Gender	Male
E-mail	robert.blitzer@mssm.edu
Education and Training	Ph.D., University of Rhode Island
	M.S., Purdue University
	B.S., Rutgers University

Blitzer Laboratory

Education and Training	Ph.D., University of Rhode Island
	M.S., Purdue University
	B.S., Rutgers University

Research in the Blitzer Laboratory addresses the mechanism of memory formation through the phenomenon of synaptic plasticity. In particular, we are interested in a persistent form of increased synaptic efficiency, termed long-term potentiation (LTP), which can be induced in the hippocampus, a brain structure concerned with memory formation and retrieval. LTP is induced by physiological stimulation, and is a highly regulated process involving numerous signaling pathways. Current projects include:

1) The detailed analysis of the roles of signaling pathways in LTP induction. This is a broad topic, and includes such topics as interactions between MAP kinase and Ca2+/calmodulin kinase II and the inhibition of protein phosphatases by the cAMP pathway.

2) The mechanism of LTP maintenance. Memories tend to be persistent, but the correspondingly persistent phase of LTP remains relatively unexplored. The underlying processes are only beginning to be understood, but are clearly different from those of LTP induction. We are gaining insight into maintenance processes using manipulations, both physiological and pharmacological, that can reverse well-established LTP.

3) The synaptic locus of LTP. LTP induction requires both presynaptic and postsynaptic events. However, a major unresolved issue in the field is whether the expression of LTP reflects a pre- or postsynaptic change. A presynaptic change might be increased glutamate release, while postsynaptic possibilities include recruitment of new glutamate channels to the membrane and regulation of existing receptors phenomenon. We are using quantal analysis methods to address this issue.

Most of our projects are collaborative and interdisciplinary in design, including biochemical, molecular biological, and imaging techniques in addition to the lab's core expertise in neurophysiology.

LTP, memory, neurophysiology, hippocampus, signaling

Tsokas P, Ma T, Iyengar R, Landau EM, Blitzer RD. Mitogen-activated protein kinase upregulates the dendritic translation machinery in long-term potentiation by controlling the mammalian target of rapamycin pathway. J Neurosci 2007 May 30; 27(22): 5885-5894.

Garcia-Osta A, Tsokas P, Pollonini G, Landau EM, Blitzer R, Alberini CM. MuSK expressed in the brain mediates cholinergic responses, synaptic plasticity, and memory formation. J Neurosci 2006 July 26; 26(30): 7919-7932.

Blitzer R. Long-term potentiation: mechanisms of induction and maintenance. Sci STKE 2005 Nov 8;(309): tr26.

Ma'ayan A, Jenkins SL, Neves S, Hasseldine A, Grace E, Dubin-Thaler B, Eungdamrong NJ, Weng G, Ram PT, Rice JJ, Kershenbaum A, Stolovitzky GA, Blitzer RD, Iyengar R. Formation of regulatory patterns during signal propagation in a Mammalian cellular network. Science 2005 Aug 12; 309(5737): 1078-83.

Ma'ayan A, Blitzer RD, Iyengar R. Toward predictive models of mammalian cells. Annu Rev Biophys Biomol Struct 2005; 34: 319-349.

Tsokas P, Grace EA, Chan P, Ma T, Sealfon SC, Iyengar R, Landau EM, Blitzer RD. Local protein synthesis mediates a rapid increase in dendritic elongation factor 1A after induction of late long-term potentiation. J Neurosci 2005 Jun 15; 25(24): 5833-5843.

Blitzer RD, Iyengar R, Landau EM. Postsynaptic signaling networks: Cellular cogwheels underlying long-term plasticity. Biol Psychiatry 2005 Jan 15; 57(2): 113-9.

Blitzer RD, Lombroso PJ. Genetics of childhood disorders: LIII. Learning and memory, Part 6: induction of long-term potentiation. J Am Acad Child Adolesc Psychiatry 2003 Aug; 42(8): 998-1001.

Blitzer RD. Genetics of childhood disorders: LIV. Learning and memory, Part 7: maintenance of long-term potentiation. J Am Acad Child Adolesc Psychiatry 2003 Sep; 42(9): 1131-1133.

Giovannini MG, Blitzer RD, Wong T, Asoma K, Tsokas P, Morrison JH, Iyengar R, Landau EM. Mitogen-activated protein kinase regulates early phosphorylation and delayed expression of Ca2+/calmodulin-dependent protein kinase II in long-term potentiation. J Neurosci 2001 Sep 15; 21(18): 7053-7062.