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体内药物诱导的神经末梢和非神经末梢γ-氨基丁酸池增加之间的解离。

Dissociation between drug-induced increases in nerve terminal and non-nerve terminal pools of GABA in vivo.

作者信息

Iadarola M J, Gale K

出版信息

Eur J Pharmacol. 1979 Oct 26;59(1-2):125-9. doi: 10.1016/0014-2999(79)90034-7.

Abstract

To examine whether increased GABA levels produced by n-dipropylacetate (DPA) and amino-oxyacetic acid (AOAA) are associated with nerve terminals, we compared the effect of these drugs on the GABA content of substantia nigra (SN) in rats in which the GABAergic afferent projections to SN had been unilaterally destroyed. In the SN largely devoid of GABAergic nerve terminals, AOAA (30 mg/kg) produced a 2-fold increase in GABA, whereas DPA (300 mg/kg) was without effect. Since DPA and AOAA both increased GABA to a similar extent in the intact SN, it appears that the GABA increase produced by DPA is associated with GABAergic nerve terminals, while AOAA primarily elevates GABA in non-nerve terminal components (neural perikarya and glial cells) which are not destroyed by our lesions.

摘要

为了研究二丙基乙酸(DPA)和氨氧基乙酸(AOAA)所引起的γ-氨基丁酸(GABA)水平升高是否与神经末梢有关,我们比较了这些药物对大鼠黑质(SN)中GABA含量的影响,这些大鼠的SN的GABA能传入投射已被单侧破坏。在基本没有GABA能神经末梢的SN中,AOAA(30毫克/千克)使GABA增加了2倍,而DPA(300毫克/千克)则没有作用。由于DPA和AOAA在完整的SN中都能使GABA升高到相似的程度,因此似乎DPA所引起的GABA升高与GABA能神经末梢有关,而AOAA主要是使未被我们的损伤破坏的非神经末梢成分(神经周核和神经胶质细胞)中的GABA升高。

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