entorhinal cortical neurons constitute the direct perforant path and the crossed temporoammonic path to the hippocampus. They terminate on dendritic branches of CA1–CA3 and the dentate fascia neurons (Van Hoesen et al., 1972). In the present study, transient sensory cortical dysfunction induced by abortive SD enhanced hippocampal activity. This suggests an inhibitory tone mediated through neocortical influence on hippocampal plasticity. Our conclusion is supported by recent evidence indicating that elimination of cortical input resulted in increased reactivity and complete disappearance of habituation, with prolongation of tonic responses in the hippocampus (Vinogradova, 2001). Lesions of the entorhinal cortex in adolescent rats also resulted in augmented spontaneous locomotor activity, an effect possibly mediated by postsynaptic hypersensitivity (Sumiyoshi et al., 2004). |
The source is mentioned once somewhere in the middle of the paragraph just like many other references to the literature. Nothing is marked as a quotation. The reader would never guess that the whole passage is taken from the source more or less literally. Only one sentence is not taken from the source and has not been counted. Note that even the expression "Our conclusion is supported by recent evidence[...]" is taken from the source (which, by the way, was five years old at the time of writing of the thesis). |
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