DISTRIBUTION AND CALCIUM-SEQUESTERING ABILITY OF SMOOTH ENDOPLASMIC-RETICULUM IN OLFACTORY AXON TERMINALS OF FROG BRAIN

DISTRIBUTION AND CALCIUM-SEQUESTERING ABILITY OF SMOOTH ENDOPLASMIC-RETICULUM IN OLFACTORY AXON TERMINALS OF FROG BRAIN
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DOI:
10.1016/0306-4522(87)90297-1
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发表时间:
1987-10-01
期刊:
影响因子:
3.3
通讯作者:
LAVERI, LA
LAVERI, LA
中科院分区:
医学3区
文献类型:
--
作者:
HARTTER, DE;BURTON, PR;LAVERI, LA

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本研究探讨牛蛙嗅神经轴突终末中滑面内质网的结构和功能。从这项研究中获得的结构证据表明,这个泡状管细胞器成为一个更复杂的网络附近的神经末梢,位于嗅叶的青蛙大脑的神经管。进一步的结构证据表明,滑面内质网膜夹断,产生一些直径约50 nm的电子透明囊泡(微泡)。超微结构细胞化学在本研究中,证明嗅轴突末端滑面内质网积极螯合钙。然而,一个变量的电子致密的产品(草酸钙)与微泡位于距离突触,相反,那些聚集在突触附近,通常不包含这种反应产物。Ca 2+,Mg 2 +-腺苷-5“-三磷酸酶(ATP酶)细胞化学的结果显示了相似的分布模式,平滑肌内质网被ATP酶反应产物(磷酸铅)密集标记,但神经末梢中聚集的微泡通常缺乏这种电子致密产物。因此,可以得出结论,嗅觉轴突滑面内质网在调节神经元内的Ca 2+水平中起作用,并且膜细胞器中的Ca 2+螯合活性依赖于ATP的酶水解。相反,微泡,特别是那些聚集在突触附近的微泡,缺乏这种Ca 2+泵送能力。因此,如果一些微泡来源于能够泵送Ca 2+的滑面内质网膜,但这些微泡本身缺乏这种能力,则可以假设Ca 2+泵从新形成的微泡膜中被移除,或者在膜中原位以某种方式丧失能力。
In the present study, the structural and functional role of smooth endoplasmic reticulum was investigated in bullfrog olfactory axon terminals. Structural evidence obtained from this study indicated that this vesiculotubular organelle becomes a more elaborate network of anastomosing tubules near the nerve terminal, located in the olfactory lobe of frog brain. Further structrural evidence suggested that membranes of the smooth endoplasmic reticulum pinch off to give rise to some electron-lucent vesicles of approximately 50- nm diameter (microvesicles). Ultrastructural cytochemistry was employed in the present study to demonstrate that olfactory axon terminal smooth endoplasmic reticulum actively sequesters Ca2+. However, a variable amount of electron-dense product (calcium oxalate) was associated with microvesicles located at a distance from the synapse, in contrast to those clustered near the synapse which usually did not contain this reaction product. Results from Ca2+, Mg2+-adenosine-5''-triphosphatase(ATPase) cytochemistry showed a similar pattern of distribution, with smooth endoplasmic reticulum being densely labeled with ATPase reaction product (lead phosphate), but aggregated microvesicles in the nerve terminal generally lacking this electron-dense product. Therefore, it is concluded that olfactory axonal smooth endoplasmic reticulum plays a role in the regulation of intraneuronal Ca2+ levels, and that the Ca2+-sequestering activity in the membranous organelle is dependent upon enzymatic hydrolysis of ATp. Conversely, the microvesicles, particularly those accumulated near the synapse, lack this Ca2+-pumping capacity. Thus, if some of the microvesicles originate from smooth endoplasmic reticulum membranes which are capable of pumping Ca2+, but these vesicles themselves lack this capacity, one can postulate that the Ca2+ pumps are either removed from the newly formed microvesicle membranes or are somehow incapacitated in situ in the membrane.