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The Journal of Neuroscience, September 30, 2009, 29(39):12255-12264; doi:10.1523/JNEUROSCI.2454-09.2009

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Cellular/Molecular
Selective Expression of ErbB4 in Interneurons, But Not Pyramidal Cells, of the Rodent Hippocampus

Detlef Vullhorst,¹ Jörg Neddens,¹ Irina Karavanova,¹ Ludovic Tricoire,² Ronald S. Petralia,³ Chris J. McBain,² and Andres Buonanno¹

¹Section on Molecular Neurobiology and ²Laboratory of Cellular and Molecular Neurophysiology, Eunice Shriver Kennedy National Institute of Child Health and Human Development, and ³Laboratory of Neurochemistry, National Institute on Deafness and other Communication Disorders, Bethesda, Maryland 20892

Correspondence should be addressed to Dr. Andres Buonanno, Section on Molecular Neurobiology, Building 35, Room 2C-1000, 35 Lincoln Drive, National Institutes of Health, Bethesda, MD 20892-3714. Email: buonanno{at}mail.nih.gov

NRG1 and ERBB4 have emerged as some of the most reproducible schizophrenia risk genes. Moreover, the Neuregulin (NRG)/ErbB4 signaling pathway has been implicated in dendritic spine morphogenesis, glutamatergic synaptic plasticity, and neural network control. However, despite much attention this pathway and its effects on pyramidal cells have received recently, the presence of ErbB4 in these cells is still controversial. As knowledge of the precise locus of receptor expression is crucial to delineating the mechanisms by which NRG signaling elicits its diverse physiological effects, we have undertaken a thorough analysis of ErbB4 distribution in the CA1 area of the rodent hippocampus using newly generated rabbit monoclonal antibodies and ErbB4-mutant mice as negative controls. We detected ErbB4 immunoreactivity in GABAergic interneurons but not in pyramidal neurons, a finding that was further corroborated by the lack of ErbB4 mRNA in electrophysiologically identified pyramidal neurons as determined by single-cell reverse transcription–PCR. Contrary to some previous reports, we also did not detect processed ErbB4 fragments or nuclear ErbB4 immunoreactivity. Ultrastructural analysis in CA1 interneurons using immunoelectron microscopy revealed abundant ErbB4 expression in the somatodendritic compartment in which it accumulates at, and adjacent to, glutamatergic postsynaptic sites. In contrast, we found no evidence for presynaptic expression in cultured GAD67-positive hippocampal interneurons and in CA1 basket cell terminals. Our findings identify ErbB4-expressing interneurons, but not pyramidal neurons, as a primary target of NRG signaling in the hippocampus and, furthermore, implicate ErbB4 as a selective marker for glutamatergic synapses on inhibitory interneurons.

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Received May 21, 2009; revised July 29, 2009; accepted Aug. 13, 2009.

Correspondence should be addressed to Dr. Andres Buonanno, Section on Molecular Neurobiology, Building 35, Room 2C-1000, 35 Lincoln Drive, National Institutes of Health, Bethesda, MD 20892-3714. Email: buonanno{at}mail.nih.gov

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