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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 >Neonatal administration of iV-acetyl-L-aspartyl-L-glutamate induces early neurodegeneration in hippocampus and alters behaviour in young adult rats
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Neonatal administration of iV-acetyl-L-aspartyl-L-glutamate induces early neurodegeneration in hippocampus and alters behaviour in young adult rats

机译：新生儿静脉注射iV-乙酰基-L-天冬氨酰-L-谷氨酸可诱导海马早期神经变性并改变成年大鼠的行为

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AbstractN-acetyl-L-aspartyl-L-glutamate (NAAG) is a dipeptide that could be considered a sequestered form of L-glutamate. As much as 25% of l-glutamate in brain may be present in the form of NAAG. NAAG is also one of the most abundant neuroactive small molecules in the CNS: it is an agonist at Group II metabotropic glutamate receptors (mGluR II) and, at higher concentrations, at the N-methyl-D-aspartate (NMDA) type of ionotropic glutamate receptors. As such, NAAG can be either neuroprotective or neurotoxic and, in fact, both characteristics have been discussed and described in the literature. In the present studies, 250 nmol NAAG was infused into each lateral cerebral ventricle of 12-day-old rat pups and, using Nissl-stained sections, neurodegeneration in the hippocampus was evaluated 24 or 96 h after the infusion. In several experiments, the neuronal death was also visualised by Fluoro-Iade B staining and studied by TUNEL technique. Some of the NAAG-treated animals were allowed to survive until 50 days post partum and subjected to behavioural (open field) tests.The administration of NAAG to 12-day-old rats resulted in extensive death of neurons particularly in the dentate gyrus of the hippocampus. The neurodegeneration was, in part, prevented by administration of an NMDA receptor antagonist MK-801 (0.lmg/kg). The nuclear DNA-fragmentation demonstrated by TUNEL technique pointed to the presence of non-specific single-strand DNA cleavage. The NAAG-associated neonatal neuronal damage may have perturbed development of synaptic circuitry during adolescence as indicated by an altered performance of the experimental animals in the open field testing (changes in grooming activity) at postnatal day 50. The results underscore the potential neurotoxicity of NAAG in neonatal rat brain and implicate neonatally induced, NMDA receptor-mediated neuronal loss in the development of abnormal behaviour in young adult rats.
机译：摘要N-乙酰基-L-天冬氨酰-L-谷氨酸（NAAG）是一种二肽，可以认为是L-谷氨酸的螯合形式。脑中多达25％的l-谷氨酸可能以NAAG的形式存在。 NAAG也是中枢神经系统中最丰富的神经活性小分子之一：它是II型代谢型谷氨酸受体（mGluR II）的激动剂，而在N-甲基-D-天冬氨酸（NMDA）型离子型激动剂中则是激动剂谷氨酸受体。这样，NAAG可以是神经保护性的或神经毒性的，并且事实上，这两个特征已经在文献中进行了讨论和描述。在本研究中，将250 nmol NAAG注入12天大的幼仔的每个侧脑室，并使用Nissl染色切片，在注入后24或96 h评估海马神经变性。在几个实验中，还通过Fluoro-Iade B染色观察了神经元的死亡，并通过TUNEL技术进行了研究。一些接受NAAG治疗的动物被允许存活至产后50天，并进行行为（开放视野）测试。向12天大的大鼠给药NAAG导致神经元的广泛死亡，特别是在大鼠齿状回中。海马。通过施用NMDA受体拮抗剂MK-801（0.1mg / kg）部分地防止了神经变性。 TUNEL技术表明核DNA片段化表明存在非特异性单链DNA切割。与NAAG相关的新生儿神经元损伤可能在青春期扰动了突触回路的发育，如出生后第50天在野外测试中实验动物的表现改变（修饰活动的变化）所表明的那样。结果强调了NAAG的潜在神经毒性。在新生大鼠大脑中，并暗示新生诱导的，NMDA受体介导的神经元丢失与年轻成年大鼠发生异常行为有关。

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