1988 Fiscal Year Final Research Report Summary
Development of the technique for recording ionic currents at motor nerve terminals
| Project/Area Number |
62870004
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| Research Category |
Grant-in-Aid for Developmental Scientific Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Kyoto University |
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Principal Investigator |
KUNO Motoi Kyoto University Faculty of Medicine, 医学部, 教授 (50142295)
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| Co-Investigator(Kenkyū-buntansha) |
YAWO Hiromu Kyoto University Faculty of Medicine, 医学部, 教授 (00144353)
TAKAHASHI Tomoyuki Kyoto University Faculty of Medicine, 医学部, 教授 (40092415)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Neuromuscular junctions / Nerve terminals / Sprouting / Ionic channels / Plasticity / CGRP |
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| Research Abstract |
Nerve terminals are the site of growth or the formation of sprouts as well as the site of transmitter release. Therefore, nerve terminals are expected to have different ionic mechanisms from those for nerve fibers. However, the analysis of ionic mechanisms is difficult at nerve terminals because of their minute structure. In the present study, attempts were made to record local ionic currents from motor nerve terminals by the technique of loose-patch clamp and to expand the nerve terminal by the formation of terminal sprouts. During the course of this study, it was accidentally found that the formation of sprouts in motor nerve terminals is inhibited by calcitonin gene-related peptide (CGRP). Consequently, the study was further extended to analyze the mechanisms opf plastic changes at neuromuscular junctions. The experiments were made in abult rats. Under the visual control with Nomarski's optics, a microelectrode was firmyl placed on the surface of a motor nerve terminal in the extens
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or digitorum muscle dissected from the hind limb. In response to nerve stimulation, the motor nerve terminal showed a tetrodotoxin-sensitive inward sodium current followed by an outward potassium current. When the potassium current was blocked, the umderlying inward calcium current was also unmasked. When sprouts were formed in motor nerve terminals by chronic conduction block of the sciatic nerve, a similar inward sodium current was also detected in the terminal sprouts. The conduction velocity at terminal sprouts was about 0.2 m/sec. When CGRP was daily applied to the snimal curing the 10-day-period of conduction block of the sciatic nerve, the formation of terminal sprouts expected in the paralyzed hind limb muscle was almost completely inhibited. To our knowledge, CGRP is the first substance which is identified to inhibit the formation of terminal sprouts. In the past, an increase of transmitter release in the paralyzed muscle has been assumed to be due to the formation of terminal sprouts. However,CGRP did not prevent increased transnitter release in the paralyzed muscle, while the formation of terminal sprouts was blocked in the muscle. It is concluded that an increase in transmitter release and the formation of terminal sprouts observed in chronically paralyzed muscle are two independent processes. Less
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