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(Stroke. 2004;35:e96.)
© 2004 American Heart Association, Inc.

Letters to the Editor

Neuroprotective Effects of MK-801 and Catecholamine Release in the Central Nervous System

Division of Cardiology, Department of Medicine, Wakayama Medical University, Wakayama, Japan

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with great interest the recent article by Gerriets and colleagues¹ dealing with the neuroprotective effects of MK-801, the N-methyl-D-aspartate (NMDA) receptor antagonist, in the different rat stroke models for the permanent middle cerebral artery occlusion (MCAO). The results of their presented study demonstrated that, because hypothalamic damage and subsequent hyperthermia can confound the results, the macrosphere MCAO models without hypothalamic damage may be more appropriate to study the neuroprotective effects of MK-801 than the suture MCAO and the macrosphere MCAO models with hypothalamic infarction.

Several studies have reported the mechanisms for the neuroprotective effects of MK-801 in the central nervous system. In a study we presented earlier, changes in norepinephrine (NE) release evoked by L-glutamate was investigated in rat central nervous system.² In an in vitro study, we showed that L-glutamate increased the release of NE from rat medulla oblongata, and further observed that the facilitative effect of L-glutamate on NE release was more pronounced in spontaneously hypertensive rats than in normotensive rats. In addition, it was demonstrated that MK-801 significantly reversed the increase in NE release evoked by L-glutamate. It would be possible that the sympatholytic action might partially explain the neuroprotective effects of MK-801 against hypertension and other neurotoxic disorders.

In the ischemic neuronal models, Nakai et al³ showed that ischemia significantly increased NE release in rat spinal cord. They also demonstrated that MK-801 suppressed the release of NE and glutamate produced by ischemia. The finding suggests that glutamate release and NMDA receptors . . . [Full Text of this Article]

Tibo Gerriets, MD; Erwin Stolz, MD; Maureen Walberer, DVM Manfred Kaps, MD

Department of Neurology, University of Giessen, Germany

Georg Bachmann, MD

Department of Radiology, Experimental Neurology Research Group, Kerckhoff Klinik Bad Neuheim, Germany

Marc Fisher, MD

Department of Neurology, University of Massachusetts Medical School, Worcester, Massachusetts