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首页> 外文期刊>Japanese Journal of Pharmacology >IMPAIRED MATURATION OF PRE-SYNAPTIC CHOLINERGIC NERVE TERMINALS IN THE SUPERIOR CERVICAL GANGLIA AFTER ADMINISTRATION OF GUANETHIDINE AND DEXAMETHASONE
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IMPAIRED MATURATION OF PRE-SYNAPTIC CHOLINERGIC NERVE TERMINALS IN THE SUPERIOR CERVICAL GANGLIA AFTER ADMINISTRATION OF GUANETHIDINE AND DEXAMETHASONE

机译:胍和地塞米松给药后颈上神经节突触前胆碱能神经终末的受损。

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References(21) Cited-By(1) The role of post-synaptic cells in the development of pre-synaptic cholinergic nerve terminals has been investigated in immature rat superior cervical ganglia (SCG) and adrenals employing chemical agents which prevent the normal maturation of postsynaptic cells. A marked atrophy of ganglion adrenergic neurons after guanethidine administration was accompanied by the complete failure of normal maturation of choline acetyltransferase (ChAc) activity in the presynaptic endings. However, the same treatment failed to alter the levels of ChAc in the mature ganglia despite the marked atrophy of adrenergic neurons. Administration of dexamethasone resulted in a growth retardation of ganglion neurons as well as adrenal chromaffin cells reflected by the lower levels of tyrosine hydroxylase and dopamine-, β-hydroxylase than those in untreated tissues. The levels of ChAc were significantly lower in the ganglia, but not in the adrenals when treatment was started immediately after birth. These results support the view that the normal synapse formation in the SCG depends on the normal maturation of adrenergic neurons, and suggest that this dependence is detectable only during a limited period of life.
机译:参考文献(21)被引用(1)在未成熟大鼠上颈神经节(SCG)和肾上腺中使用化学试剂阻止突触后细胞正常成熟,研究了突触后细胞在突触前胆碱能神经末梢发育中的作用。突触后细胞。胍乙啶给药后神经节肾上腺素能神经元明显萎缩,伴随着突触前末期胆碱乙酰转移酶(ChAc)活性的正常成熟完全失败。然而,尽管肾上腺素能神经元明显萎缩,但相同的治疗方法并不能改变成熟神经节中ChAc的水平。地塞米松的给药导致神经节神经元以及肾上腺嗜铬细胞的生长迟缓,这是由于酪氨酸羟化酶和多巴胺,β-羟化酶的水平低于未治疗组织中的水平。出生后立即开始治疗时,神经节中ChAc的水平显着降低,但肾上腺中的水平不明显。这些结果支持这样的观点,即SCG中正常突触的形成取决于肾上腺素能神经元的正常成熟,并表明这种依赖性仅在生命的有限时期内可检测到。

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