| | Staff Scientists and Clinicians
| David J. Sandstrom,
Ph.D. |
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Dr. Sandstrom is a staff scientist with Dr. Howard Nash in the Section on Molecular Genetics, Laboratory of Molecular Biology. He received a B.A. in animal physiology from the University of California, San Diego, and a Ph.D. in neurobiology from the University of California, Berkeley. Dr. Sandstrom’s graduate and postdoctoral work focused on neural and genetic mechanisms through which steroid hormones and neuronal activity induce changes in the structure and function of nervous and muscular systems. After postdoctoral work at the University of Arizona, he joined NIMH as a staff scientist in 2000. |
| Research Interests |
| At NIMH, Dr. Sandstrom is using a combination of neurophysiology and genetics to elucidate the cellular mechanisms underlying general anesthesia. Because traditional physiological and behavioral analyses have provided an incomplete picture of the molecular mechanisms of anesthetic action, the Section on Molecular Genetics is taking advantage of Drosophila genetics and genomics to uncover novel targets of volatile anesthetics. Complementing ongoing behavioral and molecular analyses, Dr. Sandstrom has developed electrophysiological methods to assess excitability, neurotransmitter release, and receptor sensitivity in the presence of anesthetics. He has shown that anesthetics robustly reduce excitability, and reduce neurotransmitter release as a consequence. In his recent work, he has characterized the role of diverse ions channels in the central and peripheral responses to volatile anesthetics. Dr. Sandstrom also maintains active collaborations with a number of labs, both intramural and extramural, and consults on the development and execution of behavioral and electrophysiological projects in the Laboratory of Molecular Biology. |
| Representative Selected Recent Publications: |
- Peabody, N.C,, J.B. Pohl, F. Diao, A.P. Vreede, D.J. Sandstrom, H. Wang, P.K. Zelensky, B.H. White : Characterization of the decision network for wing expansion in Drosophila using targeted expression of the TRPM8 channel. Neurosci., 29: 3343-3353, 2009.
- Sandstrom, D.J.: Isoflurane reduces excitability of Drosophila larval motoneurons by activating a hyperpolarizing leak conductance. Anesthesiology, 108: 434-46, 2008.
- Sandstrom D.J. Isoflurane sensitivity of Drosophila axons is enhanced in an Na+ channel mutant: Intl. Congr. Ser., 1283: 267-268, 2005.
- Sandstrom, D.J. and H.A. Nash: Drug targets: turning the channel (on) for sedation. Curr Biol., 14: R185-6, 2004.
- Sandstrom, D.J.: Isoflurane depresses glutamate release by reducing neuronal excitability at the Drosophila neuromuscular junction. J Physiol., 558: 489-502, 2004.
- Sanyal, S., D.J Sandstrom, C.A. Hoeffer and M. Ramaswami: AP1 functions upstream of CREB to control plasticity in Drosophila. Nature, 416: 870-874, 2002.
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Address:
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Building 35, Room 1B1004,
9000 Rockville Pike MSC 3736,
Bethesda, MD 20892 |
| Phone: |
301-402-3242 |
| Email Dr. Sandstrom |
| Fax: |
301-402-0245 |
| Lab Web Site: |
No website available |
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