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Impaired cognitive function is associated with changes in serotonin receptor activity following prenatal exposure to Dexamethasone
Author(s) -
Page Kathleen C,
Shah Darshan S,
Aloyo Vincent J
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.762.18
Subject(s) - medicine , endocrinology , offspring , corticosterone , basal (medicine) , prenatal stress , serotonin , dexamethasone , gestation , glucocorticoid receptor , glucocorticoid , psychology , hormone , receptor , biology , pregnancy , insulin , genetics
We investigated the effects of prenatal Dexamethasone (Dex) exposure on 5HT1A receptor activity and cognitive function in adult rat offspring. Pregnant rat dams were injected with Dex (sc; 150ug/kg/day) from gestation day 14 through 19. Control dams were treated with saline. Morris Water Maze analysis showed that at both 120 days (Adult) and 365 days (Aged) the Dex‐exposed group exhibited impairments in learning and memory. Control and Dex‐exposed adults were also challenged with an acute stressor (Adult‐Stressed). A second adult group were similarly stressed and allowed to return to baseline (Adult‐Basal). A third group of 365 day‐old control and Dex‐exposed animals were subjected to the same stress paradigm (Aged‐Stressed). Radioligand receptor binding data showed that Kd and Bmax were statistically different in Dex‐exposed hippocampi from basal and stressed adults compared to controls. This difference was not seen in the aged group. Under basal conditions, corticosterone (CORT) was significantly higher in the Dex‐exposed adults. Following stress, CORT levels were significantly lower in Dex‐exposed animals. Leptin, a hormone shown to influence cognitive function, was significantly decreased in Dex‐exposed adult males, but leptin increased in aged animals. Prenatal exposure to Dex is associated with changes in hormonal output and serotonin 5HT1A receptor activity which may impair cognitive functions.

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