Wan Y, Feng G, Calakos N. Sapap3 deletion causes mGluR5-dependent silencing of AMPAR synapses. J Neurosci. 2011;31(46):16685-91. doi:10.1523/JNEUROSCI.2533-11.2011
Chen M, Wan Y, Ade K, Ting J, Feng G, Calakos N. Sapap3 deletion anomalously activates short-term endocannabinoid-mediated synaptic plasticity. J Neurosci. 2011;31(26):9563-73. doi:10.1523/JNEUROSCI.1701-11.2011
Ren J, Qin C, Hu F, et al. Habenula "cholinergic" neurons co-release glutamate and acetylcholine and activate postsynaptic neurons via distinct transmission modes. Neuron. 2011;69(3):445-52. doi:10.1016/j.neuron.2010.12.038
Chung WS, Welsh CA, Barres BA, Stevens B. Do glia drive synaptic and cognitive impairment in disease?. Nat Neurosci. 2015;18(11):1539-1545. doi:10.1038/nn.4142
Lee PH, Perlis RH, Jung JY, et al. Multi-locus genome-wide association analysis supports the role of glutamatergic synaptic transmission in the etiology of major depressive disorder. Transl Psychiatry. 2012;2:e184. doi:10.1038/tp.2012.95
Strazisar M, Cammaerts S, Ven K, et al. MIR137 variants identified in psychiatric patients affect synaptogenesis and neuronal transmission gene sets. Mol Psychiatry. 2015;20(4):472-81. doi:10.1038/mp.2014.53
Rietveld CA, Esko T, Davies G, et al. Common genetic variants associated with cognitive performance identified using the proxy-phenotype method. Proc Natl Acad Sci U S A. 2014;111(38):13790-4. doi:10.1073/pnas.1404623111
Rudenko A, Seo J, Hu J, et al. Loss of cyclin-dependent kinase 5 from parvalbumin interneurons leads to hyperinhibition, decreased anxiety, and memory impairment. J Neurosci. 2015;35(6):2372-83. doi:10.1523/JNEUROSCI.0969-14.2015
Hyman SE. Enlisting hESCs to Interrogate Genetic Variants Associated with Neuropsychiatric Disorders. Cell Stem Cell. 2015;17(3):253-4. doi:10.1016/j.stem.2015.08.013
Zhou Y, Kaiser T, Monteiro P, et al. Mice with Shank3 Mutations Associated with ASD and Schizophrenia Display Both Shared and Distinct Defects. Neuron. 2016;89(1):147-62. doi:10.1016/j.neuron.2015.11.023