The Vollum Institute at OHSUThe Vollum Institute is a privately endowed research institute at Oregon Health & Science University dedicated to basic research that will lead to new treatments for neurological and psychiatric diseases. Vollum scientists have broad-ranging interests that coalesce around molecular neurobiology and cellular physiology. Their work has transformed the field of neuroscience and, in particular, have provided important advances in the study of synaptic transmission, neuronal development, neurotransmitter transporters, ion channels and the neurobiology of disease.

Learn more about the Vollum's mission

Meet the New Director

Marc R. Freeman, PhD, Vollum Director

Marc R. Freeman, Ph.D., joined OHSU in July 2016 as the new director of the Vollum Institute.

To learn more about his vision for the Vollum Institute and his commitment to expanding basic neuroscience research, read the Director's Message.

More about Dr. Freeman's research

The role of glial cells

Glia are cells in the brain that were long thought to be "helpers" that support neurons to perform their functions. Dr. Freeman has shown that the most predominant and least-studied glial cell, the star-shaped astrocyte, is essential to the brain's signaling network and allows for many complex behavioral outputs. His research has shown that neuromodulators, a messenger that regulates a diverse group of neurons, function not only through neurons, but signal through astrocytes as well. Currently, his research explores how neurons and glia cells communicate with one another so the nervous system runs smoothly and how their dysfunction can result in neurological disease.

Axon degeneration

Axons, slender nerve fibers, must remain intact to function, and, in cases of injury or disease, they break. His research team exploited the unique set of genetic tools available in fruit flies to label specific subsets of neurons in the intact animal, cut axons to induce degeneration, and then systematically broke each gene in the fly genome to determine which were required to promote axon destruction. They discovered that when dSarm/Sarm1 was deleted it completely blocked axon degeneration, and went on to show the same was true in mice and human cell lines. Remarkably, Freeman and colleagues have recently found that blocking the Sarm1 pathway alleviates nearly all pathological effects of traumatic brain injury in mice, and other labs have implicated Sarm1 signaling in peripheral neuropathy. These findings indicate that if researchers can find a way to block the genes that drive degeneration after injury—something Freeman's lab is currently pursuing—there's an opportunity to save the nervous system from degeneration in many cases of injury or neurodegenerative disease.

Recent News

A team of researchers from OHSU's Vollum Institute has now identified, in embryonic brains of mice, a repressor/corepressor complex consisting of Insulinoma-associated 1 (INSM1), which halts the cycle of cell division, and the RE1 Silencing Transcription factor (REST) corepressors RCOR1 and RCOR2. The findings were published in the Proceedings of the National Academy of Sciences on Jan. 3, 2017.
Learn more in OHSU Research News
Read the abstract in PubMed

A team of scientists, led by Marc Freeman, recently demonstrated that neurons release neurotransmitters that bind astrocytes and change astrocyte calcium signaling, which in turn regulates downstream neurons. The research was published online Nov. 9 in the journal Nature. Co-authors include Zhiguo Ma and Tobias Stork of the Howard Hughes Medical Institute and Dwight E. Bergles of Johns Hopkins University.
Learn more in OHSU Research News
Read the abstract in PubMed


Recent Publications

Calcium release from stores inhibits GIRK
Paul F. Kramer, John T. Williams
Cell Reports, 2016 Dec 20; 17(12):3246-3255

Neuromodulators signal through astrocytes to alter neural circuit activity and behaviour
Zhiguo Ma, Tobias Stork, Dwight E. Bergles, Marc R. Freeman
Nature, 2016 Nov 9; 539(7629):428-432

Postsynaptic, not presynaptic NMDA receptors are required for spike-timing-dependent LTD induction
Brett C. Carter, Craig E. Jahr
Nature Neuroscience, 2016 Sep; 19(9):1218-1224