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新生大鼠脚间核树突去传入后躯体突触萌发的定量证明

Quantitative demonstration of somatic synapse sprouting following dendritic deafferentation in neonatal rat interpeduncular nucleus.

作者信息

Lenn N J, Wong V, Hamill G

出版信息

Brain Res Bull. 1979 Nov-Dec;4(6):843-8. doi: 10.1016/0361-9230(79)90021-2.

Abstract

Neonatal habenular lesions deafferent the dendrites of interpeduncular nucleus (IPN) neurons by preventing formation of S and crest synapses. The small number of synapses normally contacting IPN neuronal perikarya are of unknown, but non-habenular, origin. The number of synapses on IPN perikarya is significantly increased (p less than 0.001) when 10 control animals are compared to 7 animals with unilateral habenular lesions and 7 animals with bilateral lesions. The increases with bilateral lesions are approximately twice those resulting from unilateral lesions (p less than 0.01). This phenomenon involves sprouting of both the somatic synapses which contain spherical vesicles and those with flattened vesicle endings, and is greater when the latter are considered alone (p less than 0.001). Only the small group of somatic synapses with asymmetrical contacts failed to show a change. The increases suggest a postsynaptic control mechanism which acts in the direction of preserving synaptic input, but permits displacement of the site of input from dendrites to soma. Factors which may be important in determining this outcome are the production of the lesions prior to synaptogenesis, and the presumed shrinkage of the dendrites of the IPN neurons.

摘要

新生期缰核损伤通过阻止S型和嵴状突触的形成,使脚间核(IPN)神经元的树突传入缺失。正常情况下,与IPN神经元胞体接触的少量突触来源不明,但并非来自缰核。将10只对照动物与7只单侧缰核损伤动物及7只双侧损伤动物进行比较时,IPN胞体上的突触数量显著增加(p<0.001)。双侧损伤导致的增加量约为单侧损伤的两倍(p<0.01)。这种现象涉及含有球形囊泡的体突触和具有扁平囊泡末端的体突触的发芽,单独考虑后者时增加更为明显(p<0.001)。只有一小部分具有不对称接触的体突触没有变化。这些增加表明存在一种突触后控制机制,其作用方向是保留突触输入,但允许输入部位从树突转移到胞体。在决定这一结果中可能重要的因素是在突触形成之前产生损伤,以及IPN神经元树突的假定萎缩。

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