Activation of α7-containing nicotinic receptors on astrocytes triggers AMPA receptor recruitment to glutamatergic synapses
Version of Record online: 30 SEP 2013
© 2013 International Society for Neurochemistry
Journal of Neurochemistry
Volume 127, Issue 5, pages 632–643, December 2013
How to Cite
J. Neurochem.(2013) 127, 632–643
- Issue online: 13 NOV 2013
- Version of Record online: 30 SEP 2013
- Accepted manuscript online: 28 AUG 2013 11:11AM EST
- Manuscript Accepted: 26 AUG 2013
- Manuscript Revised: 31 JUL 2013
- Manuscript Received: 17 JUL 2013
- US National Institutes of Health. Grant Numbers: NS012601, NS034569, DA034216
- Tobacco-Related Disease Research Program. Grant Numbers: 16KT-011617, FT-0053, 19XT-0072
Figure S1. Composition of astrocyte cultures used to generate ACM and A/Nic.
Figure S2. A/Nic treatment increases the number of GluA puncta in hippocampal neurons in cell culture.
Figure S3. A/Nic does not affect the number of VGluT and PSD-95 puncta or their colocalization.
Figure S4. A/Nic does not change the number or size of GABAergic synapses as indicated by immunostaining of GABAA–α1 receptors and VGAT.
Figure S5. Nicotine exposure did not change the amount of astrocyte protein in culture.
Figure S6. A/Nic increases the frequency of AMPA receptor-mediated mEPSCs in hippocampal cell culture.
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