Madison D V, Nicoll R A
Department of Pharmacology, University of California, San Francisco 94143.
Brain Res. 1988 Feb 23;442(1):131-8. doi: 10.1016/0006-8993(88)91440-0.
The effects of norepinephrine (NE) on inhibitory synaptic potentials were studied on CA1 pyramidal neurons in the hippocampal slice in vitro. Norepinephrine caused the appearance of multiple population spikes in the CA1 region of the hippocampal slice, reminiscent of the actions of gamma-aminobutyric acid (GABA) antagonists. Intracellular recording revealed that NE causes a marked and reversible reduction in inhibitory postsynaptic potentials (IPSPs) recorded in CA1 pyramidal cells. This reduced IPSP results in a larger intracellular excitatory postsynaptic potential (EPSP), which can cause the cell to fire more than one action potential. This disinhibitory effect of NE appears to be mediated by an alpha-receptor, and occurs at a site presynaptic to the pyramidal cell, since NE does not change the reversal potential of the IPSP nor does it affect the amplitude or the reversal potential of iontophoretic GABA responses. In addition to reducing evoked IPSPs, NE causes an increase in the frequency of spontaneous IPSPs, suggesting that inhibition of interneuronal firing may not account for this disinhibitory action of NE.
在体外海马脑片的CA1锥体神经元上研究了去甲肾上腺素(NE)对抑制性突触电位的影响。去甲肾上腺素导致海马脑片CA1区出现多个群体峰电位,这让人联想到γ-氨基丁酸(GABA)拮抗剂的作用。细胞内记录显示,NE可使CA1锥体细胞中记录到的抑制性突触后电位(IPSP)显著且可逆地降低。这种降低的IPSP会导致更大的细胞内兴奋性突触后电位(EPSP),进而可使细胞产生不止一个动作电位。NE的这种去抑制作用似乎是由α受体介导的,且发生在锥体细胞的突触前部位,因为NE既不改变IPSP的反转电位,也不影响离子电渗法施加GABA反应的幅度或反转电位。除了降低诱发的IPSP外,NE还会增加自发性IPSP的频率,这表明抑制中间神经元放电可能无法解释NE的这种去抑制作用。