# Axon Transport of TrkA receptors in sympathetic neurons

> **NIH NIH F31** · JOHNS HOPKINS UNIVERSITY · 2020 · $45,520

## Abstract

Project Summary/Abstract
 Axons of sympathetic neurons extend millimeters to meters to innervate peripheral tissues and organs, which
is essential for tissue homeostasis and fundamental physiological processes including cardiac output, body
temperature, regulation of blood glucose levels, and immune functions. Target-derived signals, such as the
neurotrophin, Nerve Growth Factor (NGF), recruit growing axons by binding to TrkA receptors located on axon
terminals, to initiate local and long-range retrograde signaling events to support neuron development, maturation,
and synaptic functions. To sustain functional responses to target derived ligand, TrkA receptors must be
continually localized to axon terminals. Yet, how TrkA receptors are delivered to axons remains largely
undefined.
 Previously, we reported that TrkA receptors are delivered to sympathetic axons by transcytosis, where newly
synthesized receptors are first inserted on soma surfaces, then internalized and anterogradely transported to
axons. Furthermore, we identified that TrkA transcytosis is primed by the activity of PTP1B, an ER-resident
protein tyrosine phosphatase, in cell bodies. The overall goal of my thesis project and this application is to test
the hypothesis that PTP1B phosphatase promotes a gain of TrkA biological function by controlling the long-
distance transcytosis of receptors. I will employ imaging, biochemical, and functional analyses in
compartmentalized neuron cultures in combination with in vivo analyses of genetically modified mice to
accomplish these goals. Specifically, I have generated a new mouse model, TrkAR685A knock-in mice, where a
point mutation in TrkA prevents PTP1B binding, which will allow me to test the functional relevance of TrkA-
PTP1B interactions on TrkA localization, neuron survival, and axon innervation of target tissues. Through this
fellowship application, I will develop a basic understanding of the mechanisms of Trk receptor delivery to axons,
and how this contributes to neuronal development. I will also develop the technical, communication, and
leadership skills necessary to accomplish my goal of becoming an independent investigator. My training will be
facilitated by the rigorous research plan, the expertise and guidance of my mentor and thesis committee, and
the outstanding training resources and facilities available through Johns Hopkins University.

## Key facts

- **NIH application ID:** 10049193
- **Project number:** 5F31NS113480-02
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Blaine Connor
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $45,520
- **Award type:** 5
- **Project period:** 2019-07-01 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10049193

## Citation

> US National Institutes of Health, RePORTER application 10049193, Axon Transport of TrkA receptors in sympathetic neurons (5F31NS113480-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10049193. Licensed CC0.

---

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