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树突中酪氨酸羟化酶免疫反应性的丧失是体内海藻酸诱导的大鼠黑质神经元损伤的敏感指标。

Loss of tyrosine hydroxylase immunoreactivity in dendrites is a sensitive index of kainic acid-induced damage in rat substantia nigra neurons in vivo.

作者信息

Bywood P T, Johnson S M

机构信息

Department of Clinical Pharmacology and Centre for Neuroscience, School of Medicine, Flinders University of South Australia, Adelaide, Australia.

出版信息

Neurosci Lett. 2000 Feb 11;280(1):5-8. doi: 10.1016/s0304-3940(99)00990-8.

Abstract

An early indicator of damage to substantia nigra dopamine neurons in vitro is loss of dendrites that precedes loss of the cell body. To investigate dendritic damage in vivo, rats were treated for 1 day or 1 week with kainic acid (KA; 5 or 10 mg/kg i.p.), the brain fixed and substantia nigra (SN) dopamine neurons and their dendrites labeled using an antibody to tyrosine hydroxylase (TH). KA (10 mg/kg) produced seizures initially and resulted in significant loss of TH immunoreactivity in dendrites of dopamine neurons 1 week, but not 1 day, after a single injection. Daily injections of 5 mg/kg KA, which did not produce seizures, resulted in more extensive dendritic damage. The findings indicate that loss of dendritic staining is a sensitive index of damage to SN dopamine neurons in vivo.

摘要

体外黑质多巴胺神经元损伤的一个早期指标是树突的丧失,这发生在细胞体丧失之前。为了研究体内的树突损伤,用海藻酸(KA;5或10mg/kg腹腔注射)对大鼠进行1天或1周的处理,固定大脑,并用抗酪氨酸羟化酶(TH)抗体标记黑质(SN)多巴胺神经元及其树突。单次注射后1周而非1天,10mg/kg的KA最初引发癫痫发作,并导致多巴胺神经元树突中TH免疫反应性显著丧失。每日注射5mg/kg未引发癫痫发作的KA,导致更广泛的树突损伤。这些发现表明,树突染色的丧失是体内SN多巴胺神经元损伤的一个敏感指标。

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