About

Emily Bauer is a faculty member at Columbia GSAPP. The page does not provide specific details about her research focus, background, or key contributions. Therefore, no further biographical information is available from the provided content.

Research topics

• Cognitive psychology
• Psychology
• Neuroscience

Selected publications

• Chemogenetic activation of the ventral subiculum–BNST pathway reduces context fear expression

  Learning & Memory · 2023-08-01 · 4 citations

  articleOpen accessSenior author

  An inability to reduce fear in nonthreatening environments characterizes many anxiety disorders. The pathway from the ventral subiculum (vSUB) to the bed nucleus of the stria terminalis (BNST) is more active in safe contexts than in aversive ones, as indexed by FOS expression. Here, we used chemogenetic techniques to specifically activate the vSUB-BNST pathway during both context and cued fear expression by expressing a Cre-dependent hM3D(Gq) receptor in BNST-projecting vSUB neurons. Activation of the vSUB-BNST pathway reduced context but not cued fear expression. These data suggest that the vSUB-BNST pathway contributes to behavioral responses to nonaversive contexts.

  PublisherOA PDFDOI

• Aversive Contexts Reduce Activity in the Ventral Subiculum- BNST Pathway

  Neuroscience · 2022-06-17 · 8 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Sex differences in fear responses: Neural circuits

  Neuropharmacology · 2022 · 77 citations

  1st authorCorresponding
  • Psychology
  • Neuroscience
  • Cognitive psychology
  PublisherOA PDFDOI

• Extended amygdala circuits are differentially activated by context fear conditioning in male and female rats

  Neurobiology of Learning and Memory · 2021-02-10 · 32 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Understanding Student And Faculty Attitudes With Respect To Service Learning: Lessons From The Humanitarian Engineering Program

  2020-09-03 · 5 citations

  articleOpen access

  Now entering its second year, the Humanitarian Engineering Program, which is sponsored by the Hewlett Foundation, at the Colorado School of Mines is creating curriculum that will support engineering students in developing an understanding of their responsibility for solving humanitarian problems that exist throughout the world. As part of this effort, baseline data has been collected on both the faculty and student attitudes towards service activities using the "Community Service Attitudes Scale" which was developed and validated by Shiarella, McCarthy, and Tucker 1 . During the fall of 2004, 78 students and 34 faculty responded to this assessment instrument. Student data were collected in the first semester of the Multidisciplinary Engineering Laboratory course sequence, a required course taken at the start of students' sophomore year before they have the opportunity to participate in the newly revised service learning courses. Faculty completed the attitudes survey during the first faculty meeting of the academic year. This paper describes and compares student and faculty attitudes with respect to service activities prior to the proposed intervention. Attention is given to attitudinal differences between male and female students and among students in different age groups.

  PublisherOA PDFDOI

• Yo GABA _A GABA _A : How the Structure of Human GABA _A Receptor Affects the Action of Anesthetics

  The FASEB Journal · 2018-04-01

  article

  Propofol, a powerful anesthetic, can be used safely in medical settings, but proves deadly when used recreationally. Propofol binds to the GABA A receptor, which consists of an integral ion channel protein embedded in the membrane of neurons in the brain that is activated by the neurotransmitter molecule gamma‐aminobutyric acid, or GABA. When propofol binds to the GABA A receptor, a conformational change occurs, holding the neurotransmitter GABA in its binding site and keeping the ion channel open. This allows more chloride ions to diffuse into the cell. Resting potential becomes more negative, so even with the diffusion of Na + ions during nerve stimulation, the threshold cannot be reached and the action potential is not generated. Since the neurons cannot communicate normally, a person given propofol remains unconscious. The lower part of the GABA A receptor, located in the cytoplasm of a neuron, has an unidentified molecular structure. Phe 393 variants in the A and D chains prevent propofol from acting on the GABA A receptor. The DSHA SMART (Students Modeling A Research Topic) Team modeled the similar nicotinic receptor using 3D printing technology to better understand the structure of the GABA A receptor. A greater understanding of the structure of the GABA A receptor and the role of the Phe 393 variants in the action of propofol can lead to the development of more effective anesthetics. Support or Funding Information The MSOE Center for BioMolecular Modeling would like to acknowledge and thank the National Institutes of Health Science Education Partnership Award (NIH‐SEPA 1R25OD010505‐01) and the National Institutes of Health Clinical and Translational Science Award (NIH‐CTSA UL1RR031973) for their support in funding the 2017–2018 SMART Team Team program. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

  PublisherDOI

• Rate and Temporal Coding Mechanisms in the Anterior Cingulate Cortex for Pain Anticipation

  Scientific Reports · 2018-05-23 · 29 citations

  articleOpen access

  Pain is a complex sensory and affective experience. Through its anticipation, animals can learn to avoid pain. Much is known about passive avoidance during a painful event; however, less is known about active pain avoidance. The anterior cingulate cortex (ACC) is a critical hub for affective pain processing. However, there is currently no mechanism that links ACC activities at the cellular level with behavioral anticipation or avoidance. Here we asked whether distinct populations of neurons in the ACC can encode information for pain anticipation. We used tetrodes to record from ACC neurons during a conditioning assay to train rats to avoid pain. We found that in rats that successfully avoid acute pain episodes, neurons that responded to pain shifted their firing rates to an earlier time, whereas neurons that responded to the anticipation of pain increased their firing rates prior to noxious stimulation. Furthermore, we found a selected group of neurons that shifted their firing from a pain-tuned response to an anticipatory response. Unsupervised learning analysis of ensemble spike activity indicates that temporal spiking patterns of ACC neurons can indeed predict the onset of pain avoidance. These results suggest rate and temporal coding schemes in the ACC for pain avoidance.

  PublisherOA PDFDOI

• Differential effects of stress on fear learning and activation of the amygdala in pre-adolescent and adult male rats

  Neuroscience · 2017-07-30 · 16 citations

  articleSenior authorCorresponding
  PublisherDOI

• 5-HT2C receptors in the BNST are necessary for the enhancement of fear learning by selective serotonin reuptake inhibitors

  Neurobiology of Learning and Memory · 2016-10-20 · 34 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Behavioral Neuroscience of Circuits Involved in Fear Processing

  Oxford University Press eBooks · 2016-08-01

  book1st authorCorresponding

  Normal fear regulation includes the ability to learn by experience that some circumstances predict danger. This process, which can be modeled in the laboratory using Pavlovian fear conditioning, appears to be disrupted in individuals with post-traumatic stress disorder (PTSD). Understanding of the mechanisms underlying fear learning has progressed tremendously in the last 25 years, and constitutes a promising paradigm to study the neural bases of PTSD. This chapter first reviews current knowledge of the brain structures involved in fear learning, expression and extinction, including the contributions of the amygdala and prefrontal cortex. It then addresses how these circuits are affected by PTSD and how fear processing is altered in PTSD. Understanding PTSD within a fear-conditioning and extinction framework provides insight into why certain individuals are susceptible to developing PTSD and suggests potential therapies.

  PublisherDOI

Recent grants

• Modulation of fear conditioning by extended amygdala circuits

  NIH · $411k · 2016–2020

• NIH Grant R15MH095032

  NIH · $392k · 2015

• NIH Grant F32MH076640

  NIH · $99k · 2009

• NIH Grant F31NS043899

  NIH · $58k · 2005

Frequent coauthors

• Joseph E. LeDoux

  24 shared

• Louise Urien

  18 shared

• Glenn E. Schafe

  The Graduate Center, CUNY

  15 shared

• Sarina M. Rodrigues

  15 shared

• Claudia R. Farb

  New York University

  9 shared

• Alexandrina Yakimov

  Columbia University

  8 shared

• Georgia Barbayannis

  Rutgers, The State University of New Jersey

  8 shared

• Katina C. Calakos

  Simons Foundation

  8 shared

Labs

• Emily BauerPI

Education

• M.S.

  Columbia University Graduate School of Architecture, Planning and Preservation