About

Professor Steven F. Maier is a distinguished professor in the Department of Psychology and Neuroscience at the University of Colorado Boulder. He serves as the Director of the Center for Neuroscience and is recognized for his active involvement in research, despite being retired and no longer taking students. His educational background includes a PhD from the University of Pennsylvania, obtained in 1968. Professor Maier's research interests focus on the neurochemistry and neuropharmacology of stress, drug addiction, and the bi-directional communication between the brain and the immune system, with a particular emphasis on psychoneuroimmunology. His work contributes to understanding the complex interactions between neural and immune processes, advancing knowledge in behavioral neuroscience.

Research topics

• Medicine
• Neuroscience
• Biology
• Immunology
• Psychiatry
• Psychology
• Internal medicine
• Anesthesia
• Cognitive science
• Physical therapy
• Cognitive psychology
• Social psychology
• Mathematics

Selected publications

• Effects of Oral Administration of the Probiotic Lactobacillus rhamnosus GG on the Proteomic Profiles of Cerebrospinal Fluid and Immunoregulatory Signaling in the Hippocampus of Adult Male Rats

  NeuroImmunoModulation · 2025-03-03 · 2 citations

  articleOpen access

  INTRODUCTION: The microbiome-gut-brain axis, by modulating bidirectional immune, metabolic, and neural signaling pathways in the host, has emerged as a target for the prevention and treatment of psychiatric and neurological disorders. Oral administration of the probiotic bacterium Lactobacillus rhamnosus GG (LGG; ATCC 53103) exhibits anti-inflammatory effects, although the precise mechanisms by which LGG benefits host physiology and behavior are not known. The goal of this study was to explore the general effects of LGG on the cerebrospinal fluid (CSF) proteome and a biological signature of anti-inflammatory signaling in the central nervous system (CNS) of undisturbed, adult male rats. METHODS: Liquid chromatography-tandem mass spectrometry-based proteomics were conducted using CSF samples collected after 21 days of oral treatment with live LGG (3.34 × 107 colony-forming units (CFU)/mL in the drinking water (resulting in an estimated delivery of ∼1.17 × 109 CFU/day/rat) or water vehicle. Gene enrichment analysis (using DAVID, v. 6.8) and protein-protein interactions (using STRING, v. 11) were used to explore physiological network changes in CSF. Real-time reverse transcription polymerase chain reaction (real-time RT-PCR) was performed to assess gene expression changes of anti-inflammatory cytokines in the hippocampus. Genes associated with anti-inflammatory signaling that were analyzed included Il10, Tgfb1, Il4, and IL-4-responsive genes, Cd200, Cd200r1, and Mrc1 (Cd206). RESULTS: Oral LGG administration altered the abundance of CSF proteins, increasing the abundance of five proteins (cochlin, NPTXR, reelin, Sez6l, and VPS13C) and decreasing the abundance of two proteins (CPQ, IGFBP-7) in the CSF. Simultaneously, LGG increased the expression of Il10 mRNA, encoding the anti-inflammatory cytokine interleukin 10, in the hippocampus. CONCLUSION: Oral LGG altered the abundance of CSF proteins associated with extracellular scaffolding, synaptic plasticity, and glutamatergic signaling. These data are consistent with the hypothesis that oral administration of LGG improves memory and cognition, and promotes a physiological resilience to neurodegenerative disease, by increasing glutamatergic signaling and promoting an anti-inflammatory environment in the brain.

  PublisherOA PDFDOI

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

  Brain Behavior and Immunity · 2025-08-28

  article
  PublisherDOI

• SARS-CoV-2 S1 subunit produces a protracted priming of the neuroinflammatory, physiological, and behavioral responses to a remote immune challenge: A role for corticosteroids

  Brain Behavior and Immunity · 2024-07-21 · 11 citations

  articleSenior author
  PublisherDOI

• Prior experience with behavioral control over stress facilitates social dominance

  Neurobiology of Stress · 2023-12-06 · 2 citations

  articleOpen access

  Dominance status has extensive effects on physical and mental health, and an individual's relative position can be shaped by experiential factors. A variety of considerations suggest that the experience of behavioral control over stressors should produce winning in dominance tests and that winning should blunt the impact of later stressors, as does prior control. To investigate the interplay between competitive success and stressor control, we first examined the impact of stressor controllability on subsequent performance in a warm spot competition test modified for rats. Prior experience of controllable, but not physically identical uncontrollable, stress increased later effortful behavior and occupation of the warm spot. Controllable stress subjects consistently ranked higher than did uncontrollable stress subjects. Pharmacological inactivation of the prelimbic (PL) cortex during behavioral control prevented later facilitation of dominance. Next, we explored whether repeated winning experiences produced later resistance against the typical sequelae of uncontrollable stress. To establish dominance status, triads of rats were given five sessions of warm spot competition. The development of stable dominance was prevented by reversible inactivation of the PL or NMDA receptor blockade in the dorsomedial striatum. Stable winning blunted the later stress-induced increase in dorsal raphe nucleus serotonergic activity, as well as prevented uncontrollable stress-induced social avoidance. In contrast, endocrine and neuroimmune responses to uncontrollable stress were unaffected, indicating a selective impact of prior dominance. Together, these data demonstrate that instrumental control over stress promotes later dominance, but also reveal that winning experiences buffer against the neural and behavioral outcomes of future adversity.

  PublisherDOI

• Prior experience with behavioral control over stress facilitates social dominance

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-06-07 · 1 citations

  preprintOpen access

  Dominance status has extensive effects on physical and mental health, and an individual's relative position can be shaped by experiential factors. A variety of considerations suggest that the experience of behavioral control over stressors should produce winning in dominance tests and that winning should blunt the impact of later stressors, as does prior control. To investigate the interplay between competitive success and stressor control, we first examined the impact of stressor controllability on subsequent performance in a warm spot competition test modified for rats. Prior experience of controllable, but not physically identical uncontrollable, stress increased later effortful behavior and occupation of the warm spot. Controllable stress subjects consistently ranked higher than did uncontrollable stress subjects. Pharmacological inactivation of the prelimbic (PL) cortex during behavioral control prevented later facilitation of dominance. Next, we explored whether repeated winning experiences produced later resistance against the typical sequelae of uncontrollable stress. To establish dominance status, triads of rats were given five sessions of warm spot competition. Reversible inactivation of the PL or NMDA receptor blockade in the dorsomedial striatum led to a long-term reduction in social rank. Stable dominance blunted the later stress-induced increase in dorsal raphe nucleus serotonergic activity, as well as prevented stress-induced social avoidance. In contrast, endocrine and neuroimmune responses to uncontrollable stress were unaffected, indicating a selective impact of prior dominance. Together, these data demonstrate that instrumental control over stress promotes later dominance, but also reveal that winning experiences buffer against the neural and behavioral outcomes of future adversity.

  PublisherOA PDFDOI

• Voluntary wheel running prevents formation of membrane attack complexes and myelin degradation after peripheral nerve injury

  Brain Behavior and Immunity · 2023-11-03 · 5 citations

  articleOpen access
  PublisherOA PDFDOI

• From helplessness to controllability: toward a neuroscience of resilience

  Frontiers in Psychiatry · 2023 · 40 citations

  Senior authorCorresponding
  • Psychology
  • Cognitive psychology
  • Neuroscience

  produces the debilitation by potent activation of serotonergic neurons in the brainstem dorsal raphe nucleus. Debilitation is prevented with an instrumental controlling response, which activates prefrontal circuitry detecting control and subsequently blunting the dorsal raphe nucleus response. Furthermore, learning control alters the prefrontal response to future adverse events, thereby preventing debilitation and producing long-term resiliency. The general implications of these neuroscience findings may apply to psychological therapy and prevention, in particular by suggesting the importance of cognitions and control, rather than habits of control.

  PublisherOA PDFDOI

• Sex Differences in Stress-Induced Prefrontal Circuit Plasticity

  Alcohol · 2023-05-09

  articleOpen access
  PublisherDOI

• Exploring the immunogenic properties of SARS-CoV-2 structural proteins: PAMP:TLR signaling in the mediation of the neuroinflammatory and neurologic sequelae of COVID-19

  Brain Behavior and Immunity · 2023-04-27 · 14 citations

  reviewOpen accessSenior author

  • SARS-CoV-2 structural proteins are shed from mature virions and enter the circulation. • These proteins produce inflammatory responses in innate immune cells. • Inflammatory responses are mediated by TLR receptors. • These proteins induce inflammatory responses in the periphery and brain. • Inflammatory responses might mediate the neuropsychiatric symptoms in COVID19 patients. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) produces an array of neurologic and neuropsychiatric symptoms in the acute and post-acute phase of infection (PASC; post-acute sequelae of SARS-CoV-2 infection). Neuroinflammatory processes are considered key factors in the etiology of these symptoms. Several mechanisms underpinning the development of inflammatory events in the brain have been proposed including SARS-CoV-2 neurotropism and peripheral inflammatory responses (i.e., cytokine storm) to infection, which might produce neuroinflammation via immune-to-brain signaling pathways. In this review, we explore evidence in support of an alternate mechanism whereby structural proteins (e.g., spike and spike S1 subunit) derived from SARS-CoV-2 virions function as pathogen-associated molecular patterns (PAMPs) to elicit proinflammatory immune responses in the periphery and/or brain via classical Toll-Like Receptor (TLR) inflammatory pathways. We propose that SARS-CoV-2 structural proteins might directly produce inflammatory processes in brain independent of and/or in addition to peripheral proinflammatory effects, which might converge to play a causal role in the development of neurologic/neuropsychiatric symptoms in COVID-19.

  PublisherDOI

• An Integrative Model for Endophenotypes Relevant to Posttraumatic Stress Disorder (PTSD): Detailed Methodology for Inescapable Tail Shock Stress (IS) and Juvenile Social Exploration (JSE)

  Neuromethods · 2023-01-01 · 3 citations

  book-chapter
  PublisherDOI

Recent grants

• NIH Grant R37MH050479

  NIH · $3.1M · 2007

• NIH Grant R21MH106817

  NIH · $419k · 2018

• NIH Grant R01AG028271

  NIH · $3.8M · 2018

• Stress-induced neuroinflammatory priming: Glucocorticoids, inflammasomes, alarmins

  NIH · $2.1M · 2016–2023

• NIH Grant T32MH014617

  NIH · $839k · 1996

Frequent coauthors

• Linda R. Watkins

  University of Colorado Boulder

  451 shared

• Mark R. Hutchinson

  University of Adelaide

  85 shared

• Kenner C. Rice

  National Institute on Alcohol Abuse and Alcoholism

  80 shared

• Matthew G. Frank

  University of Colorado Boulder

  80 shared

• Erin D. Milligan

  University of New Mexico

  65 shared

• Monika Fleshner

  University of Colorado Boulder

  64 shared

• Peter M. Grace

  The University of Texas MD Anderson Cancer Center

  64 shared

• Ruth M. Barrientos

  58 shared

Labs

• Maier Watkins LaboratoryPI

  1-2 sentence research focus

Education

• Ph.D.

  University of Pennsylvania

  1968