科研之友
微信
新浪微博
Facebook
分享链接
摘要
The alpha(1)-adrenoceptor agonist phenylephrine and the beta-adrenoceptor agonist isoproterenol have opposite effects on evoked EPSPs (eEPSPs) in the cerebral cortex. The suppressive effects of phenylephrine on eEPSPs are mediated by modulation of postsynaptic glutamate receptors, whereas enhancement of eEPSPs by isoproterenol is due to facilitation of glutamate release from presynaptic terminals. The present study used whole-cell patch-clamp recordings from layer V pyramidal neurons in visuocortical slice preparations to assess the effects of phenylephrine and isoproterenol on the release probability of.-aminobutyric acid (GABA). The present study recorded evoked inhibitory postsynaptic potentials (eIPSCs) by repetitive electrical stimulation (duration, 100 s; 10 stimuli at 33 Hz) and miniature IPSCs (mIPSCs). The effects of phenylephrine (100 mu M) depended on the amplitude of eIPSCs: phenylephrine decreased the paired-pulse ratios (PPRs) of eIPSCs with smaller amplitudes (%26lt;similar to 600 pA) but increased PPRs of eIPSCs with larger amplitude. Phenylephrine also exhibited amplitude-dependent modulation of mIPSCs, i.e., an increase in the frequency of smaller mIPSC events (%26lt;similar to 20 pA) and a decrease in the frequency of larger events. These findings suggest that alpha(1)-adrenoceptor activation facilitates GABA release from a subpopulation of GABAergic terminals that induce smaller-amplitude IPSCs in postsynaptic neurons. In contrast, isoproterenol (100 M) consistently decreased the PPR of eIPSCs and increased the frequency of mIPSCs, suggesting that presynaptic beta-adrenoceptors increase release probability from most GABAergic terminals. The complexity of adrenoceptor modulations in GABAergic synaptic transmission by alpha(1)-adrenoceptor and beta-adrenoceptor activation may be due to the presence of pleiotropic subtypes of GABAergic interneurons in the cerebral cortex.
- 出版日期2014-3
