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The Journal of Neuroscience, February 25, 2009, 29(8):2404-2413; doi:10.1523/JNEUROSCI.4303-08.2009

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Development/Plasticity/Repair
Neuregulin Signaling Is Dispensable for NMDA- and GABA_A-Receptor Expression in the Cerebellum In Vivo

N. Gajendran,¹ J. P. Kapfhammer,² E. Lain,¹ M. Canepari,³ K. Vogt,³ W. Wisden,⁴ and H. R. Brenner¹

Institutes of ¹Physiology and ²Anatomy, Department of Biomedicine, and ³Department of Pharmacology, Biozentrum, University of Basel, CH-4056 Basel, Switzerland, and ⁴Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, United Kingdom

Correspondence should be addressed to H. R. Brenner, Institute of Physiology, Department of Biomedicine, University of Basel, Klingelbergstrasse 50, CH-4056 Basel, Switzerland. Email: Hans-Rudolf.Brenner{at}unibas.ch

Neuregulin-1s (NRG-1s) are a family of growth and differentiation factors with multiple roles in the development and function in different organs including the nervous system. Among the proposed functions of NRG-1s in the nervous system is the regulation of genes encoding certain neurotransmitter receptors during synapse formation as well as of other aspects of synaptic function. Here, we have examined, in granule cells of the cerebellum in vivo, the role of NRGs in the induction of NMDA receptor (NMDA-R) and GABA_A receptor (GABA_A-R), which are thought to be induced by NRG-1 secreted by the synaptic inputs. To this end, we used the Cre/loxP system to genetically ablate the NRG receptors ErbB2 and ErbB4 selectively in these cells, thus eliminating all NRG-mediated signaling to them. Unlike previous reports using cultured granule cells to address the same question, we found that the developmental expression patterns of the mRNAs encoding the NR2C subunit of the NMDA-R and the β2-subunit of the GABA_A-R is normal in mice lacking the NRG receptors ErbB2 and ErbB4. Likewise, no alterations in cerebellar morphology nor in certain aspects of cerebellar wiring were resolved in these mutants. We conclude that NRG/ErbB signaling to the granule cells is dispensable for the normal development of their synaptic inputs.

Key words: synapse formation; development; neuregulin; cerebellum; granule cell; NMDA receptor

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Received Sept. 9, 2008; revised Dec. 17, 2008; accepted Jan. 22, 2009.

Correspondence should be addressed to H. R. Brenner, Institute of Physiology, Department of Biomedicine, University of Basel, Klingelbergstrasse 50, CH-4056 Basel, Switzerland. Email: Hans-Rudolf.Brenner{at}unibas.ch

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