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Maternal deprivation alters expression of neural maturation gene tbr1 in the amygdala paralaminar nucleus in infant female macaques
Author(s) -
de Campo Danielle M.,
Cameron Judy L.,
Miano Joseph M.,
Lewis David A.,
Mirnics Karoly,
Fudge Julie L.
Publication year - 2017
Publication title -
developmental psychobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 93
eISSN - 1098-2302
pISSN - 0012-1630
DOI - 10.1002/dev.21493
Subject(s) - amygdala , glutamatergic , maternal deprivation , neuroblast , biology , monocular deprivation , neuroscience , downregulation and upregulation , neural development , psychology , immediate early gene , gene expression , endocrinology , medicine , gene , neurogenesis , genetics , glutamate receptor , visual cortex , receptor , ocular dominance
Early parental loss is associated with social–emotional dysregulation and amygdala physiologic changes. Previously, we examined whole amygdala gene expression in infant monkeys exposed to early maternal deprivation. Here, we focus on an amygdala region with immature neurons at birth: the paralaminar nucleus (PL). We hypothesized that 1) the normal infant PL is enriched in a subset of neural maturation (NM) genes compared to a nearby amygdala subregion; and 2) maternal deprivation would downregulate expression of NM transcripts (mRNA). mRNAs for bcl2, doublecortin , neuroD1 , and tbr1 —genes expressed in post‐mitotic neurons—were enriched in the normal PL. Maternal deprivation at either 1 week or 1 month of age resulted in PL‐specific downregulation of tbr1 —a transcription factor necessary for directing neuroblasts to a glutamatergic phenotype. tbr1 expression also correlated with typical social behaviors. We conclude that maternal deprivation influences glutamatergic neuronal development in the PL, possibly influencing circuits mediating social learning.