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NIH grant 1R01AT014133-01: Central mechanisms of nausea and their modulation via non-invasive neurostimulation
Institute: {'code': 'AT', 'abbreviation': 'NCCIH', 'name': 'National Center for Complementary and Integrative Health', 'admin_org_id': '12500007', 'admin_funding_url': ''}. PI: Roberta Sclocco. Award: $552874.
Start: 2026-09-25T00:00:00.
Nausea is a highly aversive sensation that commonly accompanies chronic disorders and substantially
reduces quality of life. Unlike vomiting, nausea arises from distinct neurocircuitry centered in the brainstem,
particularly the nucleus tractus solitarii (NTS), which integrates vagal afferent input from visceral organs with
top-down signals from cortical, limbic, cerebellar, and vestibular regions. This integrative architecture provides
a neural basis for the strong influence of cognitive and emotional processes on nausea perception. However,
mechanistic understanding of nausea has been limited, in part because nausea is difficult to measure in animal
models.
Using a validated motion sickness paradigm, our group has pioneered human fMRI investigations of nausea,
demonstrating that activity in limbic and striatal regions precedes nausea onset and that autonomic responses
are linked to reduced insula activity, suggesting inhibitory brainstem–cortical interactions. Despite these
advances, effective anti-nausea therapies remain scarce. Standard pharmacological treatments often produce
undesirable side effects, underscoring the need for non-pharmacological alternatives.
Transcutaneous auricular vagus nerve stimulation (taVNS) is a promising, noninvasive intervention that
modulates afferent vagal signaling and engages central autonomic networks via the NTS. Emerging evidence
suggests that taVNS can reduce nausea symptoms, yet its neural mechanisms remain unknown. The objective
of this proposal is to elucidate the brain-based mechanisms underlying taVNS effects on nausea using ultra–
high-field (7T) fMRI to achieve enhanced resolution of brainstem circuitry.
We will combine continuous 7T fMRI, active or sham taVNS, autonomic monitoring, and real-time nausea
ratings in motion sickness–prone adults to characterize nausea progression and recovery. Our aims will define
brainstem mechanisms of nausea, determine how taVNS alters symptom trajectory, and link central neural
dynamics with peripheral autonomic responses. By clarifying the neural circuitry underlying taVNS-mediated
anti-nauseogenic effects, this work will advance mechanistic understanding of brain–body interactions and
support the development of targeted, non-pharmacological therapies for nausea.document fetched 2026-10-04 02:43