# Impact of autism genetic risk on cortical sensorimotor dynamics

> **NIH NIH F32** · UNIVERSITY OF FLORIDA · 2024 · $76,756

## Abstract

Project Summary
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder defined by social deficits and restricted
and repetitive behaviors. These behaviors have been associated with impaired sensory processing and
sensorimotor integration. In addition, ASD is often comorbid with intellectual disability (ID) and cognitive
impairment. This is especially true of ASD diagnoses associated with one of several major ASD risk genes.
While it is well established that sensory processing is critical for cognitive function in general and learning in
particular, it is not clear how deficits in sensory processing in ASD may contribute to cognitive and learning
impairments in patients. I hypothesize that learning impairments in ASD patients stem from sensory processing
deficits leading to a disruption in cortical functional connectivity critical for learned behaviors. I will test this idea
by using a mouse model of major ASD genetic risk that shows a tactile instrumental learning impairment.
Importantly, learning deficits require the function of the ASD risk gene in cortical excitatory projection neurons
(see preliminary data) highlighting the importance for cortical processing in this phenotype. In addition, these
animals have a reduced cortical response to touch. In Aim 1, I will assess the impact of the ASD risk gene on
sensory processing in dorsal cortex by monitoring calcium dynamics as mice receive passive sensory
stimulation. In addition, I will manipulate the ASD risk gene in sensory cortex to test its autonomous control of
calcium dynamics and connectivity. I expect that the ASD risk gene model mice will have reduced responses in
sensory cortex and disrupted functional connectivity to downstream regions in dorsal cortex. In Aim 2, I will
monitor dorsal cortex calcium dynamics as mice perform an instrumental learning task to test the idea that the
major ASD risk gene causes altered dynamics of cortical functional connectivity. Furthermore, I will determine
to what extent putative mesoscale connectivity deficits in the mouse model predict learning impairments in the
task. Lastly, I will specifically manipulate the ASD risk gene in sensory cortex to tests its autonomous role in
regulating functional connectivity during learning. The impact of this proposal will be to understand the
neurobiological underpinnings of impaired learning related to a major ASD risk gene, which may serve to
inform the development of treatments for cognitive deficits in ASD patients. In conclusion, I am an excellent
candidate for a National Research Service Award Fellowship because of my background in ASD risk gene
research and the training in cutting-edge systems neuroscience tools provided by the Rumbaugh lab.
Altogether, the training and experiments proposed here will enable me to further our understanding of ASD and
lay a strong foundation for my career goal of running an independent research laboratory.

## Key facts

- **NIH application ID:** 10864803
- **Project number:** 5F32MH130163-02
- **Recipient organization:** UNIVERSITY OF FLORIDA
- **Principal Investigator:** Randall M. Golovin
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $76,756
- **Award type:** 5
- **Project period:** 2023-07-01 → 2026-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10864803

## Citation

> US National Institutes of Health, RePORTER application 10864803, Impact of autism genetic risk on cortical sensorimotor dynamics (5F32MH130163-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10864803. Licensed CC0.

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