# Neuromodulation of brain and emotional responses to psychological stress

> **NIH NIH K01** · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · 2024 · $176,180

## Abstract

Project Summary / Abstract
Acute psychological stressors rapidly and reliably evoke emotional responses, which involve changes in
self-reported affect as well as peripheral cardiovascular physiology. These affective and physiological
responses to psychological stressors may increase the risk for negative mental and physical health
outcomes. However, the neurobiological mechanisms for these processes are not well understood. This
K01 proposal will test a novel mechanistic model in which heightened activity in the dorsal anterior
cingulate cortex (dACC) in response to acute psychological stress is causally implicated in affective and
cardiovascular responses. Human neuroimaging studies show that heightened stressor-evoked activity
in the dACC is associated with changes in affect and peripheral physiology, yet to date this evidence has
been observational and correlational. Noninvasive neuromodulation methods such as continuous theta
burst stimulation (cTBS), an advanced form of transcranial magnetic stimulation (TMS), combined with
subject-specific neuronavigational targets, electrical field modeling, and double cone coils targeting
deeper cortical structures, can rapidly depotentiate activity in the dACC. This K01 will therefore test the
proposed model using a within-subject, sham-controlled, two-armed counterbalanced design in a cohort
of 55 midlife adults ranging in mood symptomatology. Participants will undergo single sessions of cTBS
to depotentiate dACC activity (i.e., dACC-cTBS) or sham cTBS as a control condition. Immediately
following each session, participants will complete a validated psychological stress task with concurrent
functional magnetic resonance imaging (fMRI). The proposed K01 will examine effects of dACC-cTBS
on stressor-evoked (1) dACC activity, (2) dACC connectivity, (3) affective reactivity, and (4)
cardiovascular reactivity. Dr. Kraynak has expertise in stress neurobiology, multimodal functional
neuroimaging, and cardiovascular psychophysiology. To successfully complete the proposed study, he
will require additional training in (1) clinical affective neuroscience, (2) TMS methodology, and (3)
translational experimental study design. Dr. Kraynak will complete this training and research in the
Department of Psychiatry at the University of Pittsburgh, a highly collaborative environment that is an
ideal fit for his interdisciplinary training and research goals. Completion of the training and research plan
in this career development award will enable Dr. Kraynak to transition to an independent investigator
focused on the neurobiology of emotional responses to acute psychological stress. Findings from this
K01 would significantly add to our understanding of the neurobiology of emotional responses to stressors,
potentially confirm the causal contributions of the dACC to emotional reactivity in humans, and inform
future independent neuromodulation studies targeting stress-related psychopathology.

## Key facts

- **NIH application ID:** 10948563
- **Project number:** 1K01MH137517-01
- **Recipient organization:** UNIVERSITY OF PITTSBURGH AT PITTSBURGH
- **Principal Investigator:** Thomas Edward Kraynak
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $176,180
- **Award type:** 1
- **Project period:** 2024-08-01 → 2029-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10948563

## Citation

> US National Institutes of Health, RePORTER application 10948563, Neuromodulation of brain and emotional responses to psychological stress (1K01MH137517-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10948563. Licensed CC0.

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