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通过向青蛙神经肌肉接头施加高浓度细胞外钾诱导突触小泡的可逆性耗竭。

Reversible depletion of synaptic vesicles induced by application of high external potassium to the frog neuromuscular junction.

作者信息

Gennaro J F, Nastuk W L, Rutherford D T

出版信息

J Physiol. 1978 Jul;280:237-47. doi: 10.1113/jphysiol.1978.sp012382.

Abstract
  1. Reversible depletion of synaptic vesicles from frog cutaneous pectoris neuromuscular junctions was studied by application of a Ringer solution containing 115 mM-K propionate.2. During the release of transmitter, the synaptic vesicle membrane is added to the axolemmal membrane. Under the conditions of high K(+)-induced release, the synaptic vesicle membrane accumulates as folds formed in the region of the axolemmal membrane between the active zones. In depleted terminals, large vesicular structures appear and the evidence shows that some of them (possibly all) are formed as axolemmal infoldings. During formation of such infoldings the active zones remain fixed in position with respect to the post-junctional membrane.3. During recovery in normal Ringer solution, which followed 30 min depolarization in high K(+) Ringer solution, spontaneous m.e.p.p.s were detected as early as 9 min after the start of the recovery period and the average time for their reappearance was 17 min.4. At the end of a 20 min recovery period which followed K(+) depolarization, small accumulations of synaptic vesicles were again found within the terminal close to the active zones. At this time coated vesicles and coated pits were seen associated with the prejunctional axolemma and its infoldings. It appears that synaptic vesicles are re-formed directly from these coated vesicles.5. After 60 min recovery from K(+) depolarization, at which time stimulation of the motor nerve induced a muscle twitch, the structure of the terminals closely resembled that of control preparations.6. The entire synaptic vesicle recycling process can take place in the absence of the neurone soma.
摘要
  1. 通过应用含有115 mM - 丙酸钾的林格氏液,研究了青蛙胸皮神经肌肉接头处突触小泡的可逆性耗竭。

  2. 在递质释放过程中,突触小泡膜会添加到轴突膜上。在高钾诱导释放的条件下,突触小泡膜会在活性区之间的轴突膜区域形成褶皱而积累。在耗竭的终末,会出现大的囊泡结构,证据表明其中一些(可能全部)是由轴突膜内褶形成的。在这种内褶形成过程中,活性区相对于突触后膜的位置保持固定。

  3. 在高钾林格氏液中30分钟去极化后,在正常林格氏液中恢复期间,早在恢复开始后9分钟就检测到自发微小终板电位,其再次出现的平均时间为17分钟。

  4. 在钾离子去极化后的20分钟恢复期结束时,在靠近活性区的终末内再次发现了突触小泡的小聚集。此时,可见被膜小泡和被膜小窝与突触前轴突膜及其内褶相关联。似乎突触小泡是直接从这些被膜小泡重新形成的。

  5. 从钾离子去极化恢复60分钟后,此时刺激运动神经会诱发肌肉抽搐,终末的结构与对照制剂非常相似。

  6. 整个突触小泡循环过程可以在没有神经元胞体的情况下发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24fe/1282657/945476417766/jphysiol00766-0254-a.jpg

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