# Cortico-cortical Projections Driving Frontal-sensory Neural Oscillatory Synchrony to Mediate Attention

> **NIH NIH F31** · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · 2020 · $45,520

## Abstract

Project Summary
Neural oscillations had previously been considered to be a consequence of cognitive function, but recent
evidence suggests they rather play a central role in communicating neural information across distributed brain
networks during complex cognitive processes such as attention. Desynchronized neural oscillatory activity is
frequently reported in psychiatric disorders, including autism, depression, and schizophrenia, leading to
cognitive impairments, including attentional deficits. Little is known about the underlying circuit mechanisms
that drive neural oscillations supporting attention or how they are disrupted to produce desynchronization. Our
comprehensive idea to aid in the recovery of attention is to take a circuit-based approach to resynchronize
cortical regions to healthy states and subsequently reestablish proper attentional performance. This proposal
aims to identify novel circuit mechanisms driving synchronous neural oscillations required for attention. Our
preliminary study found that chemogenetic inactivation of top-down cortical projections from anterior cingulate
cortex (ACC) to the visual cortex (VIS) disrupts visual attentional behavior in mice. Furthermore, we show that
circuit-specific optogenetic activation of this top-down circuit enhances attention performance. Of note, both
attention
15q13.3
significant
schizophrenia.
is
microdeletion,
or
deficits and reduced cortical gamma oscillation
microdeletion, one of the major copy number well documented in association with a
minority of individuals diagnosed with various neurodevelopmental disorder such as autism and
Although our preliminary results implicate a circuit-specific mechanism of attentional control, it
unknown whether 1) ACC  VIS activity increased during attention and by 15q13.3
2) ACC-VIS sychronization is associated with attention and disrupted by 15q13.3 microdeletion,
if 3) the top-down circuit can be modulated to rescue attention deficits.
in mice were reported to be caused by chromosomal
variants
is disrupted
We hypothesize that this prefrontal
top-down projection to visual cortex synchronizes activity between ACC and VIS during attention and that
ACCVIS projection can be leveraged to improve synchronization and attention deficits caused by a 15q13.3
microdeletion. Our experimental design uses an intersectional viral approach and cutting-edge fiber
photometry, in vivo electrophysiology and optogenetic techniques to simultaneously monitor and manipulate
this top-down circuit as mice perform a naturalistic free moving attention task to test this hypothesis. We
anticipate our study will shed novel fundamental mechanistic insight into the role of neural synchronization
during attention and provide a unique opportunity to identify novel circuit-based targets for neuromodulation
treatments of psychiatric disorders.

## Key facts

- **NIH application ID:** 9984802
- **Project number:** 5F31MH121010-02
- **Recipient organization:** ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
- **Principal Investigator:** Kevin Jay Norman
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $45,520
- **Award type:** 5
- **Project period:** 2019-07-02 → 2022-07-01

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9984802

## Citation

> US National Institutes of Health, RePORTER application 9984802, Cortico-cortical Projections Driving Frontal-sensory Neural Oscillatory Synchrony to Mediate Attention (5F31MH121010-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9984802. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*
