One of the primary challenges for the central nervous system is decoding meaningful messages from the ongoing constant barrage of information arriving at its synapses. This challenge is even more difficult under circumstances of injury or inflammation when signals can be scrambled, amplified, or passed along inappropriate circuits. Multiple laboratories are exploring these processes and trying to unravel the mystery of how normal and adaptive pain shifts to a maladaptive chronic pain state. To explore these processes, research in my laboratory focuses on the neurons responsible for transmitting sensory information to the central nervous system; the primary afferents.
The lab uses different models to examine pain processing: inflammation, nerve injury, and spinal cord injury. Primary afferents are studied using ex vivo preparations that allow for comprehensive phenotyping of individual nerve fibers and determine how injury changes physiological properties of these neurons. Physiological characterizations of neurons are also coupled with gene expression profiling of individual afferents to examine shifts in expression patterns following injury. Genetic expression of channelrhoodopsin is also utilized to target specific populations of afferents to examine relative contributions to sensory processing. It is our hope that our results will lead to advances that aid in the treatment of pathological pain.
- Baumbauer, K.M., Anderson, M.J., & Riccio, D.C. (2002). State dependent retention: The relevance of internal context. In R.W. Flint, Jr. (Ed.), Forget it? Sources, theories, & mechanisms of alterations in mnemonic function (pp. 39-50). North Chelmsford, MA: Courier Custom Publishing, Inc.
- Baumbauer, K.M., Young, E.E., Hoy, K.C., Jr., France, J.L., & Joynes, R.L. (2006). Intrathecal infusions of anisomycin impact the learning deficit but not the learning effect observed in spinal rats that have received instrumental training. Behavioural Brain Research, 173, 299-309.
- Baumbauer, K.M., Young, E.E., Hoy, K.C., Jr., Abood, A., & Joynes, R.L. (2007). Administration of a Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibitor reverses the noncontingent shock learning deficit observed in spinal rats. Behavioral Neuroscience, 121, 570-578.
- Baumbauer, K.M., Young, E.E., Hoy, K.C., Jr., & Joynes, R.L. (2007). Intrathecal administration of neurokinin 1 and neurokinin 2 receptor antagonists undermines the savings effect in spinal rats trained in an instrumental learning paradigm. Behavioral Neuroscience, 121, 186-199.
- Baumbauer, K.M., Young, E.E., Hoy, K.C., Jr., & Joynes, R.L. (2007). Neurokinin receptors modulate the impact of uncontrollable stimulation on adaptive spinal plasticity. Behavioral Neuroscience, 121, 1082-1094.
- Gómez-Pinilla, F., Huie, J. R., Ying, Z., Ferguson, A.R., Crown, E.D., Baumbauer, K.M., Edgerton, V.R., & Grau, J.W. (2007). BDNF and Learning: Evidence that instrumental training promotes learning within the spinal cord by up-regulating BDNF expression. Neuroscience, 148, 893-906.
- Young, E.E., Baumbauer, K.M., Elliott, A.E., & Joynes, R.L. (2007). Lipopolysaccharide induces a spinal learning deficit that is blocked by IL-1 receptor antagonism. Brain, Behavior, & Immunity, 21, 748-757. Highlighted in the 8/07 issue of BBI and accompanied by an invited commentary by Dr. Terence Deak (SUNY-Binghamton).
- Young, E.E., Baumbauer, K.M., Elliot, A., & Joynes, R.L. (2007). Neonatal injury disrupts acquisition of an instrumental response in adult spinal rats. Behavioral Neuroscience, 121, 1095-1100.
- Young, E.E., Baumbauer, K.M., Hillyer, J.E., & Joynes, R.L. (2007). Local anesthetic treatment significantly attenuates acute pain responding but does not prevent the neonatal injury-induced reduction in adult spinal behavioral plasticity. Behavioral Neuroscience, 121, 1073-1081.
- Young, E.E., Baumbauer, K.M., Hillyer, J.E., Patterson, A.M., Hoy, K.C., Jr., Mintz, E.M., & Joynes, R.L. (2008). The neonatal injury-induced spinal learning deficit in adult rats: Central mechanisms. Behavioral Neuroscience, 122, 589-600.
- Baumbauer, K.M., Hoy, K.C., Jr., Huie, J.R., Hughes, A.J., Woller, S.A., Puga, D.A., Setlow, B., & Grau, J.W. (2008). Timing in the Absence of Supraspinal Input I: Variable, but not Fixed, Spaced Stimulation of the Sciatic Nerve Undermines Spinally-Mediated Instrumental Learning. Neuroscience, 155, 1030-1047.
Evaluated by Dr. Kent Berridge for Faculty of 1000 Biology. Kent Berridge: Faculty of 1000 Biology, 28 Oct 2008 www.f1000biology.com/article/id/1123485/evaluation
- Baumbauer, K.M., Huie, J.R., Hughes, A.J., & Grau, J.W. (2009). Timing in the Absence of Supraspinal Input II: Regular spaced stimulation induces a lasting alteration in spinal unction that depends on the NMDA receptor, protein synthesis, and BDNF. Journal of Neuroscience, 29, 14383-14393. This Week in the Journal featured article. http://www.jneurosci.org/cgi/content/full/29/46/i
- Baumbauer, K.M., Young, E.E., & Joynes, R.L. (2009). Pain and learning in a spinal system: Contradictory outcomes from Common Origins. Brain Research Reviews, 61, 124-143.
Featured on MDLinx.com, 10 Oct 2009 http://www.mdlinx.com/internalmdlinx/news-article.cfm/2916554
- Vichaya, E.G., Baumbauer, K.M., Carcoba, L.M., Grau, J.W, & Meagher, M.W. (2009). Spinal glia modulate both adaptive ad physiological processes. Brain, Behavior, & Immunity, 23, 969-976.
- Baumbauer, K.M., & Grau, J.W. (2011). Timing in the Absence of Supraspinal Input III: Regularly Spaced Cutaneous Stimulation Prevents and Reverses the Spinal Learning Deficit Produced by Peripheral Inflammation. Behavioral Neuroscience, 125, 37-45.
- Ferguson, A.R., Huie, J.R., Crown, E.D., Baumbauer, K.M., Hook, M.A., Garraway, S.M., Lee, K.H., Hoy, K.C., & Grau, J.W. (2012). Maladaptive spinal plasticity opposes spinal learning and recovery in spinal cord injury. Frontiers in Integrative Physiology. doi: 10.3389/fphys.2012.00399
- Grau, J.W., Huie, J.R., Garraway, S.M., Hook, M.A., Crown, E.D., Baumbauer, K.M., Lee, K.H., Hoy, K.C., & Ferguson, A.R. (2012). Impact of a behavioral control on the processing of nociceptive stimulation within the dorsal horn. Frontiers in Integrative Physiology, 3, 1-21.
- Huie, J.R., Garraway, S.M., Baumbauer, K.M., Hoy, K.C., Jr., Beas, B.S., Montgomery, K.S., Bizon, J.L., & Grau, J.W. (2012). Brain derived neurotrophic factor (BDNF) promotes adaptive plasticity within the spinal cord and mediates the beneficial effects of controllable stimulation. Neuroscience, 200, 74-90.
- Huie, J.R., Baumbauer, K.M., Lee, K.H., Beattie, M.S., Bresnahan, J.C., Ferguson, A.R., & Grau, J.W. (2012). Glial tumor necrosis factor alpha (TNFα) generates metaplastic inhibition of spinal learning. PLoS ONE, 7, e39751. doi:10.1371/journal.pone.0039751.
- Fava, E., Hull, R., Baumbauer, K.M., & Bortfeld, H. (2014). Hemodynamic Responses to Speech and Music in Preverbal Infants. Child Neuropsychology, 20, 430-448.
Grau, J.W., Huie, J.R., Lee, K.H., Hoy, K.C., Huang, Y.-J., Turtle, J.D., Strain, M.M., Baumbauer, K.M., Miranda, R.M., Hook, M.A., Ferguson, A.R., & Garraway, S.M. (in press).
- Metaplasticity and behavior: How training and inflammation affect plastic potential within the spinal cord and recovery after injury. Frontiers in Neural Circuits.
Baumbauer, K.M., Deberry, J.J., Adelman, P.C., Miller, R.H., Koerber, H.R., Davis, B.M., & Albers, K.M. (under review). Keratinocytes can initiate cutaneous sensations. Neuron.
- T32 Postdoctoral Fellowship “Mechanisms and Clinical Presentation of Pain” NS073548
- International Association for the Study of Pain (IASP) Travel Grant
- Student Led Award for Teaching Excellence (SLATE), Texas A&M University
- American Psychological Association Committee on Animal Research & Ethics (CARE) Imprinting-Interdivisional Mentoring Fellowship Award
- Recovery of Function Travel Award, Texas A&M University
- Faculty of Neuroscience Travel Award, Texas A&M University
- American Psychological Association Dissertation Award
- ONTAP Teaching Fellow, Kent State University
- Behavioural Brain Research
- Brain Research
- Growth Factors
- International Journal of Nanomedicine
- Medical Research Council, UK