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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 018 01 - Diskussion
Zuletzt bearbeitet: 2014-04-29 17:38:27 Singulus
Aeh, Fragment, Gesichtet, Gorji 2001, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 18, Zeilen: 1ff (complete)
Quelle: Gorji 2001
Seite(n): 38, Zeilen: l.col: 30ff
This suggests that glutamate evokes SD via an action at NMDA receptors.

Migraine sufferers (notably with aura) have substantially higher plasma glutamate and aspartate levels than controls and tension headache patients between attacks. During migraine attacks, glutamate and to a lesser extent aspartate levels are even further increased which show a defective cellular reuptake mechanism for these excitatory amino acids in migraineurs (Ferrari et al., 1990). Another study showed that migraine patients during attacks had higher CSF concentrations of glutamic acid than in controls (Martinez et al., 1993). Aura symptoms cause severe disability over many hours to days in patients with familial hemiplegic migraine (FHM). Intranasal application of the NMDA antagonist ketamine reversibly reduced the severity and duration of neurological deficit in FHM (Kaube et al., 2000). Subcutaneous administration of ketamine produced a marked relief of pain both as an acute treatment and as a prophylactic therapy in migraineurs (Nicolodi and Sicuteri, 1995). In addition, it was suggested that NMDA-mediated transmission is involved in nociceptive trigeminovascular transmission within the trigeminocervical complex in cats (Goadsby and Classey, 2000). The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis suggest that NMDA receptors provide a potential therapeutic target for cephalic pain (e.g., migraine) due to trigeminovascular activation from meningeal afferents (Mitsikostas et al., 1989).

5-HT1A receptor stimulation suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex (Edagawa et al., 1999). NMDA receptor blockade as well as activation of the 5-HT1A receptor attenuates the properties of KCl-induced SD in parietal cortical slices of adult rats (Kruger et al., 1999). Migraine patients have a greater cerebral 5-HT1A hypersensitivity and several anti-migraine agents exhibit marked 5-HT1A receptor activity (Leone et al., 1998).


Edagawa Y, Saito H, Abe K. Stimulation of the 5-HT1A receptor selectively suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex. Brain Res. 1999;827:225–228.

Ferrari MD, Odink J, Bos KD, Malessy MJ, Bruyn GW. Neuroexcitatory plasma amino acids are elevated in migraine. Neurology 1990; 40:1582–1586.

Goadsby PJ, Classey JD. Glutamatergic transmission in the trigeminal nucleus assessed with local blood flow. Brain Res. 2000;875:119–124.

Kaube H, Herzog J, Kaufer T, Dichgans M, Diener HC. Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine. Neurology 2000;55:139–141.

Kruger H, Heinemann U, Luhmann HJ. Effects of ionotropic glutamate receptor blockade and 5-HT1A receptor activation on spreading depression in rat neocortical slices. Neuroreport 1999;10:2651–2656.

Leone M, Attanasio A, Croci D, Ferraris A, D’Amico D, Grazzi L, Nespolo A,. Bussone G. 5- HT1A receptor hypersensitivity in migraine is suggested by the m-chlorophenylpiperazine test. Neuroreport 1998;9:2605–2608.

Martinez F, Castillo J, Rodriguez JR, Leira R, Noya M. Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks. Cephalalgia 1993;13:89–93.

Mitsikostas DD, Sanchez del Rio M, Waeber C, Moskowitz MA, Cutrer F. The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis. Pain 1998;76:239–248.

Nicolodi M, Sicuteri F. Exploration of NMDA receptors in migraine: therapeutic and theoretic implications. Int. J. Clin. Pharmacol. Res. 1995; 15:181–189.

This suggests that glutamate evokes SD via an action at NMDA receptors.

Migraine sufferers (notably with aura) have substantially higher plasma glutamate and aspartate levels than controls and tension headache patients between attacks. During migraine attacks, glutamate and to a lesser extent aspartate levels are even further increased which show a defective cellular reuptake mechanism for these excitatory amino acids in migraineurs [125]. Another study showed that migraine patients during attacks had higher CSF concentrations of glutamic acid than in controls [263]. Aura symptoms cause severe disability over many hours to days in patients with familial hemiplegic migraine (FHM). Intranasal application of the NMDA antagonist ketamine reversibly reduced the severity and duration of neurological deficit in FHM [205]. Subcutaneous administration of ketamine produced a marked relief of pain both as an acute treatment and as a prophylactic therapy in migraineurs [307]. Furthermore, it was suggested that NMDA-mediated transmission is involved in nociceptive trigeminovascular transmission within the trigeminocervical complex in cats [140]. The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis suggest that NMDA receptors provide a potential therapeutic target for cephalic pain (e.g., migraine) due to trigeminovascular activation from meningeal afferents [289].

As mentioned, migraineurs have a greater cerebral 5-HT1A hypersensitivity and several antimigraine agents exhibit marked 5-HT1A receptor activity [247,302]. 5-HT1A receptor stimulation suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex [116]. NMDA receptor blockade as well as activation of the 5-HT1A receptor attenuates the properties of KCl-induced SD in parietal cortical slices of adult rats [228].


[116] Y. Edagawa, H. Saito, K. Abe, Stimulation of the 5-HT1A receptor selectively suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex, Brain Res. 827 (1999) 225-228.

[125] M.D. Ferrari, J. Odink, K.D. Bos, M.J. Malessy, G.W. Bruyn, Neuroexcitatory plasma amino acids are elevated in migraine, Neurology 40 (1990) 1582-1586.

[140] PJ. Goadsby, J.D. Classey, Glutamatergic transmission in the trigeminal nucleus assessed with local blood flow, Brain Res. 875 (2000) 119-124.

[205] H. Kaube, J. Herzog, T. Kaufer, M. Dichgans, H.C. Diener, Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine, Neurology 55 (2000) 139-141.

[228] H. Kruger, U. Heinemann, H.J. Luhmann, Effects of ionotropic glutamate receptor blockade and 5-HT1A receptor activation on spreading depression in rat neocortical slices, Neuroreport 10 (1999) 2651-2656.

[247] M. Leone, A. Attanasio, D. Croci, A. Ferraris, D. D’Amico, L. Grazzi, A. Nespolo, G. Bussone, 5-HT1A receptor hypersensitivity in migraine is suggested by the m-chlorophenylpiperazine test, Neuroreport 9 (1998) 2605-2608.

[263] F. Martinez, J. Castillo, J.R. Rodriguez, R. Leira, M. Noya, Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks, Cephalalgia 13 (1993) 89-93.

[289] D.D. Mitsikostas, M. SancPez del Rio, C. Waeber, M.A. Moskowitz, F.M. Cutrer, The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis, Pain 76 (1998) 239-248.

[302] A. Newman-Tancredi, C. Conte, C. Chaput, L. Verriele, V. Audinot- Bouchez, S. Lochon, G. Lavielle, M.J. Millan, Agonist activity of antimigraine drugs at recombinant human 5-HT1A receptors: potential implications for prophylactic and acute therapy, Naunyn Schmtrerbrrg’s ArcP. Pharmacol. 355 (1997) 682-688.

[307] M. Nicolodi, F. Sicuteri, Exploration of NMDA receptors in migraine: therapeutic and theoretic implications, Int. J. Clin. Pharmacol. Res. 15 (1995) 181-189.

Anmerkungen

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Sichter
(Hindemith) Singulus


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