During infant maltreatment, stress targets hippocampus, but stress with mother present targets amygdala and social behavior.

Abstract:

:Infant maltreatment increases vulnerability to physical and mental disorders, yet specific mechanisms embedded within this complex infant experience that induce this vulnerability remain elusive. To define critical features of maltreatment-induced vulnerability, rat pups were reared from postnatal day 8 (PN8) with a maltreating mother, which produced amygdala and hippocampal deficits and decreased social behavior at PN13. Next, we deconstructed the maltreatment experience to reveal sufficient and necessary conditions to induce this phenotype. Social behavior and amygdala deficits (volume, neurogenesis, c-Fos, local field potential) required combined chronic high corticosterone and maternal presence (not maternal behavior). Hippocampal deficits were induced by chronic high corticosterone regardless of social context. Causation was shown by blocking corticosterone during maltreatment and suppressing amygdala activity during social behavior testing. These results highlight (1) that early life maltreatment initiates multiple pathways to pathology, each with distinct causal mechanisms and outcomes, and (2) the importance of social presence on brain development.

authors

Raineki C,Opendak M,Sarro E,Showler A,Bui K,McEwen BS,Wilson DA,Sullivan RM

doi

10.1073/pnas.1907170116

subject

Has Abstract

pub_date

2019-11-05 00:00:00

pages

22821-22832

issue

45

eissn

0027-8424

issn

1091-6490

pii

1907170116

journal_volume

116

pub_type

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