# Dissecting a neural substrate for stress-induced analgesia

> **NIH NIH F31** · DUKE UNIVERSITY · 2021 · $44,335

## Abstract

ABSTRACT
Affective modulation of pain is an important mechanism for selecting appropriate behavior given different
contexts. As an adaptive mechanism, it can aid an animal in surviving a life-threatening situation. Stress-induced
analgesia (SIA) is such a phenomenon in which an affective state of high stress, induced by such stimuli as
predator odor, produces analgesia to noxious stimuli. Previous studies of SIA have shown that stressful stimuli
increase freezing behavior and decrease nociceptive responses, a readout of analgesia. Furthermore, SIA was
shown to critically depend on the central amygdala (CeA). CeA is known to have a multitude of roles in
processing emotional responses to pain and fear. The question is whether CeA is involved in producing true
analgesia, or its role on eliciting freezing renders animals to show less motor responses to pain. Recent
advances from others and our lab have discovered two distinct CeA neuronal populations for controlling freezing
versus analgesia, respectively. Specifically, somatostatin-positive cells within the CeA (CeASST) have been
shown by numerous groups to mediate freezing behavior, while our lab has discovered a population of cells
activated by general anesthetics (CeAGA) which produces robust analgesia when optogenetically stimulated.
Using predator odor as a model of SIA, I will assess the contribution of CeASST-freezing neurons versus CeAGA
neurons in this model. Furthermore, preliminary studies revealed that CeAGA cells receive strong projections
from a region called the amygdala-piriform transition zone (AmPir), and this region is known to be activated by
predator odor. I will therefore further test the hypothesis that the AmPir-to-CeA circuit relays predator odor
information to CeA to produce SIA. I will accomplish these aims through the use of transgenic mouse lines and
viral strategies to target behaviorally-specific neural populations and optogenetically manipulate them during
predator odor SIA. This proposal will provide novel insights into the neural circuits mediating the interplay
between stress and pain, and advance our understandings of how emotions modulate pain.

## Key facts

- **NIH application ID:** 10234671
- **Project number:** 1F31NS122489-01
- **Recipient organization:** DUKE UNIVERSITY
- **Principal Investigator:** Carolyn Victoria Diaz
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $44,335
- **Award type:** 1
- **Project period:** 2021-05-01 → 2024-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10234671

## Citation

> US National Institutes of Health, RePORTER application 10234671, Dissecting a neural substrate for stress-induced analgesia (1F31NS122489-01). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10234671. Licensed CC0.

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