The Program in Neuroscience is an academic program of the Graduate School of Biomedical Sciences (GSBS) at the University of Massachusetts Medical School. Neuroscience investigators focus on: the neural, molecular, and genetic mechanisms that underlie nervous system development, learning and memory, addiction, glial responses to neuronal injury, and circadian rhythmicity; mechanisms of synaptic neurotransmitter release, analysis of how neurotransmitter receptors and membrane channels operate, and how drugs act on these processes to modify cellular function and behavior; magnetic resonance imaging technology to study and map changes in the brain associated with physiological stimuli as well as drugs of abuse; and disorders of the central nervous system, with special emphasis on neurodegenerative disorders, autism spectrum disorders, mental retardation and other developmental disabilities. This collection showcases publications and presentations authored by students in the Neuroscience program.

Attention GSBS Neuroscience students: To submit your publications, go to GSBS Student Publications and click on Submit Research in the left sidebar. You’ll need to log in or create a free account. If you have the article's PubMed ID, submission is very easy. Enter the PubMed ID and information from PubMed will be used to populate the submission form. Questions? Contact Lisa Palmer.

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Publications from 1997

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Modulation of two cloned potassium channels by 1-alkanols demonstrates different cutoffs, Benson Chu and Steven N. Treistman

Publications from 1995

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Ethanol inhibition of recombinant heteromeric NMDA channels in the presence and absence of modulators, Benson Chu, Vellareddy Anantharam, and Steven N. Treistman

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Transplanted xenogeneic neural cells in neurodegenerative disease models exhibit remarkable axonal target specificity and distinct growth patterns of glial and axonal fibres, Ole Isacson, Terrence W. Deacon, Peyman Pakzaban, Wendy R. Galpern, Jonathan H. Dinsmore, and Lindsay H. Burns

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Abolition of G protein inhibition of alpha 1A and alpha 1B calcium channels by co-expression of the beta 3 subunit, John P. Roche, Vellareddy Anantharam, and Steven N. Treistman