An up to date list of Murphy Lab publications can be found here.
Reprint requests should be sent to murphyg@umich.edu
Althaus, A.L., Moore, S.J., Zhang, H., Du, X., Murphy, G.G., and Parent, J.M., Altered synaptic drive onto birthdated dentate granule cells in experimental temporal lobe epilepsy. J Neurosci, 2019. 39(38): p. 7604-7614. PMC6750946.
Cazares, V.A., Rodriguez, G., Parent, R., Ouillette, L., Glanowska, K.M., Moore, S.J., and Murphy, G.G., Environmental variables that ameliorate extinction learning deficits in the 129S1/SvlmJ mouse strain. Genes Brain Behav, 2019. 18(7): p. e12575. PMC6718342.
Moore, S.J. and Murphy, G.G., The role of L-type calcium channels in neuronal excitability and aging. Neurobiology of Learning and Memory, 2020. 173: p. 107230.
Ghoweri, A.O., Ouillette, L., Frazier, H.N., Anderson, K.L., Lin, R.-L., Gant, J.C., Parent, R., Moore, S., Murphy, G.G., and Thibault, O., Electrophysiological and Imaging Calcium Biomarkers of Aging in Male and Female 5XFAD Mice. Journal of Alzheimer's Disease, 2020. 78: p. 1419-1438.
Moore, S.J., Murphy, G.G., and Cazares, V.A., Turning strains into strengths for understanding psychiatric disorders. Molecular Psychiatry, 2020. 25(12): p. 3164-3177. 32404949
Cazares, V.A. and Murphy, G.G., Pre- and Post-synaptic sites of plasticity., in Handbook of Amygdala Structure and Function, J. Urban and J.A. Rosenkranz, Editors. 2020, Academic Press: San Diego. p. 115-126.
Stevenson, T.K., Moore, S.J., Murphy, G.G., and Lawrence, D.A., Tissue Plasminogen Activator in Central Nervous System Physiology and Pathology: From Synaptic Plasticity to Alzheimer's Disease. Seminars in Thrombosis and Hemostasis, 2022. 48(03): p. 288-300.
Rodriguez, G., Moore, S.J., Neff, R.C., Glass, E.D., Stevenson, T.K., Stinnett, G.S., Seasholtz, A.F., Murphy, G.G., and Cazares, V.A., Deficits across multiple behavioral domains align with susceptibility to stress in 129S1/SvImJ mice. Neurobiology of Stress, 2020. 13: p. 100262.
Moore, S. J., Cazares, V. A., Temme, S. J., & Murphy, G. G. (2023). Age-related deficits in neuronal physiology and cognitive function are recapitulated in young mice overexpressing the L-type calcium channel, CaV 1.3. Aging cell, 22(3), e13781.