Article abstract
Nature Neuroscience 11, 1410 - 1418 (2008)
Published online: 26 October 2008 | doi:10.1038/nn.2215
GABAB receptor activation mediates frequency-dependent plasticity of developing GABAergic synapses
Chun Xu1, Man-xia Zhao1, Mu-ming Poo1,2 & Xiao-hui Zhang1
Abstract
Activity-induced long-term modification of glutamatergic synapses depends on the frequency of synaptic activation. We found that long-term modification of developing rat hippocampal GABAergic synapses that was induced by repetitive coincident pre- and postsynaptic spiking was also frequency dependent. Spiking at 20–50 Hz resulted in synaptic potentiation, whereas spiking at 5 Hz led to synaptic depression. The potentiation was abolished by blocking GABAB receptors (GABABRs), whereas the depression was independent of GABABR activation and could be converted to potentiation by elevating GABABR activity. The potentiation could be attributed to a local postsynaptic increase in Na+/K+/2Cl- co-transporter activity near activated synapses. The activity of postsynaptic Ca2+/calmodulin-dependent protein kinase II was necessary for long-term potentiation of these developing GABAergic synapses and its phosphorylation at Thr286 could be enhanced by activating GABABRs with baclofen. Together with our finding that activation of GABABRs is frequency dependent, these results indicate that postsynaptic GABABR activation mediates frequency-dependent potentiation of developing GABAergic synapses.
- Institute of Neuroscience, State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue-Yang Road Shanghai 200031, China.
- Division of Neurobiology, Department of Molecular & Cell Biology, Helen Wills Neuroscience Institute, University of California Berkeley, 221 LSA, Berkeley, California 94720, USA.
Correspondence to: Mu-ming Poo1,2 e-mail: mpoo@berkeley.edu
Correspondence to: Xiao-hui Zhang1 e-mail: xhzhang@ion.ac.cn
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