首页> 美国卫生研究院文献>The Journal of Physiology >Excitatory synaptic potentials dependent on metabotropic glutamate receptor activation in guinea-pig hippocampal pyramidal cells.
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Excitatory synaptic potentials dependent on metabotropic glutamate receptor activation in guinea-pig hippocampal pyramidal cells.

机译:兴奋性突触电位取决于豚鼠海马锥体细胞中代谢型谷氨酸受体的活化。

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摘要

1. Intracellular and extracellular recordings of CA1 and CA3 neurones were performed in guinea-pig hippocampal slices to examine synaptic activities dependent on metabotropic glutamate receptors (mGluRs). 2. Long burst activities were elicited by 4-aminopyridine in the presence of ionotropic glutamate receptor and GABAA receptor blockers (6-cyano-7-nitroquinoxaline-2,3-dione and 3-(RS-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, and picrotoxin). Long bursts were also elicited by alpha-dendrotoxin. 3. Long bursts consisted of a 5-25 s depolarization with overriding action potentials and occurred rhythmically at intervals ranging from 1 to 20 min. Long bursts were generated in a population of CA3 neurones and the synchronized output elicited long bursts in CA1 cells. Depolarizing potentials underlying long bursts in CA1 cells had a reversal potential of -14.8 +/- 5.1 mV. 4. Long burst-associated depolarizations in CA1 neurones were suppressed by local application of L-(+)-2-amino-3-phosphonopropionic acid (L-AP3) and of the phenylglycine derivatives (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), S-4-carboxyphenylglycine (S-4CPG) and S-4-carboxy-3-hydroxyphenylglycine (S-4C3HPG). (-)-MCPG or atropine application did not affect the long burst-associated depolarization. 5. Bath perfusion of (+)-MCPG (0.5 mM), S-4CPG (0.5 mM), S-4C3HPG (0.5 mM) or L-AP3 (1 mM) blocked the occurrence of long bursts. 6. The results suggest that the long burst-associated depolarizations are synaptic potentials dependent on mGluR activation. Activation of mGluRs may also be involved in the generation of synchronized long bursts in the CA3 region.
机译:1.在豚鼠海马切片中进行CA1和CA3神经元的细胞内和细胞外记录,以检查依赖于代谢型谷氨酸受体(mGluRs)的突触活性。 2.在离子型谷氨酸受体和GABAA受体阻滞剂(6-氰基-7-硝基喹喔啉-2,3-二酮和3-(RS-2-羧基哌嗪-4-基))存在下,4-氨基吡啶引起长时间爆发活性。 -丙基-1-膦酸和微毒素)。 α-树突毒素也引起长时间爆发。 3.长爆发包括5-25 s的去极化作用,并具有压倒性的动作电位,并有节奏地以1至20分钟的间隔发生。在CA3神经元群体中产生了长脉冲,并且同步输出在CA1细胞中引起了长脉冲。 CA1细胞长时间爆发后的去极化电位的反向电位为-14.8 +/- 5.1 mV。 4.通过局部应用L-(+)-2-氨基-3-膦酸丙酸(L-AP3)和苯基甘氨酸衍生物(+)-α-甲基-4-抑制了CA1神经元中的长脉冲相关去极化羧基苯基甘氨酸((+)-MCPG),S-4-羧基苯基甘氨酸(S-4CPG)和S-4-羧基-3-羟基苯基甘氨酸(S-4C3HPG)。 (-)-MCPG或阿托品的应用不会影响与长脉冲有关的去极化。 5.(+)-MCPG(0.5 mM),S-4CPG(0.5 mM),S-4C3HPG(0.5 mM)或L-AP3(1 mM)的浴灌注阻止了长脉冲的发生。 6.结果表明,长猝发相关的去极化是依赖于mGluR激活的突触电位。 mGluR的激活也可能参与CA3区域中同步长脉冲的产生。

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