@article{kamande_nagendran_harris_taylor_2019, title={Multi-compartment Microfluidic Device Geometry and Covalently Bound Poly-D-Lysine Influence Neuronal Maturation}, volume={7}, ISSN={["2296-4185"]}, DOI={10.3389/fbioe.2019.00084}, abstractNote={Multi-compartment microfluidic devices have become valuable tools for experimental neuroscientists, improving the organization of neurons and access to their distinct subcellular microenvironments for measurements and manipulations. While murine neurons are extensively used within these devices, there is a growing need to culture and maintain human neurons differentiated from stem cells within multi-compartment devices. Human neuron cultures have different metabolic demands and require longer culture times to achieve synaptic maturation. We tested different channel heights (100 μm, 400 μm, and open) to determine whether greater exposure to media for nutrient exchange might improve long-term growth of NIH-approved H9 embryonic stem cells differentiated into glutamatergic neurons. Our data showed an opposite result with both closed channel configurations having greater synaptic maturation compared to the open compartment configuration. These data suggest that restricted microenvironments surrounding neurons improve growth and maturation of neurons. We next tested whether covalently bound poly-D-lysine (PDL) might improve growth and maturation of these neurons as somata tend to cluster together on PDL adsorbed surfaces after long culture periods (>30 days). We found that covalently bound PDL greatly improved the differentiation and maturation of stem cell-derived neurons within the devices. Lastly, experimental paradigms using the multi-compartment platform show that axons of human stem cell derived neurons intrinsically regenerate in the absence of inhibitory cues and that isolated axons form presynaptic terminals when presented with synaptic targets.}, journal={FRONTIERS IN BIOENGINEERING AND BIOTECHNOLOGY}, author={Kamande, Joyce W. and Nagendran, Tharkika and Harris, Joseph and Taylor, Anne Marion}, year={2019}, month={May} }
 @article{nagendran_taylor_2019, title={Unique Axon-to-Soma Signaling Pathways Mediate Dendritic Spine Loss and Hyper-Excitability Post-axotomy}, volume={13}, ISSN={["1662-5102"]}, DOI={10.3389/fncel.2019.00431}, abstractNote={Axon damage may cause axon regeneration, retrograde synapse loss, and hyper-excitability, all of which affect recovery following acquired brain injury. While axon regeneration is studied extensively, less is known about signaling mediating retrograde synapse loss and hyper-excitability, especially in long projection pyramidal neurons. To investigate intrinsic injury signaling within neurons, we use an in vitro microfluidic platform that models dendritic spine loss and delayed hyper-excitability following remote axon injury. Our data show that sodium influx and reversal of sodium calcium exchangers (NCXs) at the site of axotomy, mediate dendritic spine loss following axotomy. In contrast, sodium influx and NCX reversal alone are insufficient to cause retrograde hyper-excitability. We found that calcium release from axonal ER is critical for the induction of hyper-excitability and inhibition loss. These data suggest that synapse loss and hyper-excitability are uncoupled responses following axon injury. Further, axonal ER may play a critical and underappreciated role in mediating retrograde hyper-excitability within the CNS.}, journal={FRONTIERS IN CELLULAR NEUROSCIENCE}, author={Nagendran, Tharkika and Taylor, Anne Marion}, year={2019}, month={Sep} }
 @article{pinto_alves_martins_pedro_ryu_jeon_taylor_almeida_2016, title={The proteasome controls presynaptic differentiation through modulation of an on-site pool of polyubiquitinated conjugates}, volume={212}, number={7}, journal={Journal of Cell Biology}, author={Pinto, M. J. and Alves, P. L. and Martins, L. and Pedro, J. R. and Ryu, H. R. and Jeon, N. L. and Taylor, A. M. and Almeida, R. D.}, year={2016}, pages={789–801} }
 @article{gordon_wang_allbritton_taylor_2015, title={Magnetic Alignment of Microelements Containing Cultured Neuronal Networks for High-Throughput Screening}, volume={20}, ISSN={["1552-454X"]}, DOI={10.1177/1087057115598609}, abstractNote={High-throughput screening (HTS) on neurons presents unique difficulties because they are postmitotic, limited in supply, and challenging to harvest from animals or generate from stem cells. These limitations have hindered neurological drug discovery, leaving an unmet need to develop cost-effective technology for HTS using neurons. Traditional screening methods use up to 20,000 neurons per well in 384-well plates. To increase throughput, we use “microraft” arrays, consisting of 1600 square, releasable, paramagnetic, polystyrene microelements (microrafts), each providing a culture surface for 500–700 neurons. These microrafts can be detached from the array and transferred to 384-well plates for HTS; however, they must be centered within wells for automated imaging. Here, we developed a magnet array plate, compatible with HTS fluid-handling systems, to center microrafts within wells. We used finite element analysis to select an effective size of the magnets and confirmed that adjacent magnetic fields do not interfere. We then experimentally tested the plate’s centering ability and found a centering efficiency of 100%, compared with 4.35% using a flat magnet. We concluded that microrafts could be centered after settling randomly within the well, overcoming friction, and confirmed these results by centering microrafts containing hippocampal neurons cultured for 8 days.}, number={9}, journal={JOURNAL OF BIOMOLECULAR SCREENING}, author={Gordon, Kent R. and Wang, Yuli and Allbritton, Nancy L. and Taylor, Anne Marion}, year={2015}, month={Oct}, pages={1091–1100} }
 @article{menon_boyer_winkle_mcclain_hanlin_pandey_rothenfusser_taylor_gupton_2015, title={The E3 ubiquitin ligase TRIM9 Is a filopodia off switch required for netrin-dependent axon guidance}, volume={35}, number={6}, journal={Developmental Cell}, author={Menon, S. and Boyer, N. P. and Winkle, C. C. and McClain, L. M. and Hanlin, C. C. and Pandey, D. and Rothenfusser, S. and Taylor, A. M. and Gupton, S. L.}, year={2015}, pages={698–712} }
 @article{taylor_wu_tai_schuman_2013, title={Axonal translation of beta-catenin regulates synaptic vesicle dynamics}, volume={33}, number={13}, journal={Journal of Neuroscience}, author={Taylor, A. M. and Wu, J. and Tai, H. C. and Schuman, E. M.}, year={2013}, pages={5584–5589} }