Lambert N A, Wilson W A
Department of Pharmacology, Duke University Medical Center, Durham, North Carolina.
Neuron. 1993 Dec;11(6):1057-67. doi: 10.1016/0896-6273(93)90219-h.
Release of GABA from the terminals of hippocampal inhibitory neurons is inhibited by activation of GABAB autoreceptors and mu opioid receptors. However, it is not known whether these presynaptic processes affect all inhibitory synapses equally. We examined the effects of the GABAB receptor agonist baclofen and the mu opioid receptor agonist DAGO on postsynaptic currents evoked by minimal stimulation of inhibitory fibers (meIPSCs) in area CA3. Baclofen reversibly depressed approximately half of the meIPSCs evoked in the stratum pyramidale. The remaining meIPSCs were unaffected despite a coincident depression of spontaneous IPSCs. In contrast, all meIPSCs were depressed by DAGO. In addition, minimal stimulation in the stratum radiatum evoked meIPSCs that were always depressed by baclofen. These results indicate that regulation of GABA release by GABAB autoreceptors occurs at a subset of inhibitory synapses and that GABAB-resistant inhibitory synapses are located on pyramidal neuron somata. Hippocampal inhibitory neurons may be heterogeneous with respect to presynaptic receptor-mediated regulation of GABA release.
海马抑制性神经元终末释放γ-氨基丁酸(GABA)会受到GABAB自身受体和μ阿片受体激活的抑制。然而,尚不清楚这些突触前过程是否对所有抑制性突触产生同等影响。我们研究了GABAB受体激动剂巴氯芬和μ阿片受体激动剂DAGO对CA3区抑制性纤维最小刺激诱发的突触后电流(微小抑制性突触后电流,meIPSCs)的影响。巴氯芬可逆性地抑制了在锥体层诱发的约一半meIPSCs。尽管自发性抑制性突触后电流(sIPSCs)同时受到抑制,但其余的meIPSCs未受影响。相比之下,所有meIPSCs均被DAGO抑制。此外,在辐射层的最小刺激诱发的meIPSCs总是被巴氯芬抑制。这些结果表明,GABAB自身受体对GABA释放的调节发生在一部分抑制性突触,且对GABAB有抗性的抑制性突触位于锥体神经元胞体上。海马抑制性神经元在突触前受体介导的GABA释放调节方面可能存在异质性。