# Catecholamine Neurons and Metabolic Controls

> **NIH NIH R01** · WASHINGTON STATE UNIVERSITY · 2020 · $451,986

## Abstract

Project Summary
Glucose is the required metabolic fuel for the brain. Quantities of stored glucose (glycogen) in the brain
are adequate to maintain brain function and survival for only a few minutes. Therefore, glucose must be
monitored constantly in order to control diverse behavioral, endocrine and autonomic responses that
ensure delivery of glucose from the blood. Mechanisms that detect brain glucose deficit and elicit
protective responses, referred to as counter-regulatory responses (CRRs), that mobilize and replenish the
brain's glucose supply are of vital importance for survival. These responses include stimulation of appetite,
increased glucocorticoid and adrenal medullary secretion and others. Studies employing molecular
neurosurgery with targeted immunotoxins, in situ hybridization, gene silencing and CNO/DREAAD
technology all support the essential involvement of catecholamine (CA) neuron subpopulations in elicitation
of CRRs. However, an obstacle to research in this area has been that CA neurons in the same general
areas of the hindbrain that house the glucoregulatory CA neurons are involved in multiple and equally
critical homeostatic functions that are not directly glucoregulatory (such as cardiovascular, respiratory, and
neuroendocrine controls). However, new data and techniques are available that will allow us to specifically
characterize and probe the distinct functions of the glucoregulatory CA subgroups and possibly to identify
the underlying causes of their dysregulation in hypoglycemia associated autonomic failure (HAAF), a
potentially lethal condition that constantly threatens diabetic patients on insulin therapy. Using a variety of
technical approaches, we will attempt to reveal peptides that act as co-transmitters for CA neurons
involved in specific CRRs (feeding, glucocorticoid and adrenal medullary secretion), as well as identifying
the glucosensing mechanisms they express. We will also evaluate the effect of acute and recurrent
glucoprivation on these mechanisms.

## Key facts

- **NIH application ID:** 9848546
- **Project number:** 5R01DK114187-03
- **Recipient organization:** WASHINGTON STATE UNIVERSITY
- **Principal Investigator:** W. Sue Ritter
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $451,986
- **Award type:** 5
- **Project period:** 2018-03-01 → 2022-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9848546

## Citation

> US National Institutes of Health, RePORTER application 9848546, Catecholamine Neurons and Metabolic Controls (5R01DK114187-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9848546. Licensed CC0.

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