通过毒蕈碱受体激活对大鼠海马体突触传递的突触前抑制：突触前钙内流的参与

Presynaptic inhibition of synaptic transmission in the rat hippocampus by activation of muscarinic receptors: involvement of presynaptic calcium influx.

作者信息

Qian J, Saggau P

机构信息

Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, U.S.A.

出版信息

Br J Pharmacol. 1997 Oct;122(3):511-9. doi: 10.1038/sj.bjp.0701400.

DOI:10.1038/sj.bjp.0701400

PMID:9351508

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1564959/

Abstract

Modulation of presynaptic voltage-dependent calcium channels (VDCCs) by muscarinic receptors at the CA3-CA1 synapse of rat hippocampal slices was investigated by using the calcium indicator fura-2. Stimulation-evoked presynaptic calcium transients ([Ca(pre)]t) and field excitatory postsynaptic potentials (fe.p.s.ps) were simultaneously recorded. The relationship between presynaptic calcium influx and synaptic transmission was studied. 2. Activation of muscarinic receptors inhibited [Ca(pre)]t, thereby reducing synaptic transmission. Carbachol (CCh, 10 microM) inhibited [Ca(pre)]t by 35% and reduced fe.p.s.p. by 85%. The inhibition was completely antagonized by 1 microM atropine. An approximate 4th power relationship was found between presynaptic calcium influx and postsynaptic responses. 3. Application of the N-type VDCC-blocking peptide toxin omega-conotoxin GVIA (omega-CTx GVIA, 1 microM) inhibited [Ca(pre)]t and fe.p.s.ps by 21% and 49%, respectively, while the P/Q-type VDCC blocker omega-agatoxin IVA (omega)-Aga IVA, 1 microM) reduced [Ca(pre)]t and fe.p.s.ps by 35% and 85%, respectively. 4. Muscarinic receptor activation differentially inhibited distinct presynaptic VDCCs. Omega-CTx GVIA-sensitive calcium channels were inhibited by muscarinic receptors, while omega-Aga IVA-sensitive channels were not. The percentage inhibition of omega-CTx GVIA-sensitive [Ca(pre)]t was about 63%. 5. Muscarinic receptors inhibited presynaptic VDCCs in a way similar to adenosine (Ad) receptors. The percentage inhibition of omega-CTx GVIA-sensitive [Ca(pre)]t by Ad (100 microM) was about 59%. There was no significant inhibition of omega-Aga IVA-sensitive channels by Ad. The inhibitions of [Ca(pre)]t by CCh and Ad were mutually occlusive. 6. These results indicate that inhibition of synaptic transmission by muscarinic receptors is mainly the consequence of a reduction of the [Ca(pre)]t due to inhibition of presynaptic VDCCs.

摘要

通过使用钙指示剂fura-2，研究了毒蕈碱受体对大鼠海马脑片CA3-CA1突触处突触前电压依赖性钙通道（VDCCs）的调节作用。同时记录刺激诱发的突触前钙瞬变（[Ca(pre)]t）和场兴奋性突触后电位（fe.p.s.ps）。研究了突触前钙内流与突触传递之间的关系。2. 毒蕈碱受体的激活抑制了[Ca(pre)]t，从而降低了突触传递。卡巴胆碱（CCh，10 microM）抑制[Ca(pre)]t达35%，并使fe.p.s.p降低85%。1 microM阿托品可完全拮抗这种抑制作用。发现突触前钙内流与突触后反应之间存在近似四次方关系。3. 应用N型VDCC阻断肽毒素ω-芋螺毒素GVIA（ω-CTx GVIA，1 microM）分别抑制[Ca(pre)]t和fe.p.s.ps达21%和49%，而P/Q型VDCC阻断剂ω-阿加毒素IVA（ω-Aga IVA，1 microM）分别使[Ca(pre)]t和fe.p.s.ps降低35%和85%。4. 毒蕈碱受体激活差异性地抑制不同的突触前VDCCs。毒蕈碱受体抑制ω-CTx GVIA敏感的钙通道，而ω-Aga IVA敏感的通道不受抑制。ω-CTx GVIA敏感的[Ca(pre)]t的抑制百分比约为63%。5. 毒蕈碱受体以类似于腺苷（Ad）受体的方式抑制突触前VDCCs。Ad（100 microM）对ω-CTx GVIA敏感的[Ca(pre)]t的抑制百分比约为59%。Ad对ω-Aga IVA敏感的通道无明显抑制作用。CCh和Ad对[Ca(pre)]t的抑制作用相互重叠。6. 这些结果表明，毒蕈碱受体对突触传递的抑制主要是由于抑制突触前VDCCs导致[Ca(pre)]t降低的结果。

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通过毒蕈碱受体激活对大鼠海马体突触传递的突触前抑制：突触前钙内流的参与

Presynaptic inhibition of synaptic transmission in the rat hippocampus by activation of muscarinic receptors: involvement of presynaptic calcium influx.

作者信息

Qian J, Saggau P

机构信息

Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, U.S.A.

出版信息

Br J Pharmacol. 1997 Oct;122(3):511-9. doi: 10.1038/sj.bjp.0701400.

DOI:10.1038/sj.bjp.0701400

PMID:9351508

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1564959/

Abstract

Modulation of presynaptic voltage-dependent calcium channels (VDCCs) by muscarinic receptors at the CA3-CA1 synapse of rat hippocampal slices was investigated by using the calcium indicator fura-2. Stimulation-evoked presynaptic calcium transients ([Ca(pre)]t) and field excitatory postsynaptic potentials (fe.p.s.ps) were simultaneously recorded. The relationship between presynaptic calcium influx and synaptic transmission was studied. 2. Activation of muscarinic receptors inhibited [Ca(pre)]t, thereby reducing synaptic transmission. Carbachol (CCh, 10 microM) inhibited [Ca(pre)]t by 35% and reduced fe.p.s.p. by 85%. The inhibition was completely antagonized by 1 microM atropine. An approximate 4th power relationship was found between presynaptic calcium influx and postsynaptic responses. 3. Application of the N-type VDCC-blocking peptide toxin omega-conotoxin GVIA (omega-CTx GVIA, 1 microM) inhibited [Ca(pre)]t and fe.p.s.ps by 21% and 49%, respectively, while the P/Q-type VDCC blocker omega-agatoxin IVA (omega)-Aga IVA, 1 microM) reduced [Ca(pre)]t and fe.p.s.ps by 35% and 85%, respectively. 4. Muscarinic receptor activation differentially inhibited distinct presynaptic VDCCs. Omega-CTx GVIA-sensitive calcium channels were inhibited by muscarinic receptors, while omega-Aga IVA-sensitive channels were not. The percentage inhibition of omega-CTx GVIA-sensitive [Ca(pre)]t was about 63%. 5. Muscarinic receptors inhibited presynaptic VDCCs in a way similar to adenosine (Ad) receptors. The percentage inhibition of omega-CTx GVIA-sensitive [Ca(pre)]t by Ad (100 microM) was about 59%. There was no significant inhibition of omega-Aga IVA-sensitive channels by Ad. The inhibitions of [Ca(pre)]t by CCh and Ad were mutually occlusive. 6. These results indicate that inhibition of synaptic transmission by muscarinic receptors is mainly the consequence of a reduction of the [Ca(pre)]t due to inhibition of presynaptic VDCCs.

摘要

通过使用钙指示剂fura-2，研究了毒蕈碱受体对大鼠海马脑片CA3-CA1突触处突触前电压依赖性钙通道（VDCCs）的调节作用。同时记录刺激诱发的突触前钙瞬变（[Ca(pre)]t）和场兴奋性突触后电位（fe.p.s.ps）。研究了突触前钙内流与突触传递之间的关系。2. 毒蕈碱受体的激活抑制了[Ca(pre)]t，从而降低了突触传递。卡巴胆碱（CCh，10 microM）抑制[Ca(pre)]t达35%，并使fe.p.s.p降低85%。1 microM阿托品可完全拮抗这种抑制作用。发现突触前钙内流与突触后反应之间存在近似四次方关系。3. 应用N型VDCC阻断肽毒素ω-芋螺毒素GVIA（ω-CTx GVIA，1 microM）分别抑制[Ca(pre)]t和fe.p.s.ps达21%和49%，而P/Q型VDCC阻断剂ω-阿加毒素IVA（ω-Aga IVA，1 microM）分别使[Ca(pre)]t和fe.p.s.ps降低35%和85%。4. 毒蕈碱受体激活差异性地抑制不同的突触前VDCCs。毒蕈碱受体抑制ω-CTx GVIA敏感的钙通道，而ω-Aga IVA敏感的通道不受抑制。ω-CTx GVIA敏感的[Ca(pre)]t的抑制百分比约为63%。5. 毒蕈碱受体以类似于腺苷（Ad）受体的方式抑制突触前VDCCs。Ad（100 microM）对ω-CTx GVIA敏感的[Ca(pre)]t的抑制百分比约为59%。Ad对ω-Aga IVA敏感的通道无明显抑制作用。CCh和Ad对[Ca(pre)]t的抑制作用相互重叠。6. 这些结果表明，毒蕈碱受体对突触传递的抑制主要是由于抑制突触前VDCCs导致[Ca(pre)]t降低的结果。

通过毒蕈碱受体激活对大鼠海马体突触传递的突触前抑制：突触前钙内流的参与

Presynaptic inhibition of synaptic transmission in the rat hippocampus by activation of muscarinic receptors: involvement of presynaptic calcium influx.

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通过毒蕈碱受体激活对大鼠海马体突触传递的突触前抑制：突触前钙内流的参与

Presynaptic inhibition of synaptic transmission in the rat hippocampus by activation of muscarinic receptors: involvement of presynaptic calcium influx.

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机构信息

出版信息