Document Detail


Prospective investigation of stress inoculation in young monkeys.
MedLine Citation:
PMID:  15351772     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Retrospective studies in humans have identified characteristics that promote stress resistance, including childhood exposure to moderately stressful events (ie, stress inoculation). OBJECTIVE: Because of limited opportunities for prospective studies in children, we tested whether exposure to moderate stress early in life produces later stress resistance in a primate model. DESIGN AND MAIN OUTCOME MEASURES: Twenty squirrel monkeys were randomized to intermittent stress inoculation (IS; n = 11) or a nonstress control condition (NS; n = 9) from postnatal weeks 17 to 27. At postnatal week 35, each mother-offspring dyad underwent testing in a moderately stressful novel environment for inferential measures of offspring anxiety (ie, maternal clinging, mother-offspring interactions, object exploration, and food consumption) and stress hormone concentrations (corticotropin [ACTH] and cortisol). At postnatal week 50, after acclimation to an initially stressful wire-mesh box attached to the home cage, independent young monkeys underwent testing for inferential measures of anxiety (ie, voluntary exploration and play) in the box. RESULTS: In the novel environment test, IS compared with NS offspring demonstrated diminished anxiety as measured by decreased maternal clinging (P =.02), enhanced exploratory behavior (P =.005), and increased food consumption (P =.02). Mothers of IS offspring accommodated offspring-initiated exploration (P =.009) and served as a secure base more often compared with NS mothers (P =.047). Compared with NS offspring, IS offspring had lower basal plasma ACTH (P =.001) and cortisol (P =.001) concentrations and lower corticotropin (P =.04) and cortisol (P =.03) concentrations after stress. In the subsequent home-cage wire-box test, IS offspring demonstrated enhanced exploratory (P<.001) and play (P =.008) behaviors compared with NS offspring. CONCLUSIONS: These results provide the first prospective evidence that moderately stressful early experiences strengthen socioemotional and neuroendocrine resistance to subsequent stressors. This preclinical model offers essential opportunities to improve our understanding and enhance prevention of human stress-related psychiatric disorders by elucidating the etiology and neurobiology of stress resistance.
Authors:
Karen J Parker; Christine L Buckmaster; Alan F Schatzberg; David M Lyons
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Archives of general psychiatry     Volume:  61     ISSN:  0003-990X     ISO Abbreviation:  Arch. Gen. Psychiatry     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-09-07     Completed Date:  2004-09-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0372435     Medline TA:  Arch Gen Psychiatry     Country:  United States    
Other Details:
Languages:  eng     Pagination:  933-41     Citation Subset:  AIM; IM    
Affiliation:
Department of Psychiatry and Behavioral Sciences, Stanford University Medical School, Stanford, Calif. 94305-5485, USA. kjparker@stanford.edu
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological* / physiology*
Adrenocorticotropic Hormone / blood
Animals
Behavior, Animal / physiology*
Disease Models, Animal
Exploratory Behavior / physiology
Female
Habituation, Psychophysiologic / physiology
Humans
Hydrocortisone / blood
Hypothalamo-Hypophyseal System / physiology
Male
Pituitary-Adrenal System / physiology
Prospective Studies
Random Allocation
Saimiri / growth & development*
Social Behavior
Social Isolation / psychology
Stress, Psychological / physiopathology*,  psychology
Grant Support
ID/Acronym/Agency:
DA016902/DA/NIDA NIH HHS; F32 MH066537/MH/NIMH NIH HHS; MH47573/MH/NIMH NIH HHS; MH50604/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
50-23-7/Hydrocortisone; 9002-60-2/Adrenocorticotropic Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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