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Angaben zur Quelle [Bearbeiten]

Autor     Brigitta Wernsmann, Hans-Christian Pape, Erwin-Josef Speckmann, Ali Gorji
Titel    Effect of cortical spreading depression on synaptic transmission of rat hippocampal tissues
Zeitschrift    European Journal of Neuroscience
Ausgabe    23
Datum    March 2006
Nummer    5
Seiten    1103–1110
DOI    10.1111/j.1460-9568.2006.04643.x
URL    http://onlinelibrary.wiley.com/doi/10.1111/j.1460-9568.2006.04643.x/abstract

Literaturverz.   

yes
Fußnoten    yes
Fragmente    7


Fragmente der Quelle:
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The hippocampus has direct and important functional interactions with brain areas likely to be important to migraine, such as the areas associated with vision, emotions and neuroendocrine homeostasis. The connection between entorhinal cortex and hippocampus is regarded as an important loop responsible for the processing of sensory information (Vaisanen et al., 1999). Thus, these medial temporal lobe structures may play a crucial role in the development of somatosensory and neuropsychotic symptoms in neurological disorders such as epilepsy and migraine (Eid et al. 1995). As memories in humans depend initially on the medial temporal lobe system, including the [hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966).] The hippocampus has direct and important functional interactions with brain areas likely to be important to migraine, such as the areas associated with vision, emotions and neuroendocrine homeostasis. The connection between entorhinal cortex and hippocampus is regarded as an important loop responsible for the processing of sensory information (Vaisanen et al., 1999). Thus, these medial temporal lobe structures may play a crucial role in the development of somatosensory and neuropsychotic symptoms in neurological disorders such as epilepsy and migraine (Eid et al., 1995). As memories in humans depend initially on the medial temporal lobe system, including the hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966; Kapp & Schneider, 1971).
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[As memories in humans depend initially on the medial temporal lobe system, including the] hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966). Furthermore, propagation of SD in the hippocampus was believed to play a role in migraine pain by triggering nociceptive activation of the caudal trigeminal nucleus (Kunkler and Kraig, 2003). Classical studies investigated hippocampal SD more often by implantation of KCl into the hippocampus and induction of SD directly in the tissue. Little information is available on the effects of cortical SD on hippocampal activity. Because altered neural circuit function can be seen remote from the SD propagation site, using in vitro brain models, the effects of different substances as well as electrical stimulation on propagation of SD between the neocortex and the hippocampus was investigated. As memories in humans depend initially on the medial temporal lobe system, including the hippocampus, it was suggested that interictal memory dysfunction in patients with migraine might be attributed to the hippocampus involvement (Kupfermann, 1966; Kapp & Schneider, 1971). Furthermore, propagation of SD in the hippocampus was believed to play a role in migraine pain by triggering nociceptive activation of the caudal trigeminal nucleus (Kunkler & Kraig, 2003). Classical studies investigated hippocampal SD more often by implantation of KCl into the hippocampus and induction of SD directly in the tissue. Little information is available on the effects of cortical spreading depression (CSD) on hippocampal activity. Because altered neural circuit function can be seen remote from the SD propagation site (Bures et al., 1961; Albe-Fessard et al., 1984; Moskowitz et al., 1993; Kunkler & Kraig, 2003; Gorji et al., 2004), using in vitro and ex vivo / in vitro brain models, the effects of neocortical SD on the synaptic plasticity of hippocampal tissues were tested.
Anmerkungen

The source is not mentioned.

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Intrinsic optical imaging as well as bioelectrical recordings revealed different patterns of SD propagation in hippocampal and entorhinal slices (Buchheim et al., 2002; Wernsmann et al., 2006). All data indicated of a resistance of the entorhinal cortex for penetration by cortical SD. Although the exact mechanisms responsible for difficulty of cortical SD propagation to the entorhinal cortex are not clear, some hypotheses can be derived from experimental data. A traditional view assumes that the entorhinal cortex faithfully transmits neocortical inputs to the hippocampus and the hippocampus inputs to the neocortex (Naber et al., 1999). More recent evidence suggests that the entorhinal cortex is more than a simple relay between the neocortex and hippocampus. The entorhinal cortices contribute to the gating of impulses between these brain structures. Local inhibition and intrinsic membrane properties of entorhinal neurons are major factors limiting impulse traffic across the entorhinal cortex (Pelletier et al., 2004). Intrinsic optical imaging also revealed different patterns of SD propagation in hippocampal and entorhinal slices (Buchheim et al., 2002). Although the exact mechanisms responsible for different propagation patterns of SD are not clear, some hypotheses can be derived from experimental data. A traditional view assumes that the entorhinal cortices faithfully transmit neocortical inputs to the hippocampus and vice versa (Naber et al., 1999). More recent evidence suggests that the entorhinal cortices are more than a simple relay between the neocortex and hippocampus. Entorhinal cortices contribute to the gating of impulses between these structures. Local inhibition and intrinsic membrane properties of entorhinal neurons are major factors limiting impulse traffic across the entorhinal cortex (Pelletier et al., 2004).
Anmerkungen

The source is given, but not as reference for the entire passage, but as one of two references for the statement "Intrinsic optical imaging as well as bioelectrical recordings revealed different patterns of SD propagation in hippocampal and entorhinal slices"

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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.

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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.

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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).

Anmerkungen

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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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.

Anmerkungen

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.

Sichter
(Hindemith) Agrippina1

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