1992 Fiscal Year Final Research Report Summary
Long term potentiation of paintransmission at the spinal level
| Project/Area Number |
03670096
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
YOSHIOKA Koichi Faculty of Medicine, Tokyo Medical and Dental University, Associate Professor, 医学部, 助教授 (00143579)
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| Project Period (FY) |
1991 – 1992
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| Keywords | substance P / tachykinins / spinal cord / pain / serotonin |
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| Research Abstract |
1. Transmitter mechanisms of a long-lasting inhibition of the monosynaptic reflex (MSR)induced by stimulation of the descending pathway was investigated in the isolated spinal cord of the neonatal rat. The descending inhibition was markedly potentiated by a 5-hydroxytryptamine (5-HT) uptake blocker and was blocked by a 5-HT antagonist, suggesting the involvement of 5-HT in this inhibition.
2. The mechanisms of a cutaneous nerve-evoked inhibition of MSR were studied in the spinal cord-peripheral nerve preparation. Conditioning stimulation of the saphenous nerve evoked an inhibition of the MSR. This inhibition was potentiated by an anticholinesterase and almost completely blocked by atropine. From the effects of muscarinic agonists and antagonists, it was suggested that the receptors involved in the inhibition of MSR are of M2 type.
3. A possible mechanism of inactivation of tachykinins released from nerve terminals is enzymatic degradation. To investigate this possibility, effect of peptidase inhibitors on C-fiber evoked responses was examined using an isolated spinal cord-saphenous nerve preparation of the newborn rat. A slow depolarization of the L3 ventral root evoked by the saphenous nerve stimulation was enhanced by application of a mixture of peptidase inhibitors in the presence of naloxone. This result suggests that enzymatic degradation plays a physiological role in termination of neurotransmitter action of tachykinins.
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