About

Michael Baratta is an Assistant Professor in the Department of Psychology and Neuroscience at the University of Colorado Boulder. He holds a PhD from the University of Colorado Boulder, earned in 2008. His research focuses on how experiential factors modify an organism's response to future challenge. He is affiliated with the Baratta Laboratory located in the Muenzinger D244 building, and his contact information includes an email address (Michael.Baratta@colorado.edu) and a phone number (303-492-0777). His work is situated within the field of behavioral neuroscience, and he is involved in advancing understanding of the neural mechanisms underlying behavioral responses to environmental and experiential influences.

Research topics

• Neuroscience
• Medicine
• Immunology
• Biology
• Internal medicine
• Physiology
• Mathematics
• Psychiatry
• Social psychology
• Psychology
• Cognitive science
• Cognitive psychology

Selected publications

• A novel soil-derived Mycolicibacterium decreases anxiety-like defensive behavioral responses in association with decreases in biomarkers of neuroinflammation and hippocampal microglial priming in adult male rats

  Brain Behavior and Immunity · 2026-05-01

  articleOpen access
  PublisherOA PDFDOI

• Caudal Granular Insular Cortex to Somatosensory Cortex I: A Critical Pathway for the Transition of Acute to Chronic Pain

  Journal of Neuroscience · 2025-12-16 · 1 citations

  articleOpen access

  Allodynia (perceiving touch as painful) is an enduring symptom of neuropathic pain. While acute pain is initiated by afferent signaling from the periphery to spinal cord, pain chronification recruits ongoing activity in supraspinal sites. One such site that has been proposed to be important in pain chronification is the caudal granular insular cortex (CGIC). The present studies of allodynia in response to sciatic nerve injury in male and female rats focus on the role of CGIC in pain chronification by analyzing: circuit-specific mGreenLantern expression to define CGIC-to-somatosensory cortex I (SI) projections; behavioral and electrophysiological effects of chemogenetic (DREADD) excitation and inhibition of CGIC; behavioral and immediate-early gene effects of pathway-specific activation and inhibition of CGIC-to-SI projections; and mGreenLantern expression in dendritic arbors of CGIC-to-SI projection neurons to assess CGIC dendritic spine changes following neuropathic pain. These studies demonstrate that signals from CGIC-to-SI are necessary for neuropathic pain. Nerve injury induces plasticity in CGIC dendritic spine morphology, multiweek chemogenetic inhibition of CGIC or CGIC-to-SI projection neurons produces an enduring reversal of neuropathic pain, and DREADD-induced excitation of this pathway in non-neuropathic rats induces allodynia and increases c-Fos expression in CGIC, SI, and pain responsive laminae in spinal cord dorsal horn. Together with recent findings showing that SI modifies incoming nociceptive and touch information, these data demonstrate that input from CGIC-to-SI input shapes SI gating of nociceptive signals and promotes the transition to chronic pain following peripheral nerve injury.

  PublisherOA PDFDOI

• Active coping mitigates the effects of stress on glucocorticoid levels in the prefrontal cortex

  Brain Behavior and Immunity · 2025-08-28

  articleSenior author
  PublisherDOI

• Interpeduncular GABAergic neuron function controls threat processing and innate defensive adaptive learning

  Molecular Psychiatry · 2025-08-08 · 1 citations

  articleOpen access

  The selection of appropriate defensive behaviors in the face of potential threat is fundamental to survival. Equally important is learning to adjust and optimize defensive behaviors when there is no real danger. Despite extensive research on innate threat processing, little is known about the mechanisms by which individuals adapt their defensive behaviors in response to repeated threats that lack real danger. Insight into this process is critical as its dysregulation may contribute to neuropsychiatric conditions, such as anxiety disorders. Here, we used the visual looming stimulus (VLS) paradigm in mice to investigate innate threat processing and adaptive defensive learning. Repeated exposure to VLS over consecutive sessions reduced immediate freezing responses and time spent inside a sheltered area upon VLS events, leading to an increase in exploratory behaviors. Fiber photometry recordings and optogenetic manipulations revealed that VLS innate adaptive defensive learning is associated with reduced recruitment of the midbrain interpeduncular nucleus (IPN), a structure associated with fear and anxiety-related behaviors. Functional circuit-mapping identified a role for select IPN projections to the laterodorsal tegmental nucleus in gating defensive learning. Finally, we uncovered a subpopulation of IPN neurons that express the neuropeptide somatostatin and encode avoidance signals in response to VLS. These results identify critical behavioral signatures of innate defensive responses and a circuit that regulates the essential features of threat processing.

  PublisherOA PDFDOI

• Modulation of dorsal raphe nucleus connectivity and serotonergic signalling to the insular cortex in the prosocial effects of chronic fluoxetine

  Neuropharmacology · 2025-03-11 · 1 citations

  articleOpen access

  Long-term exposure to fluoxetine and other selective serotonin reuptake inhibitors alters social and anxiety-related behaviours, including social withdrawal, which is a symptom of several neuropsychiatric disorders. Adaptive changes in serotonergic neurotransmission likely mediate this delayed effect, although the exact mechanisms are still unclear. Here we investigated the functional circuitry underlying the biphasic effects of fluoxetine on social approach-avoidance behaviour and explored the place of serotonergic dorsal raphe nucleus (DR) ensembles in this network, using c-Fos-immunoreactivity as a correlate of activity. Graph theory-based network analysis revealed changes in patterns of functional connectivity and identified neuronal populations in the insular cortex (IC) and serotonergic populations in the DR as central targets to the prosocial effects of chronic fluoxetine. To determine the role of serotonergic projections to the IC, a retrograde tracer was micro-injected in the IC prior to fluoxetine treatment and social behaviour testing. Chronic fluoxetine increased c-Fos immunoreactivity in insula-projecting neurons of the rostral, ventral part of the DR (DRV). Using a virally delivered Tet-Off platform for temporally-controlled marking of neuronal activation, we observed that chronic fluoxetine may affect social behaviour by influencing independent but interconnected populations of serotonergic DR ensembles. These findings suggest that sustained fluoxetine exposure causes adaptive changes in functional connectivity due to altered serotonergic neurotransmission in DR projection targets, and the increased serotonergic signalling to the IC likely mediate some of the therapeutic effects of fluoxetine on social behaviour. • Fluoxetine treatment alters patterns of functional connectivity across the brain • Correlated activity of dorsal raphe serotonergic neurons is altered by fluoxetine • Insula and dorsal raphe connectivity are important for the effects of fluoxetine • Prosocial effects of fluoxetine engage insula-projecting DRV serotonergic neurons • Distinct serotonergic clusters in the DR mediate social behaviour and SSRI response

  PublisherDOI

• Salience Signaling and Stimulus Scaling of Ventral Tegmental Area Glutamate Neuron Subtypes

  Journal of Neuroscience · 2025-06-05 · 3 citations

  articleOpen access

  Ventral tegmental area (VTA) glutamatergic neurons participate in reward, aversion, drug-seeking, and stress. Subsets of these neurons cotransmit glutamate and GABA (VGluT2 + VGaT + neurons), transmit glutamate without GABA (VGluT2 + VGaT − neurons), or cotransmit glutamate and dopamine (VGluT2 + TH + neurons), but whether these molecularly distinct subpopulations show behavior-related differences is not wholly understood. We identified in male and female mice that VGluT2 + subpopulations are sensitive to the reward value in unique ways. VGluT2 + VGaT + neurons increased maximum activity with increased sucrose concentration, whereas VGluT2 + VGaT − neurons increased maximum and sustained activity with increased sucrose concentration, and VGluT2 + TH + neurons increased sustained but not maximum activity with increased sucrose concentration. VGluT2 + subpopulations also uniquely signaled consumption of sweet/noncaloric (saccharine) and nonsweet/high-calorie rewards (fat). VGluT2 + VGaT + neurons uniquely signaled lower-calorie sucrose over fat, whereas both VGluT2 + VGaT − neurons and VGluT2 + TH + neurons showed a signaling preference for higher-calorie fat over sucrose but in temporally distinct ways. Further experiments suggested that VGluT2 + VGaT + consummatory reward-related activity was related to sweetness, partially modulated by prefeeding, and not dependent on caloric content. Additionally, aversive stimuli increased activity for each VGluT2 + subpopulation, but VGluT2 + VGaT + neurons uniquely scaled their magnitude and sustained activity with footshock intensity. Optogenetic activation of VGluT2 + VGaT + neurons during low-intensity footshock enhanced fear-related behavior without inducing place preference or aversion. About half of VGluT2 + VGaT + sucrose-sensitive neurons were transcriptionally activated by footshock. We interpret these data such that VTA glutamatergic subpopulations signal different elements of rewarding and aversive experiences and highlight the unique role of VTA VGluT2 + VGaT + neurons in salience signaling.

  PublisherOA PDFDOI

• Timing of Changes in Alzheimer's Disease Plasma Biomarkers as Assessed by Amyloid and Tau <scp>PET</scp> Clocks

  Annals of Neurology · 2025-06-20 · 20 citations

  articleOpen access

  OBJECTIVE: The objective of this study was to evaluate the timing of change of Alzheimer's disease (AD) plasma biomarkers (Aβ42/Aβ40, p-tau217, p-tau181, GFAP, and NfL) from six different assay platforms, alongside established AD biomarkers, using amyloid and tau positron emission tomography (PET)-based AD progression timelines. METHODS: Data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), including 784 individuals with longitudinal amyloid PET and 359 with longitudinal tau PET, were analyzed to estimate the age at amyloid and tau PET positivity, respectively. Longitudinal plasma biomarker measurements were available from 190 individuals with an estimated amyloid PET positivity age and from 70 individuals with an estimated tau PET positivity age. In a subset of 17 clinical progressors, age at tau PET positivity strongly predicted symptom onset, allowing for estimation of symptom onset age. Biomarker trajectories based on time from amyloid or tau PET positivity or symptom onset were modelled using Generalized Additive Mixed models. Time intervals of significant biomarker change and the earliest timepoints at which biomarkers exceeded predefined abnormality thresholds were identified. RESULTS: All plasma biomarkers except NfL became abnormal prior to established thresholds for amyloid and tau PET positivity. Plasma Aβ42/Aβ40 became abnormal very early in both amyloid PET and tau PET timelines, while plasma GFAP became abnormal early in the tau PET timeline. Plasma Aβ42/Aβ40 levels plateaued, whereas plasma p-tau217, p-tau181, GFAP, and NfL levels increased throughout the modeled disease progression. Some variations in the timing of these changes were observed across different biomarker assays. INTERPRETATION: These findings suggest that the plasma Aβ42/Aβ40 may be useful in identifying individuals with very low levels of amyloid pathology, whereas p-tau, GFAP, and NfL may be useful in staging disease progression. ANN NEUROL 2025;98:508-523.

  PublisherOA PDFDOI

• Dr. Steven F. Maier: A fearless scientist, a rigorous mentor, and a legacy of excellence

  Brain Behavior and Immunity · 2025-04-14

  articleOpen access

  For more than 40 years, Dr. Steven F. Maier has shaped the field of psychoneuroimmunology through innovative research, influential mentorship, and dedicated service to the scientific community. As he concludes his tenure as Associate Editor of Brain, Behavior, and Immunity, this tribute reflects on his most transformative scientific contributions-from conceptualizing learned helplessness to uncovering the neural and immune mechanisms linking stress to disease vulnerability. Drawing from our experiences as longtime mentees and later colleagues, we also share reflections on his unique mentoring style, unwavering commitment to scientific rigor, and enduring influence on the field.

  PublisherDOI

• Interpeduncular GABAergic neuron function controls threat processing and innate defensive adaptive learning

  Research Square · 2024-09-20

  preprintOpen access
  PublisherOA PDFDOI

• Timing of changes in Alzheimer’s disease plasma biomarkers as assessed by amyloid and tau PET clocks

  medRxiv · 2024-10-28 · 2 citations

  preprintOpen access

  Abstract Plasma biomarkers for Alzheimer’s disease (AD) are increasingly being used to assist in making an etiological diagnosis for cognitively impaired (CI) individuals or to identify cognitively unimpaired (CU) individuals with AD pathology who may be eligible for prevention trials. However, a better understanding of the timing of plasma biomarker changes is needed to optimize their use in clinical and research settings. The aim of this study was to evaluate the timing of change of key AD plasma biomarkers (Aβ42/Aβ40, p-tau217, p-tau181, GFAP and NfL) from six different companies, along with established AD biomarkers, using AD progression timelines based on amyloid and tau PET. We used data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), including 784 individuals with longitudinal 18 F-florbetapir amyloid PET and 359 individuals with longitudinal 18 F-flortaucipir tau PET, to estimate age at amyloid and tau positivity, defined as the age at the first positive PET scan. Of these, longitudinal plasma biomarker measures were available from 190 individuals with an estimated age at amyloid positivity and 70 individuals with an estimated age at tau positivity. Age at tau positivity was a stronger predictor of symptom onset than age at amyloid positivity in 17 individuals who progressed from CU to CI during their participation in the ADNI study (Adj R 2 = 0.86 vs. Adj R 2 = 0.38), and therefore was used to estimate symptom onset age for all individuals with an estimated age at tau positivity. Generalized additive mixed models (GAMMs) were used to model biomarker trajectories across years since amyloid positivity, tau positivity, and symptom onset, and to identify the earliest timepoint of biomarker abnormality when compared to a reference group of amyloid- and tau-negative CU individuals, as well as time periods of significant change in biomarkers. All plasma biomarkers except NfL became abnormal prior to amyloid and tau positivity. Plasma Aβ42/Aβ40 was the first biomarker to reach abnormality consistently across timelines and plasma GFAP became abnormal early in the tau timeline. Plasma Aβ42/Aβ40 levels reached a plateau, while plasma p-tau217, p-tau181, GFAP and NfL increased throughout disease progression. Some differences in the timing of change were observed across biomarker assays. The primary utility of plasma Aβ42/Aβ40 may lie in early identification of individuals at high risk of AD. In contrast, p-tau217, p-tau181, GFAP and NfL increase throughout the estimated timelines, supporting their potential as biomarkers for staging and monitoring disease progression.

  PublisherOA PDFDOI

Recent grants

• NIH Grant R21MH106817

  NIH · $419k · 2018

• Behavioral control recruits prefrontal circuits that modulate conditioned fear

  NIH · $424k · 2019–2022

• NIH Grant F31MH075213

  NIH · $56k · 2007

• Stressor controllability: Prefrontal circuits that produce resilience and dominance

  NIH · $8.9M · 1993–2029

Frequent coauthors

• Steven F. Maier

  University of Colorado Boulder

  46 shared

• Linda R. Watkins

  University of Colorado Boulder

  30 shared

• Donald Cooper

  Mobile Assay (United States)

  27 shared

• César Venero

  Hurley Medical Center

  25 shared

• Samuel D Dolzani

  University of Colorado Boulder

  23 shared

• Sandra A. Brown

  University of California, San Diego

  20 shared

• Susan F. Tapert

  University of California, San Diego

  20 shared

• José Amat

  University of Colorado Boulder

  19 shared

Education

• Ph.D.

  University of Colorado Boulder

  2008