Craig Harrison Bailey, PhD

  • Associate Professor of Clinical Neuroscience (in Psychiatry)
Profile Headshot


Dr. Bailey's career highlights include the following:

1969 NSF Summer Traineeship

1969-72 Chester W. Kingsley Memorial Fellowship

1972-73 Katherine Comstock Thorne Fellowship

1973-75 MDAA Postdoctoral Fellow, Department of Biology, University of Pennsylvania

1974-75 Biomedical Image and Image Processing Resource, Biotechnology Resources Branch, Division of Research Resources, NIH funds for research of HVEM Resource, University of Colorado

1975-77 NIMH Postdoctoral Fellow, Division of Neurobiology & Behavior, College of Physicians and Surgeons, Columbia University

1979-81 NSF BNS7824476; Cellular Approach to Neurobiology of Aging; P.I.

1980-85 Irma T. Hirschl Career Scientist Award

1982-85 NIH MH35729; Cellular Basis of Age-Impaired Learning and Memory, P.I.

1983-85 Office of Naval Research N00014-83; Molecular Mechanisms of Learning and Memory; Co-P.I., Morphological Scope

1988-91 Development Award from the McKnight Endowment Fund for Neuroscience

1981-97 NIH GM32099; Cellular Analysis of Behavior, Co-P.I. of Neuromorphology Scope

1982- 2006 NIH MH37134; Morphological Basis of Synaptic Plasticity; P.I.

2008-2010 Simons Foundation Autism Research Initiative, Investigator Award; The Role of Wild-Type and Autism-Linked Mutant Forms of Neuroligin in Activity-Dependent Synaptic Plasticity; Co-P.I.

Academic Appointments

  • Associate Professor of Clinical Neuroscience (in Psychiatry)


  • Male

Credentials & Experience

Committees, Societies, Councils

Member, The Kavli Institute for Brain Science


Our primary interest is the analysis of behaviorally relevant structural plasticity as it occurs at the level of identified synapses. Toward that end, we have extensively studied the storage of long-term memory for sensitization of the gill-withdrawal reflex in Aplysia and have found that it is associated with the growth of new synapses by the sensory neurons onto their postsynaptic target neurons. Despite the association of synaptic growth with various forms of long-term memory, surprisingly little is known about the cell biological mechanisms that regulate and couple the structural changes to the molecular changes that govern learning-induced synaptic plasticity and the relative functional contribution each may make to the initiation of the long-term process on the one hand and its stable maintenance on the other. To address these questions, we have combined time-lapse imaging and molecular biological analysis (using gene transfer) of living sensory-to-motor neuron synapses in culture and have monitored both functional and structural changes simultaneously so as to follow remodeling and growth at the same specific synaptic connections continuously over time. This approach has allowed us to examine directly the functional contribution of learning-related structural changes to the different time-dependent phases of memory storage. Insights provided by these studies suggest the synaptic differentiation and growth induced by learning in the mature nervous system are highly dynamic and often rapid processes that can recruit both molecules and mechanisms important for de novo synapse formation during development.

Research Interests

  • Cellular/Molecular/Developmental Neuroscience
  • Neurobiology of Learning and Memory
  • Synapses and Circuits

Selected Publications

  • Bailey, C.H., Kandel, E.R., Si, K. and Choi, Y-B. (2005). Toward a molecular biology of learning-related synaptic growth in Aplysia. Cellscience Reviews 2, 27-57.
  • Hawkins, R.D., Kandel, E.R. and Bailey, C.H. (2006). Molecular mechanisms of memory storage in Aplysia. Biol. Bull. 210, 174-191.
  • Bailey, C.H. and Kandel, E.R. (2008). Synaptic remodeling, synaptic growth and the storage of long-term memory in Aplysia. In: W. Sossin, J.- C. Lacaille, V.F. Castellucci and S. Belleville (eds), The Essence of Memory, Progress in Brain Research, Elsevier Press, 169: 179-198.
  • Miniaci, M.C., Kim, J-H., Puthanveettil, S.V., Si, K., Zhu, H., Kandel, E.R., and Bailey, C.H. (2008). Sustained CPEB-dependent local protein synthesis is required to stabilize synaptic growth for persistence of long-term facilitation in Aplysia. Neuron 59, 1024-1036.
  • Bailey, C.H. and Kandel, E.R. (2008). Activity-dependent remodeling of presynaptic boutons. In: L. Squire (ed), New Encyclopedia of Neuroscience, Elsevier Press, 67-74.
  • Bailey, C.H., Barco, A., Hawkins, R.D. and Kandel, E.R. (2008). Molecular studies of learning and memory in Aplysia and the hippocampus: a comparative analysis of implicit and explicit memory storage. In: J. H. Byrne (ed), Learning and Memory:A Comprehensive Reference, Volume 4: Molecular Mechanisms of Memory, Elsevier Press:11-29.
  • Li, H-L., Huang, B.S.,Vishwasrao, H., Sutedja, N., Chen, W., Jin, I., Hawkins, R.D., Bailey, C.H., and Kandel, E.R. (2009). Dscam mediates remodeling of glutamate receptors in Aplysia during de novo and learning-related synapse formation. Neuron, 61: 527-540.
  • Bailey CH, Kandel ER: Synaptic and cellular basis of learning. (2009). In: JT Cacioppo and GG Berntson (eds), Handbook of Neuroscience for Behavioral Sciences, John Wiley and Sons, Chapter 27: 528-551.
  • Jung SY, Kim J, Kwon OB, Jung JH, An K, Jeong AY, Lee CJ, Choi Y-B, Bailey CH, Kandel ER, Kim J-H. (2010). Input-Specific Synaptic Plasticity in the Amygdala is Regulated by Neuroligin-1 via Postsynaptic NMDA Receptors Proc. Nat. Acad. Sci., USA,107(10): 4710-4715.
  • Hawkins RD, Bailey CH, Kandel ER. (2010). The neuronal circuit for simple forms of learning in Aplysia. In: G M Shepherd and S Grillner (eds), Handbook of Brain Microcircuits, Oxford University Press, Chapter 52: 485-502.
  • Jung, S.Y., Kim, J., Kwon, O.B., Jung, J.H., An, K., Jeong, A.Y., Lee, C.J., Choi, Y-B, Bailey, C.H., Kandel, E.R. and Kim, J-H. (2010) Input-specific synaptic plasticity in the amygdala is regulated by neuroligin-1 via postsynaptic NMDA receptors. Proc. Nat. Acad. Sci., USA., 107 (10): 4710- 4715.
  • Choi, Y.-B., Li, H.-L., Kassabov, S.R., Jin, I., Puthanveettil, S.V., Karl, K.A., Lu, Y., Kim, J.- H., Bailey, C.H.,and Kandel, E.R. (2011) Neurexin-Neuroligin trans-synaptic interaction mediates learning-related synaptic remodeling and long-term facilitation in Aplysia. Neuron, 70: 1-14.
  • Lee, S-H, Kwak, C., Shim, J.,Kim, Choi, S-L, Kim, H.F., D-J, Jang, D-J, Lee, J-A, Lee, K., Lee, C-H, Lee,Y-D, Miniaci, M.C., Bailey, C.H., Kandel, E.R. and B-K, Kaang. (2012) A cellular model of memory reconsolidation involves reactivation-induced destabilization and restabilization at the sensorimotor synapse in Aplysia. Proc. Nat. Acad. Sci., USA., 109 (35): 14200- 14205.
  • Lee, S-H, Shim, J., Choi, S-L, Lee, N., Lee, C-H, Bailey, C.H., Kandel, E.R., Jang, D-J, and Kaang, B-K. (2012) Learning-related synaptic growth mediated by internalization of Aplysia cell adhesion molecule is controlled by membrane phosphatidylinositol 4,5-bisphosphate synthetic pathway. J. Neuroscience, 32 (46): 16296-16305.
  • Kassabov, S.R., Choi , Y-B, Karl , K.A. Vishwasrao, H.D., Bailey, C.H. and Kandel, E.R. (2013) A single Aplysia neurotrophin mediates synaptic facilitation via differentially processed isoforms secreted as mature or precursor forms. Cell Reports, 3: 1-15.
  • Bailey, C.H., Kandel, E.R., and Harris, K.M., (2015) Structural components of synaptic plasticity and memory consolidation. In: Mayford, Y. Dudai and E.Kandel (eds), Learning and Memory Cold Spring Harbor Press, Chapter 10: (in press).