An Analysis of Disuse Effects on Central Synapses
| Project/Area Number |
61480107
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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) |
HARADA Yoshio Kyoto University Faculty of Medicine, 医学部, 助手 (30181027)
TAKAHASHI Tomoyuki Kyoto University Faculty of Medicine, 医学部, 講師 (40092415)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1987: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1986: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Keywords | Spinal cord / Motoneurons / Synapses / Plasticity / Disuse / テトロドトキシン / 脊髄 / ラット / 筋紡錘 / EPSP |
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| Research Abstract |
In the mammal, spinal motoneurons receive direct excitatory synaptic inputs from Group Ia sensory fibers arising from muscle spindles. The efficiency of this synapse can be quantified in terms of the mean amplitude of monosynaptic excitatory postsynaptic potentials (EPSPs) recoeded from motoneurons with intracellular electrodes in response to stimulation of a muscle nerve. When a muscle nerve is sectioned in the rat, monosynaptic EPSPs evoked by stimulation of the muscle nerve show a transient enhancement for a few days but are significantly depressed in a few weeks. The mechanisms underlying these two phenomena which occur with different latencies have been investigated. When the conduction of a peripheral nerve was blocked with the local application of tetrodotoxin for a few days, the monosynaptic EPSPs elicited by stimulation of the peripheral nerve were significantly enhanced. This plastic change at Ia synapses on motoneurons was maximally expressed by a conduction block of the per
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ipheral nerve for 2 days. Thus, the early enhancement of Ia synaptic transmission in motoneurons observed for a few days after periphral nerve section can be attributed to plastic changes of the synapses induced by the deprivation of sensory impulse activity.
Depression of Ia synaptic transmission observed with a long latency following section of the peripheral nerve proceeded slowly as long as reinnervation by the cut nerve had been prevented. This depression could be restored to normal levels when the cut nerve had been allowed to rein- nervate the muscle. Therefore, this synaptic depression appears to be induced by interruption of the peripheral axonal continuity of sensory fibers. The normal function of sensory neurons is known to be maintained by nerve growth factor (NGF) supplied from the target tissue. There- fore, NGF was daily applied to neonatal rats after crushing the peripheral nerve on the day after birth. This treatment significantly prevented depression of Ia synaptic transmission expected to occur after the peripheral nerve injury. Thus, it is concluded that depression of Ia synaptic transmission produced by peripheral nerve section is due to interruption of NGF or an analogous trophic supply from the target tissue to the sensory neurons. Less
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Report
(2 results)
Research Products
(10 results)
