# Projections of opioid-sensitive KF neurons

> **NIH NIH F31** · UNIVERSITY OF FLORIDA · 2021 · $2,500

## Abstract

PROJECT SUMMARY/ABSTRACT
 Individuals who overdose on opioids die from respiratory depression due to activation of the mu opioid
receptors, but the precise mechanism remains elusive. Respiratory output is generated and controlled by nuclei
in the brainstem, including the Kölliker-Fuse (KF) in the pons and the Bӧtzinger Complex, preBötzinger Complex
and rostral ventral respiratory group in the ventrolateral medulla. All of these structures express postsynaptic
and/or presynaptic mu opioid receptors and therefore are vulnerable to opioid modulation. The work of this
proposal focuses on understanding if and how opioids modulate respiratory-controlling KF neurons that project
to respiratory nuclei in the ventrolateral medulla, namely the Bӧtzinger Complex, preBötzinger Complex and
rostral ventral respiratory group. Opioids could modulate KF neurons by hyperpolarization and/or inhibition of
neurotransmitter release from axon terminals. Recently, it was found that mu opioid receptor agonists
hyperpolarize a population of KF neurons, but it is unknown how these opioid-sensitive neurons integrate into
the pontomedullary respiratory circuitry. I will determine if these opioid-sensitive KF neurons project to respiratory
nuclei (Aim 1), and if KF projections to respiratory nuclei are vulnerable to presynaptic opioid modulation (Aim
2). I hypothesize that opioid-sensitive KF neurons project to and synapse onto neurons within the Bӧtzinger
Complex, preBötzinger Complex and/or rostral ventral respiratory group, thereby changing respiratory output. In
Aim 1, the projection target of opioid-sensitive KF neurons will be determined using brain-slice electrophysiology
and retrograde tracing. In Aim 2, brain-slice electrophysiology, in combination with optogenetics, will be used to
determine if opioids inhibit neurotransmitter release from KF axon terminals. Results from this project will 1)
identify respiratory neurocircuitry vulnerable to opioid modulation and 2) provide insight into the mechanism by
which opioids change respiratory output. My work will be supervised by Drs. Levitt (sponsor) and Mitchell (co-
sponsor), two NIH-funded investigators with extensive publications in their respective fields. Together, we
developed a training plan that will help me learn new experimental techniques important to neuropharmacology
and neuroscience research, develop my writing and oral dissemination skills, and foster my teaching and career
development. This work and Drs. Levitt and Mitchell’s mentorship will give me the necessary skills to pursue a
competitive post-doctoral fellowship and eventual faculty position.

## Key facts

- **NIH application ID:** 10438059
- **Project number:** 3F31DA053798-01S1
- **Recipient organization:** UNIVERSITY OF FLORIDA
- **Principal Investigator:** Jordan T Bateman
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $2,500
- **Award type:** 3
- **Project period:** 2021-05-16 → 2023-05-15

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10438059

## Citation

> US National Institutes of Health, RePORTER application 10438059, Projections of opioid-sensitive KF neurons (3F31DA053798-01S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10438059. Licensed CC0.

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