Calcium-activated release of nitric oxide potentiates excitatory synaptic potentials in immature rat sympathetic preganglionic neurons.
Calcium-activated release of nitric oxide potentiates excitatory synaptic potentials in immature rat sympathetic preganglionic neurons.
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钙激活的一氧化氮的释放增强了未成熟大鼠交感神经节前神经元的兴奋性突触电位。
DOI：
10.1152/jn.1995.74.6.2600
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Dun,NJ
中科院分区：
文献类型：
--
作者：
Wu,SY;Dun,NJ
1. 对12 ~ 16日龄大鼠横断脊髓切片中大部分含有脑一氧化氮合酶的交感神经节前神经元（SPNs）进行全细胞膜片记录。2. 在去极化电流脉冲（40 Hz. 10 s）诱导的spn重复放电后，75个spn中有50个的侧索刺激引起的兴奋性突触后电位（epsp）振幅持续增加（140 +/- 22%，平均+/- SD）。3. 在用一氧化氮合酶抑制剂ng -单甲基- l-精氨酸（L-NMA: 100微米）或nw -硝基- l-精氨酸（L-NARG； 30微米）或牛血红蛋白（100微米）预处理的切片中，重复放电spn后epsp没有显著增加。4. 用l -精氨酸（L-Arg， 300微米）而不是D-Arg对切片进行超级处理，可使EPSPs平均可逆提高140 +/- 19%。5. 在膜片电极中加入Ca2+螯合剂1.2-双（2-氨基苯氧基）-乙烷-N，N，N‘，N’-四乙酸（BAPTA, 1 mM）后，在所研究的所有细胞中重复放电后，epsp没有显著增加。6. 结果表明，在spn反复放电过程中，Ca2+通过电压门控通道内流激活bNOS，导致一氧化氮的释放和epsp的增强。
1. Whole cell patch recordings were made from sympathetic preganglionic neurons (SPNs), the majority of which contain brain nitric oxide synthase (bNOS), in transverse spinal cord slices of 12- to 16-day-old rats. 2. Repetitive discharge of SPNs induced by a train of depolarizing current pulses (40 Hz. 10 s) was followed by a long-lasting increase (140 +/- 22%, mean +/- SD) of the amplitude of excitatory postsynaptic potentials (EPSPs) evoked by stimulation of lateral funiculus in 50 of 75 SPNs. 3. In slices pretreated with the nitric oxide synthase inhibitors, NG-monomethyl-L-arginine (L-NMA: 100 microM) or Nw-nitro-L-arginine (L-NARG; 30 microM) or with bovine hemoglobin (100 microM), repetitive discharge of SPNs was not followed by a significant increase of EPSPs. 4. Superfusing the slices with L-arginine (L-Arg, 300 microM) but not D-Arg reversibly increased the EPSPs by an average of 140 +/- 19%. 5. Inclusion of the Ca2+ chelator 1.2-bis(2-aminophenoxy)- ethane-N,N,N',N'-tetraacetic acid (BAPTA, 1 mM) in the patch electrodes resulted in no significant increase of EPSPs after repetitive discharge in all cells studied. 6. It is concluded that during repetitive discharge of SPNs, Ca2+ influx via voltage-gated channels activates bNOS, resulting in a release of nitric oxide and potentiation of EPSPs.