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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Repeated injection of MK801: an animal model of schizophrenia?
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Repeated injection of MK801: an animal model of schizophrenia?

机译：重复注射MK801：精神分裂症的动物模型吗？

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摘要

Glutamate-induced neurotoxicity plays an important role in neurological and psychiatric diseases. Thus, much attention has been given to the potential neuroprotective role of glutamate receptor antagonists, especially to those acting on the N-methyl-d-aspartate (NMDA) subtype. However, in addition to their neuroprotective potential, these compounds have also neurotoxic and psychotogenic properties. In the present study we used repeated injections of MK801 to examine if this non-competitive NMDA receptor antagonist could be used to produce schizophrenia-like alterations in behavior and brain metabolism in animals. Rats were given injections of MK801 (0.1 mg/kg) on six consecutive days, the last dose together with [1-(13)C]glucose and [1,2-(13)C]acetate, to probe neuronal and astrocytic metabolism, respectively. Analyses of extracts from parts of the frontal cortex plus cingulate and retrosplenial cortices and temporal lobes were performed using (13)C and (1)H magnetic resonance spectroscopy. Changes in glutamate and glutamine were restricted to the temporal lobe, in which amounts and labeling from [1-(13)C]glucose and [1,2-(13)C]acetate were increased compared to control. Locomotor activity was slightly higher in rats treated with MK801 compared to untreated animals. Metabolic changes did not resemble the alterations occurring in schizophrenia and those after repeated high dose (0.5 mg/kg) [Kondziella, D., Brenner, E., Eyjolfsson, E.M., Markinhuhta, K.R., Carlsson, M., Sonnewald, U., 2005. Glial-neuronal interactions are impaired in the schizophrenia model of repeated MK801 exposure. Neuropsychopharmacology, Epub ahead of print] but rather those caused by MK801 seen after a single high dose (0.5 mg/kg) [Brenner, E., Kondziella, D., Haberg, A., Sonnewald, U., 2005. Impaired glutamine metabolism in NMDA receptor hypofunction induced by MK801. J. Neurochem. 94, 1594-1603.].
机译：谷氨酸引起的神经毒性在神经和精神疾病中起重要作用。因此，已经对谷氨酸受体拮抗剂的潜在神经保护作用，特别是对作用于N-甲基-d-天冬氨酸（NMDA）亚型的那些给予了极大的关注。然而，除了它们的神经保护潜力之外，这些化合物还具有神经毒性和精神病原性。在本研究中，我们使用了重复注射的MK801来检查这种非竞争性NMDA受体拮抗剂是否可用于在动物行为和脑代谢中产生精神分裂症样改变。连续六天给大鼠注射MK801（0.1 mg / kg），最后一剂与[1-（13）C]葡萄糖和[1,2-（13）C]乙酸盐一起注射，以探测神经元和星形细胞的代谢， 分别。使用（13）C和（1）H磁共振波谱分析额叶皮层，扣带状和后脾皮层和颞叶的部分提取物。谷氨酸和谷氨酰胺的变化仅限于颞叶，与对照相比，[1-（13）C]葡萄糖和[1,2-（13）C]乙酸盐的量和标记增加。与未治疗的动物相比，用MK801治疗的大鼠的运动能力略高。代谢变化与精神分裂症以及反复高剂量（0.5 mg / kg）后发生的变化不同[Kondziella，D.，Brenner，E.，Eyjolfsson，EM，Markinhuhta，KR，Carlsson，M.，Sonnewald，U. ，2005。神经胶质-神经元的相互作用在反复MK801暴露的精神分裂症模型中受损。神经心理药理学，Epub提前出版]，而是由单次高剂量（0.5 mg / kg）观察到的由MK801引起的那些[Brenner，E.，Kondziella，D.，Haberg，A.，Sonnewald，U.，2005。谷氨酰胺受损MK801诱导的NMDA受体功能减退中的新陈代谢。 J.神经化学。 94，1594-1603。]。

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