# Plasticity of Layer 6 corticothalamic pyramidal cell circuits in the adult primary auditory cortex following visual deprivation

> **NIH NIH F31** · JOHNS HOPKINS UNIVERSITY · 2024 · $48,974

## Abstract

Project Summary
Individuals with deafness and hearing loss face significant communication challenges that impact their social,
educational, and professional lives, leading to potential mental health and cognitive issues and increased
physical safety risks. In the United States, around 48 million people report experiencing hearing loss,
exceeding the combined cases of diabetes and cancer. Cochlear implants have allowed for the restoration of
hearing in those suffering from debilitating hearing-related impairments; however, children show higher post-
implantation success than adults due to their increased neural plasticity. Prior research from our laboratories
suggests adult auditory plasticity can be enhanced by visual deprivation. Circuits involved in sensory gating
control likely facilitate this restoration of adult plasticity, as we have found that these changes coincide with the
weakening of inhibitory inputs from the thalamic reticular nucleus (TRN) to the primary auditory thalamus (the
ventromedial geniculate bodies: MGBv) and the strengthening of inhibitory synaptic transmission originating
from cortical parvalbumin interneurons (PV-IN) onto A1 layer 4 (L4) principal neurons. Key circuits involved in
gain control originate in layer 6 (L6) and involve corticothalamic projection neurons (L6-CTNs), which receive
sensory information from other cortical areas (e.g. vision), in addition to auditory information from MGBv, and
send excitatory signals onto the MGBv, TRN, and PV-INs within A1. Thus, I hypothesize that layer 6
corticothalamic projection neurons (L6-CTNs) in A1 play a critical role in coordinating the adult thalamocortical
plasticity observed in A1 following visual deprivation and that dark-exposure (DE) will lead to plasticity of
circuits involving L6-CTNs in adult mice. I propose to investigate whether DE leads to changes in the strength
of L6-CTN outputs to the TRN, L4 principal neurons, and L6 PV-INs (Aim1) as well as changes in the strength
of inputs onto L6-CTNs from the MGBv and within A1 (Aim2) to determine how DE alters layer 6 sensory
gating circuits in adults. Additionally, I will investigate how acute L6-CTN activity effects feed-forward
thalamocortical auditory processing from the MGBv to A1 L4 and whether DE alters these interactions (Aim3).

## Key facts

- **NIH application ID:** 10997925
- **Project number:** 1F31DC022195-01
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Anthony Tyrone Collins
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $48,974
- **Award type:** 1
- **Project period:** 2025-01-01 → 2027-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10997925

## Citation

> US National Institutes of Health, RePORTER application 10997925, Plasticity of Layer 6 corticothalamic pyramidal cell circuits in the adult primary auditory cortex following visual deprivation (1F31DC022195-01). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/10997925. Licensed CC0.

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