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The Journal of Neuroscience, January 25, 2006, 26(4):1199-1210; doi:10.1523/JNEUROSCI.2964-05.2006

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Development/Plasticity/Repair
Simultaneous NMDA-Dependent Long-Term Potentiation of EPSCs and Long-Term Depression of IPSCs in Cultured Rat Hippocampal Neurons

Miriam Ivenshitz and Menahem Segal

Department of Neurobiology, The Weizmann Institute of Science, Rehovot, 76100, Israel

Correspondence should be addressed to Menahem Segal at the above address. Email: menahem.segal{at}weizmann.ac.il

A fundamental issue in understanding activity-dependent long-term plasticity of neuronal networks is the interplay between excitatory and inhibitory synaptic drives in the network. Using dual whole-cell recordings in cultured hippocampal neurons, we examined synaptic changes occurring as a result of a transient activation of NMDA receptors in the network. This enhanced transient activation led to a long-lasting increase in synchrony of spontaneous activity of neurons in the network. Simultaneous long-term potentiation of excitatory synaptic strength and a pronounced long-term depression of inhibitory synaptic currents (LTDi) were produced, which were independent of changes in postsynaptic potential and Ca²⁺ concentrations. Surprisingly, miniature inhibitory synaptic currents were not changed by the conditioning, whereas both frequency and amplitudes of miniature EPSCs were enhanced. LTDi was mediated by activation of a presynaptic GABA_B receptor, because it was blocked by saclofen and CGP55845 [(2S)-3-{[(15)-1-(3, 4-dichlorophenyl)ethyl]amino-2-hydroxypropyl)(phenylmethyl)phosphinic acid]. The cAMP antagonist Rp-adenosine 3 ', 5 ' -cyclic monophosphothioate abolished all measured effects of NMDA-dependent conditioning, whereas a nitric oxide synthase inhibitor was ineffective. Finally, network-induced plasticity was not occluded by a previous spike-timing-induced plasticity, indicating that the two types of plasticity may not share the same mechanism. These results demonstrate that network plasticity involves opposite affects on inhibitory and excitatory neurotransmission.

Key words: LTP; LTD; NMDA; conditioning; activity-dependent plasticity; culture

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Received Apr. 4, 2005; revised Nov. 8, 2005; accepted Dec. 10, 2005.

Correspondence should be addressed to Menahem Segal at the above address. Email: menahem.segal{at}weizmann.ac.il

This article has been cited by other articles:

				A. Vlachos, E. Korkotian, E. Schonfeld, E. Copanaki, T. Deller, and M. Segal Synaptopodin Regulates Plasticity of Dendritic Spines in Hippocampal Neurons J. Neurosci., January 28, 2009; 29(4): 1017 - 1033. [Abstract] [Full Text] [PDF]

				K. C. Marsden, J. B. Beattie, J. Friedenthal, and R. C. Carroll NMDA Receptor Activation Potentiates Inhibitory Transmission through GABA Receptor-Associated Protein-Dependent Exocytosis of GABAA Receptors J. Neurosci., December 26, 2007; 27(52): 14326 - 14337. [Abstract] [Full Text] [PDF]

				S. Sapoznik, M. Ivenshitz, and M. Segal Age-dependent glutamate induction of synaptic plasticity in cultured hippocampal neurons Learn. Mem., November 1, 2006; 13(6): 719 - 727. [Abstract] [Full Text] [PDF]

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