Patric K. Stanton, Ph.D.
Professor of Cell Biology and Anatomy
Department of Cell Biology & Anatomy
Basic Sciences Building, Room 217
Valhalla, NY 10595
For 20 years, my lab has been engaged in work across the range of neuronal plasticity, including: 1) properties of long-term activity-dependent potentiation (LTP) and depression (LTD) of synaptic strength; 2) links between LTD and cascades underlying LTP; 3) changes in synaptic function associated with the development of epileptic seizures; and 4) cellular mechanisms that both trigger and prevent ischemia-induced delayed neuronal death. We were the first to show that induction of mammalian LTP requires cyclic AMP and new protein synthesis, and to demonstrate a novel form of LTD evoked when presynaptic inputs are active while postsynaptic neurons are hyperpolarized. This led to our describing a NO-mediated cyclic GMP-dependent biochemical cascade that is part of bi-directional cyclic nucleotide regulation of synaptic strength, discovering chemical methods of inducing this and other forms of LTD, and direct two-photon fluorescence imaging of presynaptic transmitter release to demonstrate that this form of LTD persistently modulates release from the rapidly-recycling pool of transmitter vesicles. We employ extracellular and whole-cell patch clamp recordings, two-photon excitation and confocal fluorescence imaging in both acute and organotypic cultures of in vitro slices from hippocampus and neocortex. As a more physiologically intact network of synaptically connected neurons and glia, brain slices are ideal for the study of cellular and synaptic properties of neural systems.
Post Graduate Studies Johns Hopkins University, Max Planck Institute for Psychiatry
Graduate Degree: Ph.D. - Pharmacology
Graduate Degree Institution: Uniformed Services University of the Health Sciences
Undergraduate Institution: Johns Hopkins University
Goldstein LE, Fisher AM, Tagge CA, Zhang XL, Velisek L, Sullivan JA, Upreti C, Kracht JM, Ericsson M, Wojnarowicz MW, Goletiani CJ, Maglakelidze GM, Casey N, Moncaster JA, Minaeva O, Moir RD, Nowinski CJ, Stern RA, Cantu RC, Geiling J, Blusztajn JK, Wolozin BL, Ikezu T, Stein TD, Budson AE, Kowall NW, Cargin D, Sharon A, Saman S, Hall GF, Moss WC, Cleveland RO, Tanzi RE, Stanton PK, McKee AC (2012) Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model. Science Translational Medicine, 4(134):134ra60.
Upreti C, Otero R, Partida C, Skinner F, Thakker R, Pacheco, L, Zhou ZY, Maglakelidze G, Velíšková J, Velíšek L, Romanovicz D, Jones T, Stanton PK, and Garrido-Sanabria ER (2012) Altered transmitter release, vesicle recycling and presynaptic structure in limbic epilepsy. Brain, 135:869-885.
Zhang XL, Upreti C, Stanton PK (2011) G beta gamma and the C-terminus of SNAP-25 are necessary for long-term depression of transmitter release, PLoS ONE, 6:1-13.
Bailey CP, Nicholls RE, Zhang XL, Zhou ZY, Müller W, Kandel ER, Stanton PK (2008) Galphai2 inhibition of adenylate cyclase regulates presynaptic activity and unmasks cGMP-dependent long-term depression at Schaffer collateral-CA1 hippocampal synapses, Learning & Memory,15:261-270.
Zhang XL, Zhou ZY, Winterer J, Müller W, Stanton PK (2006) NMDA-dependent, but not group I mGluR-dependent, LTD is associated with long-term reduction in presynaptic transmitter release at hippocampal Schaffer collateral-CA1 synapses, Journal of Neuroscience,26:10270-10280.
Nicholls RE, Zhang XL, Bailey CP, Conklin BR, Kandel ER, Stanton PK (2006) mGluR2 acts through inhibitory Galpha subunits to regulate transmission and long-term plasticity at hippocampal mossy fiber-CA3 synapses, Proceedings of the National Academy of Sciences (USA),103:6380-6385.
Tyler WJ, Zhang XL, Hartman K, Winterer J, Müller W, Stanton PK, Pozzo-Miller L (2006) BDNF increases release probability and the size of the rapidly-recycling vesicle pool within rat hippocampal excitatory synapses, Journal of Physiology,574:787-803.