Samuel M. Young, Jr., PhD

Samuel M. Young, Jr., PhD

Research Group Leader
Molecular Mechanisms of Synaptic Function

One Max Planck Way
Jupiter, FL 33458
(561) 972-9402

Visit Sam Young's Lab Website

Researcher Bio

Dr. Samuel M. Young, Jr. joined the Max Planck Florida Institute for Neuroscience (MPFI) as Research Group Leader of Molecular Mechanisms of Synaptic Function in 2010. Prior to joining MPFI, Dr. Young was an Internal Research Group Leader in the Department of Membrane Biophysics at the Max Planck Institute for Biophysical Chemistry in Goettingen, Germany.

Dr. Young conducted his postdoctoral work at the University of North Carolina-Chapel Hill (2000) in the Gene Therapy Center; at the Howard Hughes Medical Institute and the Salk Institute in La Jolla, California (2000-2004) in the Molecular Neurobiology Laboratories; and at the Max Planck Institute for Biophysical Chemistry in the Department of Membrane Biophysics (2004-2009) in Goettingen, Germany.

He carried out his doctoral work at University of North Carolina-Chapel Hill (1996-2000) in the Gene Therapy Center while enrolled in the Curriculum in Genetics and Molecular Biology program. Dr. Young completed his undergraduate at Princeton University, graduating in 1996 with an A.B in Molecular Biology. He has been a recipient of the Alexander von Humboldt fellowship and is currently a member of the Society for Neuroscience and the Association for Research in Otolaryngology (ARO).

Selected Publications

  1. Chen, C., Arai, I., Satterfield, R., Young, S.M., and Jonas, P. (2017). Synaptotagmin 2 Is the Fast Ca2+ Sensor at a Central Inhibitory Synapse. Cell Reports. 18, 723–736.

  2. Montesinos, M.S., Satterfield, R., and Young, S.M. (2016). Helper-Dependent Adenoviral Vectors and Their Use for Neuroscience Applications. Methods Mol. Biol.. 1474, 73–90.

  3. Montesinos, M., Dong, W., Goff, K., Das, B., Guerrero-Given, D., Schmalzigaug, R., Premont, RT., Satterfield, R., Kamasawa, N., Young, SM, Jr. (2015) Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse. Neuron, 88, 918–925.

  4. Chen, Z., Das B., Nakamura, Y., DiGregorio, D., Young, SM Jr. (2015) Ca2+ Channel to Synaptic Vesicle Distance Accounts for the Readily Releasable Pool Kinetics at a Functionally Mature Auditory Synapse. J Neurosci. 35(5):2083-2100

  5. Maltecca F, Baseggio E, Consolato F, Mazza D, Podini P, Young SM, Jr., Drago I, Bahr BA, Puliti A, Codazzi F, Quattrini A, Casari G (2015) Purkinje neuron Ca2+ influx reduction rescues ataxia in SCA28 model. The Journal of Clinical Investigation 2015;125(1):263–274. doi:10.1172/JCI74770.

  6. Tong H, Kopp-Scheinpflug C, Pilati N, Robinson SW, Sinclair JL, Steinert JR, Barnes-Davies M, Allfree R, Grubb BD, Young SM Jr, Forsythe ID. Protection from Noise-Induced Hearing Loss by Kv2.2 Potassium Currents in the Central Medial Olivocochlear System. J Neurosci. 2013 May 22;33(21):9113-9121.

  7. Chen, Z., Cooper, B., Kalla, S., Varoqueaux, F., and Young, SM, Jr. The Munc13 Proteins Differentially Regulate Readily Releasable Pool Dynamics and Calcium-Dependent Recovery at a Central Synapse. The Journal of Neuroscience, 8 May 2013, 33(19):8336-8351

  8. Montesinos, M., Chen, Z., and Young, SM, Jr. pUNISHER: A high level expression cassette for use with recombinant viral vectors for rapid and long term in vivo neuronal expression in the CNS. J Neurophysiol. 106:3230-3244. (2011)

  9. Dusonchet, J., Kochubey, O., Stafa K., Young, S.M. Jr., Zufferey, R., Moore, D.J., Schneider, B.L., Aebischer, P. (2011) A Rat Model of Progressive Nigral Neurodegeneration Induced by the Parkinson’s Disease-Associated G2019S Mutation in LRRK2. J Neurosci. 31(3):907-12.