Suppression of inhibitory synaptic potentiation by presynaptic activity through postsynaptic GABAB receptors in a Purkinje neuron
Suppression of inhibitory synaptic potentiation by presynaptic activity through postsynaptic GABAB receptors in a Purkinje neuron
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DOI：
10.1016/s0896-6273(00)00041-6
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发表时间：
2000-08-01
期刊：
影响因子：
16.2
通讯作者：
Hirano, T
中科院分区：
文献类型：
--
作者：
Kawaguchi, S;Hirano, T
在小脑浦肯野神经元上的抑制性突触处，异突触攀爬纤维激活引起的去极化诱导了持久的增强，伴随着GABA（A）受体反应性的增加。在这里，我们表明，激活突触前抑制性中间神经元在条件突触后去极化抑制增强。这种抑制是由于突触前末梢释放的GABA激活突触后GABA（B）受体所致。结果表明GABA（B）受体激活通过G（j）/G（o）蛋白降低cAMP依赖性蛋白激酶的活性。突触可塑性的突触前活动依赖性抑制是一种新的调节机制，在个别突触的突触效能，并可能有助于小脑皮质的学习和计算能力。
At inhibitory synapses on a cerebellar Purkinje neuron, the depolarization caused by heterosynaptic climbing fiber activation induces long-lasting potentiation accompanied by an increase in GABA(A) receptor responsiveness. Here we show that activation of a presynaptic inhibitory interneuron during the conditioning postsynaptic depolarization suppresses the potentiation. The suppression is due to postsynaptic GABA(B) receptor activation by GABA released from presynaptic terminals. The results suggest that GABA(B) receptor activation decreases the activity of cAMP-dependent protein kinase through the G(j)/G(o) proteins. The presynaptic activity-dependent suppression of synaptic plasticity is a novel regulatory mechanism of synaptic efficacy at individual synapses and may contribute to the learning and computational ability of the cerebellar cortex.