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Pharmacological investigation of spreading depression propagation in rat neocortical tissues

von Dr. Aziza El Harrak

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[1.] Aeh/Fragment 019 01 - Diskussion
Zuletzt bearbeitet: 2014-04-29 16:58:37 Schumann
Aeh, Fragment, Gesichtet, Gorji 2001, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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Hindemith
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Untersuchte Arbeit:
Seite: 19, Zeilen: 1-15
Quelle: Gorji 2001
Seite(n): 38, Zeilen: r.col: 14ff
Magnesium is known to block the NMDA receptor. The available evidence suggests that up to 50% of patients during an acute migraine attack have lowered levels of ionized magnesium (Ramadan et al., 1999). Erythrocytes and lymphocytes magnesium concentrations are significantly lower in migraine patients as compared to controls (James et al., 2000). Infusion of magnesium results in a rapid and sustained relief of an acute migraine in such patients (Mauskop et al., 1995). However, it should be mentioned that magnesium concentration has an effect on serotonin receptors, nitric oxide synthesis and release, and a variety of other migraine-related receptors and neurotransmitters (Mauskop and Altura, 1998). It is well known that reduced magnesium facilitates the development of SD in animal models and human tissues (Mody et al., 1987). Intravenous magnesium as well as the NMDA receptor antagonist MK-801 significantly reduced the frequency of SD evoked by cortical KCl application in rats. On the other hand, SD affects magnesium metabolism in the central nervous system (van der Hel et al., 1998). The magnesium sulphate anesthesia was considerably shortened approximately four times by CSD in functional decorticated mice in comparison with control animals (Bohdanecky and Necina 1963).

Bohdanecky Z, Necina J. Course of some pharmacological tests in functionally decorticated animals. Physiol. Bohemoslov. 1963;12:55–61.

Mauskop A, Altura BM. Role of magnesium in the pathogenesis and treatment of migraines. Clin. Neurosci. 1998;5:24–27.

Mauskop A, Altura BT, Cracco RQ, Altura BM. Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study. Clin. Sci. 1995;89:633–636.

Mody I, Lambert JD, Heinemann U. Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices. J. Neurophysiol. 1987;57:869– 888.

Ramadan NM, Halvorson H, Vande-Linde A, Levine SR, Helpern JA, Welch KM. Low brain magnesium in migraine. Headache 1989;29:590–593.

van der Hel WS, van den Bergh WM, Nicolay K, Tulleken KA, Dijkhuizen RM. Suppression of cortical spreading depressions after magnesium treatment in the rat. Neuroreport 1998;9:2179–2182.

Magnesium is known to block the NMDA receptor [271]. The available evidence suggests that up to 50% of patients during an acute migraine attack have lowered levels of ionized magnesium [348,455]. Erythrocytes and lymphocytes magnesium concentrations are significantly lower in migraine patients as compared to controls [426]. Infusion of magnesium results in a rapid and sustained relief of an acute migraine in such patients [270]. However, it should be mentioned that magnesium concentration has an effect on serotonin receptors, nitric oxide synthesis and release, and a variety of other migraine-related receptors and neurotransmitters [269]. It is well known that reduced magnesium facilitates the development of SD in animal models and human tissues [16,291]. Intravenous magnesium as well as the NMDA receptor antagonist MK-801 significantly reduced the frequency of SD evoked by cortical KCl application in rats [439]. On the other hand, SD affects magnesium metabolism in the central nervous system. The magnesium sulphate anesthesia was considerably shortened approximately four times by CSD in functional decorticated mice in comparison with control animals [35].

[16] M. Avoli, C. Drapeau, J. Louvel, R. Pumain, A. Olivier, J.G. Villemure, Epileptiform activity induced by low extracellular magnesium in the human cortex maintained in vitro, Ann. Neurol. 30 (1991) 589-596.

[35] Z. Bohdanecky, J. Necina, Course of some pharmacological tests in functionally decorticated animals, Physiol. Bohemoslov. 12 (1963) 55-61.

[269] A. Mauskop, B.M. Altura, Role of magnesium in the pathogenesis and treatment of migraines, Clin. Neurosci. 5 (1998) 24-27.

[270] A. Mauskop, B.T. Altura, R.Q. Cracco, B.M. Altura, Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study, Clin. Sci. 89 (1995) 633-636.

[271] M.L. Mayer, G.L. Westbrook, PB. Guthrie, Voltage-dependent block by Mg21 of NMDA responses in spinal cord neurones, Nature 309 (1984) 261-263.

[291] I. Mody, J.D. Lambert, U. Heinemann, Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices, J. NeuropPysiol. 57 (1987) 869-888.

[348] N.M. Ramadan, H. Halvorson, A. Vande-Linde, S.R. Levine, J.A. Helpern, K.M. Welch, Low brain magnesium in migraine, Headache 29 (1989) 590-593.

[426] J. Thomas, J.M. Millot, S. Sebille et al., Free and total magnesium in lymphocytes of migraine patients: effect of magnesium-rich mineral water intake, Clin. Chim. Acta 295 (2000) 63-75.

[439] W.S. van der Hel, W.M. van den Bergh, K. Nicolay, K.A. Tulleken, R.M. Dijkhuizen, Suppression of cortical spreading depressions after magnesium treatment in the rat, Neuroreport 9 (1998) 2179-2182.

[455] K.M. Welch, G.L. Barkley, N. Tepley, N.M. Ramadan, Central neurogenic mechanisms of migraine, Neurology 43 (1993) S21- S25.

Anmerkungen

The source is not mentioned.

Note: there is no entry "James et al., 2000" in the bibliography.

Sichter
(Hindemith) Schumann

[2.] Aeh/Fragment 019 19 - Diskussion
Zuletzt bearbeitet: 2014-04-29 22:32:44 Schumann
Aeh, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2009

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Untersuchte Arbeit:
Seite: 19, Zeilen: 19-25
Quelle: Sheikh 2009
Seite(n): 23, 24, Zeilen: 23: 24ff - 24: 1-5
Increasing of potassium concentration may further impairs GABA mediated inhibition and leads to appearance of ictaform burst discharges. Higashima et al. (1996) have shown that activation of GABAergic mechanisms is necessary for the generation of afterdischarges recorded in hippocampal slices after electrical stimuli. Experimental and computational data obtained by Traub et al. (1996) also suggest a role played by GABAA-mediated depolarizing conductance in the epileptiform synchronization that occurs in some models of epileptiform discharge (in [particular that induced by 4AP application).] Increasing of potassium concentration may further impairs GABA mediated inhibition and leads to appearance of ictaform burst discharges. Higashima et al. (1996) have shown that

[Seite 24]

activation of GABAergic mechanisms is necessary for the generation of afterdischarges recorded in hippocampal slices after electrical stimuli. Experimental and computational data obtained by Traub et al. (1996) also suggest a role played by GABAA-mediated depolarizing conductance in the epileptiform synchronization that occurs in some models of epileptiform discharge (in particular that induced by 4AP application).

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith) Schumann


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