# Defining the Neural Circuitry of Agency Deficits in Psychotic Disorders

> **NIH NIH R01** · UNIVERSITY OF CALIFORNIA AT DAVIS · 2020 · $496,821

## Abstract

PROJECT SUMMARY
 Psychosis is a mental disorder that manifests as a range of symptoms, including hallucinations and
delusions. These symptoms reflect a diminished ability to accurately recognize self-generated sensations
from externally caused actions or thoughts. This difficulty in differentiating and classifying actions and
thoughts as self-initiated or external has been collectively referred to as a disturbance in sense of agency
(SoA). One theory is that disruptions in corollary discharge (CD, the internally generated copy of issued
motor commands) underlie the SoA defects demonstrated in psychosis. However, due to the inherent
subjectivity of quantifying self-experience there is difficulty in objectively evaluating abnormal experiences
of agency across patient populations. This difficulty subsequently prevents defining the role of CD in
agency, as well as identifying the disrupted neural circuits that convey these signals. The research
objective of this application is to develop a sensitive, quantitative perceptual assessment of CD utilization
in order to define the continuum of abnormalities in SoA in psychotic disorders, and isolate the principal
neural circuit disruptions associated with the behavioral abnormalities. The central hypothesis of the
application is that (1) deficits in CD transmission contribute to visual perception impairments in patient
populations that experience psychosis and (2) a neural circuit, previously characterized in primates, that
conveys the saccade CD underlies the visual perception impairments observed in human psychotic
disorders. The research uses human psychophysics, clinical evaluations, statistical analysis and brain
imaging to isolate the continuum of neural circuit disruptions associated with the range of observed
behavioral abnormalities. The hypothesis of the application has been formulated on the basis of strong
preliminary data that (1) demonstrate that a visual perception behavioral paradigm can isolate and
quantitatively assess CD utilization, (2) identify the associated CD neural circuitry in monkeys, (3) probe
the perceptual consequences when this circuit is reversibly disrupted and (4) confirm similar perceptual
deficits in schizophrenia patients. The long-term goal of the research is to understand the role of CD in
SoA, and how the disruption of these signals contribute to the clinical symptoms of psychosis. The
expected outcome of the research is to provide detailed information, from behavior to the neural
pathways, on the contribution of CD disruption to SoA disorders. This contribution is significant because
it will provide a precise neurobehavioral model to develop analytical diagnostics and treatment strategies
for abnormal self-experience.

## Key facts

- **NIH application ID:** 10001007
- **Project number:** 5R01MH113701-04
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **Principal Investigator:** Wilsaan M Joiner
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $496,821
- **Award type:** 5
- **Project period:** 2018-09-01 → 2022-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10001007

## Citation

> US National Institutes of Health, RePORTER application 10001007, Defining the Neural Circuitry of Agency Deficits in Psychotic Disorders (5R01MH113701-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10001007. Licensed CC0.

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