Neurogenetic mechanisms underlying effects of chronic stress on vocal learning in adults and juveniles

NIH RePORTER · NIH · R21 · $412,519 · view on reporter.nih.gov ↗

Abstract

PROJECT SUMMARY Chronic stress can have diverse and often detrimental effects on cognitive function and overall health. When an individual is in a stressful situation, glucocorticoid (GC) hormones are released that bind to neurons and other cells expressing GC receptors, thereby altering gene expression and cellular activities. Although some changes driven by GC hormones can be beneficial in the short term, like mobilization of energy stores, repeated or chronic exposure to stressors can have many detrimental effects. Among these are a variety of behavioral and cognitive disorders, including diminished language learning. These effects have been well-studied in the context of early-life stress and vocal learning, in part through the use of avian model systems that are capable of learning early in life. How chronic stress experienced by adults affects their language learning is less understood, largely because of the lack of a suitable animal model. In this study we will employ a parrot model (the budgerigar, Melopsittacus undulatus) that, like humans, is capable of life-long learning to test the hypothesis that chronic stress reduces the ability of adults to learn new vocalizations via impacts on neuronal gene expression in the underlying neural centers of the brain. We will subject groups of adult budgerigars to either elevated or baseline chronic stress via environmental disruption and compare levels of circulating GC’s, speed and accuracy of vocal learning, and degree of social integration in the two treatments. We will also examine changes in the expression of GC receptors and key language-related genes in brain nuclei devoted to vocal learning. In a separate experiment, we will examine the interactions between early-life and adult chronic stress using a fully crossed experiment in which groups of budgerigars will experience either high or baseline stress as juveniles and again as adults (i.e. a double-hit model). We will then monitor the same behavioral and neural measures of vocal learning to test whether early life stress buffers individuals from the effects of stress during adulthood, or compounds the effects of later stress. In sum, these aims will comprehensively investigate the impacts of chronically elevated glucocorticoids on the cellular mechanisms mediating a key cognitive trait that underlies human speech and language.

Key facts

NIH application ID
10527057
Project number
1R21NS126079-01A1
Recipient
NEW MEXICO STATE UNIVERSITY LAS CRUCES
Principal Investigator
TIMOTHY F WRIGHT
Activity code
R21
Funding institute
NIH
Fiscal year
2022
Award amount
$412,519
Award type
1
Project period
2022-09-01 → 2025-08-31