Haul S, Gödecke A, Schrader J, Haas H L, Luhmann H J
Institute of Neurophysiology, University of Düsseldorf, D-40001 Dusseldorf, Germany.
J Neurophysiol. 1999 Feb;81(2):494-7. doi: 10.1152/jn.1999.81.2.494.
The role of the possible retrograde messenger nitric oxide (NO) in the induction of long-term potentiation (LTP) was studied in supragranular layers of somatosensory cortical slices obtained from adult mice. High-frequency stimulation produced a slowly rising, long-lasting (50 min) and significant (P < 0.001) increase in the extracellular synaptic response by 23%. The induction of LTP was independent from activation of N-methyl-D-aspartate (NMDA) receptors, but prevented by bath application of NG-nitro-L-arginine methyl ester (L-NAME), indicating that one or several of the different NO synthases (NOS) produced NO within the postsynaptic neuron. No LTP could be induced in knockout mice lacking the endothelial NOS (eNOS) isoform. These data suggest that eNOS is involved in an NMDA receptor-independent form of LTP in the rodent cerebral cortex.
在从成年小鼠获取的体感皮层切片的颗粒上层中，研究了可能的逆行信使一氧化氮（NO）在长时程增强（LTP）诱导中的作用。高频刺激使细胞外突触反应缓慢上升、持续时间长（50分钟）且显著增加（P < 0.001），增幅达23%。LTP的诱导独立于N-甲基-D-天冬氨酸（NMDA）受体的激活，但通过浴槽应用NG-硝基-L-精氨酸甲酯（L-NAME）可阻止其诱导，这表明一种或几种不同的一氧化氮合酶（NOS）在突触后神经元内产生了NO。在缺乏内皮型NOS（eNOS）亚型的基因敲除小鼠中无法诱导出LTP。这些数据表明，eNOS参与了啮齿动物大脑皮层中一种不依赖NMDA受体的LTP形式。
