Plasticity of synaptic inhibition in mouse spinal cord lamina II neurons during early postnatal development and after inactivation of the glycine receptor α3 subunit gene
Version of Record online: 10 DEC 2009
© The Authors (2009). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 30, Issue 12, pages 2284–2292, December 2009
How to Cite
Rajalu, M., Müller, U. C., Caley, A., Harvey, R. J. and Poisbeau, P. (2009), Plasticity of synaptic inhibition in mouse spinal cord lamina II neurons during early postnatal development and after inactivation of the glycine receptor α3 subunit gene. European Journal of Neuroscience, 30: 2284–2292. doi: 10.1111/j.1460-9568.2009.07018.x
- Issue online: 15 DEC 2009
- Version of Record online: 10 DEC 2009
- Received 27 February 2009, revised 6 October 2009, accepted 7 October 2009
Table S1. Miniature inhibitory postsynaptic current (mIPSC) properties throughout postnatal development.
Table S2. Amplitude contribution of mixed GABA/glycine miniature inhibitory postsynaptic currents (mIPSCs) during development.
Table S3. Unitary current and conductance of glycine receptor (GlyR) miniature inhibitory postsynaptic currents (mIPSCs) recorded from adult Glra3+/+ and Glra3–/– mice (six mice per group).
As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer-reviewed and may be re-organized for online delivery, but are not copy-edited or typeset by Wiley-Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors.
|EJN_7018_sm_Table S1.doc||29K||Supporting info item|
|EJN_7018_sm_Table S2.doc||26K||Supporting info item|
|EJN_7018_sm_Table S3.doc||28K||Supporting info item|
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.