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豚鼠海马锥体细胞中依赖代谢型谷氨酸受体激活的兴奋性突触电位

Excitatory synaptic potentials dependent on metabotropic glutamate receptor activation in guinea-pig hippocampal pyramidal cells.

作者信息

Bianchi R, Wong R K

机构信息

Department of Pharmacology, State University of New York Health Science Center, Brooklyn 11203, USA.

出版信息

J Physiol. 1995 Sep 15;487 ( Pt 3)(Pt 3):663-76. doi: 10.1113/jphysiol.1995.sp020908.

Abstract
  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.
摘要
  1. 在豚鼠海马切片中对CA1和CA3神经元进行细胞内和细胞外记录,以研究依赖于代谢型谷氨酸受体(mGluRs)的突触活动。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)-丙基-1-膦酸,以及印防己毒素)存在的情况下,4-氨基吡啶引发长串活动。α-树眼镜蛇毒素也能引发长串活动。3. 长串活动由5至25秒的去极化以及叠加的动作电位组成,有节奏地间隔1至20分钟出现。长串活动在一群CA3神经元中产生,同步输出在CA1细胞中引发长串活动。CA1细胞中长串活动背后的去极化电位的反转电位为-14.8±5.1毫伏。4. CA1神经元中与长串活动相关的去极化被局部应用L-(+)-2-氨基-3-膦丙酸(L-AP3)以及苯基甘氨酸衍生物(+)-α-甲基-4-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)所抑制。应用(-)-MCPG或阿托品不影响与长串活动相关的去极化。5. 浴灌流(+)-MCPG(0.5毫摩尔)、S-4CPG(0.5毫摩尔)、S-4C3HPG(0.5毫摩尔)或L-AP3(1毫摩尔)可阻断长串活动的发生。6. 结果表明,与长串活动相关的去极化是依赖于mGluR激活的突触电位。mGluRs的激活可能也参与了CA3区域同步长串活动的产生。

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