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Reconsolidation: Propagation of spreading depression between the neocortex and the hippocampus: the barrier of the entorhinal cortex

von Dr. Tanja Martens-Mantai

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[1.] Tmm/Fragment 039 01 - Diskussion
Zuletzt bearbeitet: 2014-04-28 17:01:56 Hindemith
Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Verschleierung, Wernsmann et al 2006

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Verschleierung
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Hindemith
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Untersuchte Arbeit:
Seite: 39, Zeilen: 1-17
Quelle: Wernsmann et al 2006
Seite(n): 1108, Zeilen: r.col: 28-47
In line with this, physiological studies have disclosed the existence of powerful inhibition in the entorhinal cortex (Finch et al., 1986; Jones & Buhl, 1993; Funahashi & Stewart, 1998), which may act to abort the propagation of SD.

In addition, some studies indicated relative difficulties of SD occurrence in the hippocampus compared with the entorhinal cortex (Dalby & Mody, 2003; Faria & Mody, 2004). The failure of cortical SD to spread to the hippocampus was reported earlier (Fifkova, 1964). The release of glutamate is essential to the propagation of cortical SD (Van Harreveld & Fifkova, 1973). Several studies have shown that glutamate acts via NMDA receptors during the generation and propagation of SD (Mody et al., 1987; Gorji, 2001). The NMDA receptors are assembled from NR1 subunits and at least one subtype of the four members of the NR2(A–D) subunits family. NR2B subunits are essential to the generation and propagation of SD in the entorhinal cortical slices (Faria & Mody, 2004). The physiological characteristics and possibly the localization of NR2B subunits at synapses differ between the entorhinal cortex and the hippocampus (Gordey et al., 2001; Faria & Mody, 2004), which, in turn, may influence SD penetration into the hippocampus.

Consistent with this, physiological studies have disclosed the existence of powerful inhibition in the entorhinal cortex (Finch et al., 1986; Jones & Buhl, 1993; Funahashi & Stewart, 1998), which may act to abort the propagation of SD.

Furthermore, some studies indicated a relative resistance of SD occurrence in the hippocampus compared with entorhinal cortex (Dalby & Mody, 2003; Faria & Mody, 2004). The failure of cortical SD to propagate to the hippocampus was reported earlier (Fifkova, 1964). The release of glutamate is essential to the propagation of cortical SD (Van Harreveld & Fifkova, 1973). Several studies have shown that glutamate acts via NMDA receptors during the generation and propagation of SD (Mody et al., 1987; Gorji, 2001). The NMDA receptor is a heterotetramer assembled from NR1 subunits and at least one subtype of the four members of the NR2(A–D) subunits family. NR2B subunits are essential to the generation and propagation of SD in entorhinal cortical slices (Faria & Mody, 2004). The physiological characteristics and possibly the localization of NR2B subunits at synapses differ between the entorhinal cortex and the hippocampus (Gordey et al., 2001; Faria & Mody, 2004), which, in turn, may influence SD penetration into the hippocampus.

Anmerkungen

The source is not mentioned here. It will be mentioned in passing in the next paragraph.

Sichter
(Hindemith) Agrippina1

[2.] Tmm/Fragment 039 23 - Diskussion
Zuletzt bearbeitet: 2014-04-28 21:16:02 Hindemith
BauernOpfer, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Tmm, Wernsmann et al 2006

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Hindemith
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Untersuchte Arbeit:
Seite: 39, Zeilen: 23-29
Quelle: Wernsmann et al 2006
Seite(n): 1108, Zeilen: r.col: 48-55
Seventy per cent of CSD waves propagating from temporal cortex slices penetrated to adjacent entorhinal cortex slices and stopped there, whereas the remaining 30% reached CA1 and CA3 regions of the hippocampal slices (Wernsmann et al., 2006). On the other hand, CSD elicited from the somatosensory neocortex of anaesthetized rats did not penetrate into the hippocampus (Wernsmann et al., 2006). This suggests that the CSD recording in slices offers better conditions for SD propagation probably due to weakening of intrahippocampal inhibitory mechanisms. Seventy per cent of CSD waves propagating from temporal cortex slices penetrated to adjacent entorhinal cortex slices and stopped there, whereas the remaining 30% reached CA1 and CA3 regions of the hippocampal slices. On the other hand, CSD elicited from the somatosensory neocortex of anaesthetized rats did not penetrate into the hippocampus. This suggests that the CSD recording in slices offers better conditions for SD propagation probably due to weakening of intrahippocampal inhibitory mechanisms.
Anmerkungen

The source is mentioned twice, but the copied text continues after the second reference and includes a conclusion the reader will attribute to the author of the thesis, not to Wernsmann et al (2006). Furthermore, nothing is marked as a quotation although the text has been taken literally.

Sichter
(Hindemith) Agrippina1


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