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Daniel Storm, Ph.D.,

Lab Website
Course Websites
  phcol402  phcol519
  phcol530  phcol563
Box 357750

Office: 206.543.7028
Lab: 206.543.3347
Fax: 206.616.8621







Our lab is interested in the molecular basis of neuroplasticity with an emphasis on the role of signal transduction crosstalk between the cAMP, calcium and the MAP kinase signaling pathways. Our lab uses an interdisciplinary approach which includes transgenic mouse technology, signaling mechanisms in cultured neurons, electrophysiology and behavioral studies.

Memory has two functionally and mechanistically distinct components: a short-term phase that lasts no more than several hours, and a long-term component that can continue for days or longer. The formation of long-term memory requires transcription of specific genes and de novo translation.

Another property of long-term memory is a dependency on the cAMP, calcium and MAP kinase signal transduction systems.

A key event in the generation of hippocampus-dependent long-term memory is activation of NMDA receptors with increases in intracellular free calcium. This triggers a series of events required for long-term changes at the synapse including the activation of calcium-stimulated adenylyl cyclases and MAP kinase. Transgenic ice lacking calcium-stimulated adenylyl cyclases do not develop long-term memory; mice overexpressing a calcium-stimulated adenylyl cyclase have superior memory for novel projects. Our recent data indicates that calcium-stimulated adenylyl cyclases are required for the activation and nuclear translocation of MAP kinase. These studies identify the calcium-stimulated adenylyl cyclase as a pharmacological window of opportunity for the development of drugs to enhance memory.



Recent Publications 

Phan, T, Chan, G, Sindreu, C, Eckel-Mahan, K, and Storm, DR (2011) The diurnal oscillation of MAP kinase and adenylyl cyclase activities in the hippocampus depends on the SCN. J. Neuroscience 31:10640-10647.

Wang, Z, Phan, T and Storm, DR (2011) The type 3 adenylyl cyclase is required for novel object learning and extinction of contextual memory: role of cAMP signaling in primary cilia. J. Neuroscience 31: 5557-5561.

Wang, Z and Storm, DR (2011) Maternal behavaior is impaired in female mice lacking Type 3 adenylyl cyclase. Neuropsychopharmacology 36, 772–781.

Sindreu, C, Palmiter, RD, and Storm, DR (2011) Zinc transporter ZnT-3 regulates presynaptic Erk1/2 signaling and hippocampus-dependent memory. Proc. Natl. Acad Sci. USA 108: 3366–3370.

Garelick, MG, Chan, G and Storm, DR (2009) Age dependent spatial memory deficit in mice overexpressing type 1 adenylyl cyclase J Neuroscience 29:10835-10842.

Mahan KL, Phan, T, Han, S, Wang, H, Chan, G, Scheiner, ZS, and Storm, DR (2008) Circadian Oscillation of MAPK Activity and cAMP in the Hippocampus: Implications for Memory Persistence. Nature Neuroscience 11, 1074-1082 (2008).

Shimizu, K, Phan T, Mansuy, I, and Storm, DR (2007) Proteolytic Degradation of SCOP in the Hippocampus Contributes to Activation of MAP Kinase and Memory For Novel Objects. Cell 128:1219-1229.

Sindreu, CB, Scheiner, ZS & Storm, DS (2007) Ca2+-Stimulated Adenylyl Cyclases Regulate ERK-Dependent Activation of MSK1 During Fear Conditioning. Neuron 53:79-89.

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