Zilberter Y
Karolinska Institute, Department of Neuroscience, Division of Neuroanatomy and Brain Development, Berzelius v g 3, plan 5, S-17177 Stockholm, Sweden.
J Physiol. 2000 Nov 1;528(Pt 3):489-96. doi: 10.1111/j.1469-7793.2000.00489.x.
Dual whole-cell recordings were made in layer 2/3 of the rat neocortex in synaptically connected pyramidal cells and fast-spiking non-accommodating (FSN) interneurons. In 75% of cell pairs (n = 80), the cells formed reciprocal synaptic connections. Trains of backpropagating action potentials in pyramidal cells induced Ca2+ transients in dendrites followed by inhibition of unitary IPSPs. IPSP depression was prevented by loading pyramidal cells with 5 mM BAPTA or EGTA. IPSP depression was mimicked by the metabotropic glutamate receptor (mGluR) agonist ACPD and was prevented by a mixture of the mGluR antagonists CPCCOEt and EGLU.IPSP depression was prevented by loading pyramidal cells with the antagonists of vesicular exocytosis botulinum toxin D (light chain) and GDP-beta-S. It is concluded that Ca2+-dependent release of a retrograde messenger, most probably glutamate, from pyramidal cell dendrites suppresses the inhibition of pyramidal neurons via activation of mGluRs located in FSN interneuron nerve terminals.
在大鼠新皮层第2/3层的突触连接锥体细胞和快速发放非适应性(FSN)中间神经元中进行了双细胞全细胞膜片钳记录。在75%的细胞对(n = 80)中,细胞形成了相互的突触连接。锥体细胞中的一串反向传播动作电位在树突中诱导Ca2+瞬变,随后抑制单突触IPSP。通过向锥体细胞中加载5 mM BAPTA或EGTA可防止IPSP抑制。代谢型谷氨酸受体(mGluR)激动剂ACPD模拟了IPSP抑制,而mGluR拮抗剂CPCCOEt和EGLU的混合物可防止这种抑制。通过向锥体细胞中加载囊泡胞吐拮抗剂肉毒杆菌毒素D(轻链)和GDP-β-S可防止IPSP抑制。得出的结论是,锥体细胞树突中Ca2+依赖性释放逆行信使,很可能是谷氨酸,通过激活位于FSN中间神经元神经末梢的mGluR来抑制锥体细胞的抑制作用。