About

Dr. Douglas Baxter is the associate dean of medical education at Texas A&M University School of Engineering Medicine (EnMed). He is a founding leader of EnMed, playing a key role in transforming the concept into one of the nation's most forward-thinking medical education models. With a career spanning 45 years in academic medicine and research, Baxter helped establish the innovative curriculum, shape clinical and research priorities, and mentor faculty and students during the program's formative years. His leadership was instrumental in launching EnMed in 2017, a program designed to merge engineering and medicine into an integrated educational pathway. Throughout his tenure, Baxter demonstrated clarity, humility, and unwavering belief in the mission of EnMed. He was recognized for bringing people together, asking insightful questions, and fostering a culture of innovation, resilience, and compassion. His influence extended beyond his official role, serving as a cornerstone for the program's growth and success. Baxter's contributions have left a lasting legacy of visionary thinking, a culture of excellence, and a standard of empathy that will guide EnMed into the future. His career includes work across hospitals, medical schools, and research institutions, with his time at EnMed being the most rewarding of his professional life.

Research topics

• Computer Science
• Cognitive psychology
• Psychology
• Biology
• Physics
• Social psychology
• Neuroscience

Selected publications

• A New Way to Understand the Color Rendition Performance of Multi-Primary LED Lighting Systems: Color Rendition Variability (CRV)

  LEUKOS The Journal of the Illuminating Engineering Society of North America · 2025-06-11

  articleSenior author
  PublisherDOI

• A transdisciplinary dual degree curriculum yields novel and successful learning outcomes: early lessons from training physicianeers

  Frontiers in Medicine · 2025-02-28 · 4 citations

  articleOpen access

  The evolving needs in healthcare education and delivery have led to diverse MD-based dual degree programs offering trainees broader experiences and credential-based credibility after graduation. Medical schools typically implement multidisciplinary or interdisciplinary dual degree training with designs that separate the contributing disciplines chronologically and experientially. As a result, these designs fail to maximize the cohesive learning environment and outcomes possible with a transdisciplinary dual degree design, which integrates the contributing disciplines chronologically, experientially, and conceptually. Though rare, transdisciplinary dual degrees promise transformative educational outcomes and discipline convergence by dissolving traditional discipline boundaries and fostering a new learning environment and professional identity. Therefore, we hypothesize that a transdisciplinary dual degree curriculum yields novel-and potentially better-learning outcomes. ENMED, a transdisciplinary dual degree program collaboratively developed, sponsored, and implemented by Texas A&M University and Houston Methodist Hospital, is testing this hypothesis by training "physicianeers." This new type of healthcare professional trains simultaneously for the MD and Master of Engineering degrees, thereby integrating medical and engineering expertise to advance health system innovations. Supporting the hypothesis, ENMED's early experiences suggest its transdisciplinary dual-degree model leads physicianeer trainees to novel perspectives with the potential to transform healthcare systemically.

  PublisherOA PDFDOI

• Digital twin

  Elsevier eBooks · 2023-06-10 · 1 citations

  book-chapterCorresponding
  PublisherDOI

• Voltage- and Calcium-Gated Membrane Currents Tune the Plateau Potential Properties of Multiple Neuron Types

  Journal of Neuroscience · 2023-09-12 · 3 citations

  articleOpen access

  Many neurons exhibit regular firing that is limited to the duration and intensity of depolarizing stimuli. However, some neurons exhibit all-or-nothing plateau potentials that, once elicited, can lead to prolonged activity that is independent of stimulus intensity or duration. To better understand this diversity of information processing, we compared the voltage-gated and Ca 2+ -gated currents of three identified neurons from hermaphroditic Aplysia californica . Two of these neurons, B51 and B64, generated plateau potentials and a third neuron, B8, exhibited regular firing and was incapable of generating a plateau potential. With the exception of the Ca 2+ -gated potassium current ( I KCa ), all three neuron types expressed a similar array of outward and inward currents, but with distinct voltage-dependent properties for each neuron type. Inhibiting voltage-gated Ca 2+ channels with Ni + prolonged the plateau potential, indicating I KCa is important for plateau potential termination. In contrast, inhibiting persistent Na + ( I NaP ) blocked plateau potentials, empirically and in simulations. Surprisingly, the properties and level of expression of I NaP were similar in all three neurons, indicating that the presence of I NaP does not distinguish between regular-firing neurons and neurons capable of generating plateau potentials. Rather, the key distinguishing factor is the relationship between I NaP and outward currents such as the delayed outward current ( I D ), and I KCa . We then demonstrated a technique for predicting complex physiological properties such as plateau duration, plateau amplitude, and action potential duration as a function of parameter values, by fitting a curve in parameter space and projecting the curve beyond the tested values. SIGNIFICANCE STATEMENT Plateau potentials are intrinsic properties of neurons that are important for information processing in a wide variety of nervous systems. We examined three identified neurons in Aplysia californica with different propensities to generate a plateau potential. No single conductance was found to distinguish plateau generating neurons. Instead, plateau generation depended on the ratio between persistent Na + current ( I NaP ), which favored plateaus, and outward currents such as I KCa , which facilitated plateau termination. Computational models revealed a relationship between the individual currents that predicted the features of simulated plateau potentials. These results provide a more solid understanding of the conductances that mediate plateau generation.

  PublisherOA PDFDOI

• Neuronal population activity dynamics reveal a low-dimensional signature of operant learning in Aplysia

  Communications Biology · 2022-01-24 · 10 citations

  articleOpen access

  Learning engages a high-dimensional neuronal population space spanning multiple brain regions. However, it remains unknown whether it is possible to identify a low-dimensional signature associated with operant conditioning, a ubiquitous form of learning in which animals learn from the consequences of behavior. Using single-neuron resolution voltage imaging, here we identify two low-dimensional motor modules in the neuronal population underlying Aplysia feeding. Our findings point to a temporal shift in module recruitment as the primary signature of operant learning. Our findings can help guide characterization of learning signatures in systems in which only a smaller fraction of the relevant neuronal population can be monitored.

  PublisherDOI

• Computational analysis of memory consolidation following inhibitory avoidance (IA) training in adult and infant rats: Critical roles of CaMKIIα and MeCP2

  PLoS Computational Biology · 2022-06-27 · 2 citations

  articleOpen access

  Key features of long-term memory (LTM), such as its stability and persistence, are acquired during processes collectively referred to as consolidation. The dynamics of biological changes during consolidation are complex. In adult rodents, consolidation exhibits distinct periods during which the engram is more or less resistant to disruption. Moreover, the ability to consolidate memories differs during developmental periods. Although the molecular mechanisms underlying consolidation are poorly understood, the initial stages rely on interacting signaling pathways that regulate gene expression, including brain-derived neurotrophic factor (BDNF) and Ca2+/calmodulin-dependent protein kinase II α (CaMKIIα) dependent feedback loops. We investigated the ways in which these pathways may contribute to developmental and dynamical features of consolidation. A computational model of molecular processes underlying consolidation following inhibitory avoidance (IA) training in rats was developed. Differential equations described the actions of CaMKIIα, multiple feedback loops regulating BDNF expression, and several transcription factors including methyl-CpG binding protein 2 (MeCP2), histone deacetylase 2 (HDAC2), and SIN3 transcription regulator family member A (Sin3a). This model provides novel explanations for the (apparent) rapid forgetting of infantile memory and the temporal progression of memory consolidation in adults. Simulations predict that dual effects of MeCP2 on the expression of bdnf, and interaction between MeCP2 and CaMKIIα, play critical roles in the rapid forgetting of infantile memory and the progress of memory resistance to disruptions. These insights suggest new potential targets of therapy for memory impairment.

  PublisherOA PDFDOI

• Computational analysis of memory consolidation following inhibitory avoidance (IA) training in adult and infant rats: critical roles of CaMKIIα and MeCP2

  bioRxiv (Cold Spring Harbor Laboratory) · 2022-04-01

  preprintOpen access

  Abstract Key features of long-term memory (LTM), such as its stability and persistence, are acquired during processes collectively referred to as consolidation. The dynamics of biological changes during consolidation are complex. In adult rodents, consolidation exhibits distinct periods during which the engram is more or less resistant to disruption. Moreover, the ability to consolidate memories differs during developmental periods. Although the molecular mechanisms underlying consolidation are poorly understood, the initial stages rely on interacting signaling pathways that regulate gene expression, including brain-derived neurotrophic factor (BDNF) and Ca 2+ /calmodulin-dependent protein kinase II α (CaMKIIα) dependent feedback loops. We investigated the ways in which these pathways may contribute to developmental and dynamical features of consolidation. A computational model of molecular processes underlying consolidation following inhibitory avoidance (IA) training in rats was developed. Differential equations described the actions of CaMKIIα, multiple feedback loops regulating BDNF expression, and several transcription factors including methyl-CpG binding protein 2 (MeCP2), histone deacetylase 2 (HDAC2), and SIN3 transcription regulator family member A (Sin3a). This model provides novel explanations for the (apparent) rapid forgetting of infantile memory and the temporal progression of memory consolidation in adults. Simulations predict that dual effects of MeCP2 on the expression of bdnf , and interaction between MeCP2 and CaMKIIα, play critical roles in the rapid forgetting of infantile memory and the progress of memory resistance to disruptions. These insights suggest new potential targets of therapy for memory impairment. Author Summary Long-term memories (LTMs) are enduring and resistant to disruption These features are acquired via processes collectively referred to as consolidation. In adults, the initial stages of consolidation follow complex dynamics that are believed to emerge from interacting biochemical signaling pathways [1], including BDNF and CaMKIIα dependent feedback loops. Similarly, the acquisition of ability to consolidate memory in infantile animals is believed to emerge from the functional maturation of these molecular pathways [2]. Here, the ways in which these pathways contribute to consolidation were investigated using a computational model. This model provides novel explanations for the apparent rapid forgetting of infantile memory and for development of resistance to disruption during memory consolidation.

  PublisherOA PDFDOI

• Genesis of bursting activity: Role of inhibitory constraints on persistent Na ⁺ currents

  bioRxiv (Cold Spring Harbor Laboratory) · 2022-02-08

  preprintOpen access

  SUMMARY Some neurons express a plateau of spike activity greatly outlasting a stimulus, whereas others do not. This difference could be due to differential expression of ion channels (e.g., persistent Na + , and Ca 2+ ) or similar expression of channels that differ in their properties. We compared three Aplysia neurons with varying capacity to generate plateau potentials: B51 with self-terminating plateaus, B64 with plateau potentials that do not self-terminate, and the regular spiking neuron B8. Our results indicate the three neurons expressed outward currents I A and I D , voltage-gated Ca 2+ currents I CaL and I CaR , and persistent inward I NaP . The most notable difference observed was a larger I A , I D , and I KCa currents in B8, and the plateau generating B64 did not express I KCa . Computational models suggest outward currents suppress and temporally constrain the plateau potential and that inward Ca 2+ currents suppress plateau potentials when coupled with I KCa .

  PublisherOA PDFDOI

• Specific plasticity loci and their synergism mediate operant conditioning

  bioRxiv (Cold Spring Harbor Laboratory) · 2021-12-03 · 1 citations

  preprintOpen access

  Abstract Despite numerous studies examining the mechanisms of operant conditioning (OC), the diversity of plasticity loci and their synergism have not been examined sufficiently. In the well-characterized feeding neural circuit of Aplysia , appetitive OC increases neuronal excitability and electrical coupling among several neurons. Here we found OC decreased the intrinsic excitability of B4 and the strength of its inhibitory connection to a key decision-making neuron, B51. The OC-induced changes were specific without affecting the B4-to-B8 inhibitory connection or excitability of another neuron critical for feeding behavior, B8. A conductance-based circuit model indicated certain sites of plasticity mediated the OC phenotype more effectively and that plasticity loci acted synergistically. This synergy was specific in that only certain combinations of loci synergistically enhanced feeding. Taken together, these results suggest modifications of diverse loci work synergistically to mediate OC. Significance Statement The diversity and synergism of plasticity loci mediating operant conditioning (OC) is poorly understood. Here we found that OC decreased the intrinsic excitability of a critical neuron mediating Aplysia feeding behavior and specifically reduced the strength of one of its inhibitory connections to a key decision-making neuron. A conductance-based computational model indicated that the known plasticity loci showed a surprising level of synergism to mediate the behavioral changes associated with OC. These results highlight the importance of understanding the diversity, specificity and synergy among different types of plasticity that encode memory. Also, because OC in Aplysia is mediated by dopamine (DA), the present study provides insights into specific and synergistic mechanisms of DA-mediated reinforcement of behaviors.

  PublisherOA PDFDOI

• Neuronal population activity dynamics reveal a low-dimensional signature of operant learning

  bioRxiv (Cold Spring Harbor Laboratory) · 2021-12-07

  preprintOpen access

  Abstract Learning engages a high-dimensional neuronal population space spanning multiple brain regions. We identified a low-dimensional signature associated with operant conditioning, a ubiquitous form of learning in which animals learn from the consequences of behavior. Using single-neuron resolution voltage imaging, we identified two low-dimensional motor modules in the neuronal population underlying Aplysia feeding. Our findings point to a temporal shift in module recruitment as the primary signature of operant learning.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01RR011626

  NIH · $1.9M · 2008

• NIH Grant P01NS038310

  NIH · $17.2M · 2011

Frequent coauthors

• John H. Byrne

  158 shared

• Paul Smolen

  The University of Texas Health Science Center at Houston

  48 shared

• Carmen C. Canavier

  Louisiana State University Health Sciences Center New Orleans

  15 shared

• John W. Clark

  13 shared

• Yili Zhang

  Georgetown University

  10 shared

• Curtis L. Neveu

  The University of Texas Health Science Center at Houston

  9 shared

• H. Lechner

  Salk Institute for Biological Studies

  9 shared

• Yidao Cai

  9 shared

Awards & honors

• EnMed Appreciation Gift during the 2024 M4 Awards Ceremony