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The Journal of Neuroscience, October 12, 2005, 25(41):9378-9383; doi:10.1523/JNEUROSCI.2100-05.2005

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Neuregulin-1 Reverses Long-Term Potentiation at CA1 Hippocampal Synapses

Oh-Bin Kwon,^1 * Marines Longart,^1 * Detlef Vullhorst,¹ Dax A. Hoffman,² and Andres Buonanno¹

¹Section on Molecular Neurobiology and ²Unit on Molecular Neurophysiology and Biophysics, National Institute of Child Health and Human Development-National Institutes of Health, Bethesda, Maryland 20892-3714

Neuregulin-1 (NRG-1) has been identified genetically as a schizophrenia susceptibility gene, but its function in the adult brain is unknown. Here, we show that NRG-1 does not affect basal synaptic transmission but reverses long-term potentiation (LTP) at hippocampal Schaffer collateralCA1 synapses in an activity- and time-dependent manner. Depotentiation by NRG-1 is blocked by two structurally distinct and selective ErbB receptor tyrosine kinase inhibitors. Moreover, ErbB receptor inhibition increases LTP at potentiated synapses and blocks LTP reversal by theta-pulse stimuli. NRG-1 selectively reduces AMPA, not NMDA, receptor EPSCs and has no effect on paired-pulse facilitation ratios. Live imaging of hippocampal neurons transfected with receptors fused to superecliptic green fluorescent protein, as well as quantitative analysis of native receptors, show that NRG-1 stimulates the internalization of surface glutamate receptor 1-containing AMPA receptors. This novel regulation of LTP by NRG-1 has important implications for the modulation of synaptic homeostasis and schizophrenia.

Key words: neuregulin; depotentiation; ErbB receptor; LTP; LTD; schizophrenia; superecliptic GFP

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Received May 24, 2005; revised September 2, 2005; accepted September 2, 2005.

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