# Steroid Hormone-Regulated Plasticity of Sensorimotor Integration Circuitry Supports Behavioral Change

> **NIH NIH F31** · WASHINGTON UNIVERSITY · 2024 · $34,623

## Abstract

Project Summary
Steroid hormones enrich behavior through actions on sensory and motor circuits, but it remains unclear how these parallel
actions are coordinated to generate a coherent behavioral phenotype. This proposal will investigate the effects of steroids
on neurons that convey predictive motor signals, termed corollary discharges (CD), which modify sensory processing to
account for the sensory feedback predicted to arise from an animal’s own actions, termed reafference. CDs are ubiquitous
in sensorimotor systems, and their disruption is thought to underlie some behavioral and sensory deficits in psychiatric
conditions including schizophrenia and autism. Hormonal regulation of CD is especially intriguing given that steroid
hormone levels also appear to be dysregulated in these conditions. However, the mechanisms by which steroids regulate
CD circuitry in nonpathological states remain unknown. The central hypothesis of this proposal is that steroid hormones
directly alter the physiology of corollary discharge neurons to match internal motor representations to altered reafferent
feedback. This hypothesis will be tested using a well-characterized CD that modulates sensory processing in mormyrid
electric fish. Mormyrids communicate using a stereotyped electric pulse known as an electric organ discharge (EOD). Self-
generated EODs and EODs of nearby fish activate electroreceptors in the skin, which project to a dedicated communication
pathway. To ensure that this pathway only responds to EODs of other fish, a CD signals the timing of EOD production to
selectively inhibit responses to self-generated EODs. EODs are elongated in response to increases in testosterone (T) levels
in male mormyrids during the breeding season. This T-induced EOD elongation delays electroreceptor activation, shifting
the timing of reafferent sensory feedback. To match these shifts in sensory feedback, T concurrently acts in the brain to
delay and elongate CD inhibition.
Preliminary data from extracellular recordings reveal the locus in the CD pathway whereby activity is delayed and elongated
by T. Importantly, the hormonal pathways and physiological mechanisms underlying timing shifts at this site are still
unknown. The experiments in Aim 1 will identify the steroid receptors that drive CD plasticity and determine whether these
receptors act directly in CD neurons. The experiments in Aim 2 will reveal the physiological mechanisms by which T shifts
CD timing in affected neurons. By focusing on a hormone-sensitive circuit that conveys a simple internal model, the timing
of EOD production, these investigations will yield mechanistic insight into the seasonal effects of steroid hormones on gene
expression and neural excitability in the context of a quantifiable behavioral change. Further, the results of these experiments
promise to offer insight into the neural basis of multiple psychiatric conditions in which steroid hormone levels and CD
appear to be dysregulated. With the...

## Key facts

- **NIH application ID:** 10995613
- **Project number:** 1F31NS139904-01
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** Martin William Jarzyna
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $34,623
- **Award type:** 1
- **Project period:** 2024-07-01 → 2027-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10995613

## Citation

> US National Institutes of Health, RePORTER application 10995613, Steroid Hormone-Regulated Plasticity of Sensorimotor Integration Circuitry Supports Behavioral Change (1F31NS139904-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10995613. Licensed CC0.

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