Dopaminergic and cholinergic regulation of respiratory rhythm and anesthetic respiratory suppression mechanism
| Project/Area Number |
13671595
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Miyazaki Medical College |
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Principal Investigator |
HAMAKAWA Toshiro Miyazaki University, Anesthesiology, Research Associate, 医学部, 助手 (90284835)
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| Co-Investigator(Kenkyū-buntansha) |
HAMAKAWA Toshiro Miyazaki University, Anesthesiology, Assistant Professor, 医学部, 講師 (50253836)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Dopamine / Inhibitory synapse / Excitatory synapse / Lymnaea / Volatile anesthetic / Sevoflurane / D2 receptor / Lymmaea / アセチルコリン |
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| Research Abstract |
In this study, the identified dopaminergic excitatory synapse was reconstructed between the somata of two identified Lymnaea neurons, right pedal dorsal 1 (RPeD1 -the giant dopaminergic neuron ; presynaptic cell) and visceral dorsal, 2/3 (VD2/3 ; postsynaptic cell). Current clamp technique was used to determine whether clinically relevant concentrations (0.5-2%) of sevoflurane could block both the (synaptic) response of VD2/3 to depolarizing currents induced to RPeD land the (non-synaptic) responses of RPeD1 and VD2/3 to exogenously applied dopamine (DA). The application of DA (10 μ M) was directed to the soma-soma superfusing or non-superfusing sites on the synapse. Sevoflurane was found to suppress both synaptic and non synaptic DA responses in VD2/3 (0.5% ;>60%, 2% ;>90%), while weakly suppress the non synaptic DA response response in RPeD1. Sevoflurane's ability to suppress those responses was then comapred with DA antagonists. The D2 antagonist (+-) sulpiride almost completely (>85%) blocked those all responses in RPeD1 and VD2/3, though the general DA antagonist d-tubocurarine did not block only the non synaptic DA response in RPeD1. The effects of all drugs used did not differ the superfusing versus the non-superfusing sites of DA application. Our data demonstrate that sevoflurane-induced suppression of responses on the excitatory synapse between RPeD1 and VD2/3 is predominantly postsynaptic.
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Report
(3 results)
Research Products
(2 results)
