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孕鼠经乙酸甲基氧化偶氮甲醇处理后纹状体内源性神经元的丧失。

Loss of intrinsic striatal neurons after methylazoxymethanol acetate treatment in pregnant rats.

作者信息

Balduini W, Abbracchio M P, Lombardelli G, Cattabeni F

出版信息

Brain Res. 1984 Jul;317(1):133-6. doi: 10.1016/0165-3806(84)90149-4.

DOI:10.1016/0165-3806(84)90149-4
PMID:6467029
Abstract

Treatment of pregnant rats with methylazoxymethanol (MAM) induces a marked microencephaly in the offspring. The striatum is one of the brain areas affected by treatment. We show that in striatum there is a 30% loss of dopamine (DA)-dependent adenylate-cyclase activity: this indicates that cells bearing type 1 DA receptors are affected by MAM treatment. Moreover, since kainic acid retains its neurotoxic activity, corticostriatal fibers do not seem to be affected, despite the dramatic reduction of cortex size.

摘要

用甲基氧化偶氮甲醇(MAM)处理怀孕大鼠会导致其后代出现明显的小头畸形。纹状体是受该处理影响的脑区之一。我们发现,纹状体中多巴胺(DA)依赖性腺苷酸环化酶活性丧失了30%:这表明表达1型DA受体的细胞受到了MAM处理的影响。此外,由于 kainic 酸保留了其神经毒性活性,尽管皮质大小显著减小,但皮质纹状体纤维似乎并未受到影响。

相似文献

1
Loss of intrinsic striatal neurons after methylazoxymethanol acetate treatment in pregnant rats.孕鼠经乙酸甲基氧化偶氮甲醇处理后纹状体内源性神经元的丧失。
Brain Res. 1984 Jul;317(1):133-6. doi: 10.1016/0165-3806(84)90149-4.
2
Effects of prenatal methylazoxymethanol treatment on the development of central monoamine neurons.产前甲基氧化偶氮甲醇治疗对中枢单胺能神经元发育的影响。
Brain Res. 1981 Nov;254(4):513-30. doi: 10.1016/0165-3806(81)90020-1.
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Effects of fetal methylazoxymethanol acetate lesion on the synaptic neurochemistry of the adult rat striatum.胎儿醋酸甲基氧化偶氮甲醇损伤对成年大鼠纹状体突触神经化学的影响。
J Neurochem. 1981 Oct;37(4):878-87. doi: 10.1111/j.1471-4159.1981.tb04474.x.
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Prenatal exposure to methylazoxymethanol (MAM) acetate: effects on ultrasonic vocalization and locomotor activity in rat offspring.产前暴露于乙酸甲基偶氮甲醇(MAM):对大鼠后代超声发声和运动活动的影响。
Arch Toxicol Suppl. 1987;11:148-51. doi: 10.1007/978-3-642-72558-6_21.
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The sleep-wakefulness cycle and spindle bursts during paradoxical sleep in microencephalic rats induced by prenatal administration of methylazoxymethanol (MAM) acetate.产前给予乙酸甲基偶氮甲醇(MAM)诱导的小头畸形大鼠在异相睡眠期间的睡眠-觉醒周期和纺锤波爆发。
Tokushima J Exp Med. 1982 Jun;29(1-2):1-9.
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Effect of methylazoxymethanol acetate on adenylate cyclase and 5'-nucleotidase in rat liver plasma membranes.
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Fetal methylazoxymethanol acetate-induced lesions cause reductions in dopamine receptor-mediated catalepsy and stereotypy.胎儿醋酸甲基偶氮甲醇诱导的损伤会导致多巴胺受体介导的僵住症和刻板行为减少。
Neuropharmacology. 1985 Nov;24(11):1057-62. doi: 10.1016/0028-3908(85)90191-1.
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Methylazoxymethanol-induced microencephaly: persistent increase of cortical somatostatin-like immunoreactivity.甲基氧化偶氮甲醇诱导的小头畸形:皮质生长抑素样免疫反应性持续增加。
Brain Res Dev Brain Res. 1989 May 1;47(1):156-9. doi: 10.1016/0165-3806(89)90120-x.
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Excitatory amino acid receptors in brains of rats with methylazoxymethanol-induced microencephaly.甲基偶氮甲醇诱导的小头畸形大鼠脑中的兴奋性氨基酸受体
Neurosci Res. 1992 Jun;14(1):13-25. doi: 10.1016/s0168-0102(05)80003-3.
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Impaired selective attention in methylazoxymethanol-induced microencephalic rats.甲基偶氮甲醇诱导的小头畸形大鼠的选择性注意力受损。
Pharmacol Biochem Behav. 1986 Apr;24(4):975-81. doi: 10.1016/0091-3057(86)90445-4.

引用本文的文献

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Modeling epileptic spasms during infancy: Are we heading for the treatment yet?婴儿痉挛症建模:我们是否即将迎来治疗方法?
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2
Effect of prenatal treatment with methylazoxymethanol on carbachol-, norepinephrine- and glutamate-stimulated phosphoinositide metabolism in the neonatal, young, and adult offspring.产前用甲基氧化偶氮甲醇治疗对新生、幼年及成年子代中由卡巴胆碱、去甲肾上腺素和谷氨酸刺激的磷酸肌醇代谢的影响。
Neurochem Res. 1995 Oct;20(10):1211-16. doi: 10.1007/BF00995385.
3
Methylazoxymethanol (MAM)-induced brain lesion and oral dyskinesia in rats.
甲基偶氮甲醇(MAM)诱导的大鼠脑损伤和口腔运动障碍。
Psychopharmacology (Berl). 1990;100(1):72-6. doi: 10.1007/BF02245793.
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Increased uptake sites for serotonin and dopamine with decreased S2 serotonin receptors in microencephalic rat brain.小头畸形大鼠大脑中5-羟色胺和多巴胺摄取位点增加,而5-羟色胺S2受体减少。
Neurochem Res. 1990 Oct;15(10):1017-22. doi: 10.1007/BF00965748.
5
Cholinergic hyperinnervation in the cerebral cortex of microencephalic rats does not result in muscarinic receptor down-regulation or in alteration of receptor-stimulated phosphoinositide metabolism.小头畸形大鼠大脑皮质中的胆碱能神经支配过强不会导致毒蕈碱受体下调,也不会改变受体刺激的磷酸肌醇代谢。
Neurochem Res. 1992 Aug;17(8):761-6. doi: 10.1007/BF00969009.