von Tanja Martens-Mantai
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| [1.] Tmm/Fragment 041 01 - Diskussion Zuletzt bearbeitet: 2014-04-28 17:01:53 Hindemith | BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Wernsmann et al 2006 |
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| Untersuchte Arbeit: Seite: 41, Zeilen: 1-26 |
Quelle: Wernsmann et al 2006 Seite(n): 1109, Zeilen: l.col: 23-39, 50-62, r.col: 1-4 |
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| LTP is an experimental phenomenon, which can be used to demonstrate the repertoire of long-lasting modifications of which individual synapses are capable. LTP remains one of the prime candidates for mediating learning and memory as well as many other forms of experience-dependent plasticity (Malenka & Bear, 2004). Functional disruption of neocortical input to the hippocampus induced by abortive SD in both in vitro and ex vivo experiments enhanced the LTP in the CA1 hippocampal area ipsilateral to SD initiation (Wernsmann et al., 2006). Enhancement of LTP by abortive SD was NMDA receptor dependent. Our data indicate the modulatory role of the changes of synaptic strength by LTP induction on SD propagation. In line with our results, CSD visualized using manganese-enhanced MRI following topical application of KCl to the exposed rat cortex revealed signal enhancement in CA1–3 areas, the subiculum and the dentate gyrus of the hippocampus (Henning et al., 2005).
Some evidence implicates the hippocampus in spatial memory and navigation, learning and emotion (Jensen & Lisman, 2005). This structure is also related primarily to the control of gross movements, such as locomotion and changes in posture, and involved in certain aspects of the pituitary–adrenocortical system. Amnesia, emotional disturbances, hyperactivity, yawning, and fluid retention were observed in hippocampal dysfunction as well as during migraine attacks (Bures et al., 1974; Isaacson & Pribram, 1975; Dalessio, 1980; Daquin et al., 2001). SD in animal experiments also elicits similar symptoms (Gorji, 2001). SD-like changes occur with visual aura in patients with migraine (Hadjikhani et al., 2001). Propagation of depolarizing waves in sensory systems of the neocortex may directly affect primary sensory modalities and induce aura symptoms such as visual hallucinations. SD, both indirectly via the effect on entorhinal input to the hippocampus or directly by propagation to the hippocampal structure, may disturb the hippocampal function and lead to symptoms such as amnesia or hyperactivity during migraine attacks. |
LTP is an experimental phenomenon, which can be used to demonstrate the repertoire of long-lasting modifications of which individual synapses are capable. LTP remains one of the prime candidates for mediating learning and memory as well as many other forms of experience-dependent plasticity (Malenka & Bear, 2004). In the present study, functional disruption of neocortical input to the hippocampus induced by abortive SD in both in vitro and ex vivo experiments enhanced the LTP in the CA1 hippocampal area ipsilateral to SD initiation. Enhancement of LTP by abortive SD was NMDA receptor dependent, as APV blocked LTP induction. Further propagation of SD to the hippocampus, conversely, inhibits LTP. These data indicate the modulatory role of SD on the efficacy of the hippocampal synaptic transmission. In line with our results, CSD visualized using manganese-enhanced MRI following topical application of KCl to the exposed rat cortex revealed signal enhancement in CA1–3 areas, the subiculum and the dentate gyrus of the hippocampus (Henning et al., 2005).
[...] Some evidence implicates the hippocampus in spatial memory and navigation, learning and emotion (Jensen & Lisman, 2005). This structure is also related primarily to the control of gross movements, such as locomotion and changes in posture, and involved in certain aspects of the pituitary–adrenocortical system. Amnesia, emotional disturbances, hyperactivity, yawning and fluid retention were observed in hippocampal dysfunction as well as during migraine attacks (Bures et al., 1974; Isaacson & Pribram, 1975; Dalessio, 1980; Daquin et al., 2001). SD in animal experiments also elicits similar symptoms (Gorji, 2001). SD-like changes occur with visual aura in patients with migraine (Hadjikhani et al., 2001). Propagation of depolarizing waves in sensory systems of the neocortex may directly affect primary sensory modalities and induce aura symptoms such as visual hallucinations. SD, either indirectly via the effect on entorhinal input to the hippocampus or directly by propagation to the hippocampal structure, may disturb the hippocampal function and lead to symptoms such as amnesia or hyperactivity during migraine attacks. |
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. |
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