FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2897688507> ?p ?o ?g. }

• W2897688507 endingPage "16" @default.
• W2897688507 startingPage "1" @default.
• W2897688507 abstract "Studies in clinical populations and preclinical models have shown that prenatal alcohol exposure (PAE) is associated with impairments in the acquisition, consolidation and recall of information, with deficits in hippocampal formation-dependent learning and memory being a common finding. The glucocorticoid receptor (GR), mineralocorticoid receptor (MR), and extracellular signal-regulated kinase 2 (ERK2) are key regulators of hippocampal formation development, structure and functioning and, thus, are potential mediators of PAE’s effects on this brain region. In the present studies, we employed a well-characterized mouse model of PAE to identify biochemical mechanisms that may underlie activity-dependent learning and memory deficits associated with PAE. Mouse dams consumed either 10% (w/v) ethanol in 0.066% (w/v) saccharin (SAC) or 0.066% (w/v) SAC alone using a limited (4-h) access, drinking-in-the-dark paradigm. Male and female offspring (∼180-days of age) were trained using a delay conditioning procedure and contextual fear responses (freezing behavior) were measured 24 h later. Hippocampal formation tissue and blood were collected from three behavioral groups of animals: 20 min following conditioning (conditioning only group), 20 min following the re-exposure to the context (conditioning plus re-exposure group), and behaviorally naïve (naïve group) mice. Plasma corticosterone levels were measured by enzyme immunoassay. Immunoblotting techniques were used to measure protein levels of the GR, MR, ERK1 and ERK2 in nuclear and membrane fractions prepared from the hippocampal formation. Adult SAC control male and female mice displayed similar levels of contextual fear. However, significant sex differences were observed in freezing exhibited during the conditioning session. Compared to same-sex SAC controls, male and female PAE mice demonstrated context fear deficits While plasma corticosterone concentrations were elevated in PAE males and females relative to their respective SAC naïve controls, plasma corticosterone concentrations in the conditioning only and conditioning plus re-exposure groups were similar in SAC and PAE animals. Relative to the respective naïve group, nuclear GR protein levels were increased in SAC, but not PAE, male hippocampal formation in the conditioning only group. In contrast, no difference was observed between nuclear GR levels in the naïve and conditioning plus re-exposure groups. In females, nuclear GR levels were significantly reduced by PAE but there was no effect of behavioral group or interaction between prenatal treatment and behavioral group. In males, nuclear MR levels were significantly elevated in the SAC conditioning plus re-exposure group compared to SAC naïve mice. In PAE females, nuclear MR levels were elevated in both the conditioning only and conditioning plus re-exposure groups relative to the naïve group. Levels of activated ERK2 (phospho-ERK2 expressed relative to total ERK2) protein were elevated in SAC, but not PAE, males following context re-exposure, and a significant interaction between prenatal exposure group and behavioral group was found. No main effects or interactions of behavioral group and prenatal treatment on nuclear ERK2 were found in female mice. These findings suggest a sex difference in which molecular pathways are activated during fear conditioning in mice. In PAE males, the deficits in contextual fear were associated with the loss of responsiveness of hippocampal formation nuclear GR, MR and ERK2 to signals generated by fear conditioning and context re-exposure. In contrast, the contextual fear deficit in PAE female mice does not appear to be associated with activity-dependent changes in GR and MR levels or ERK2 activation during training or memory recall, although an overall reduction in nuclear GR levels may play a role. These studies add to a growing body of literature demonstrating that, at least partially, different mechanisms underlie learning, memory formation and memory recall in males and females and that these pathways are differentially affected by PAE." @default.
• W2897688507 created "2018-10-26" @default.
• W2897688507 creator A5011502162 @default.
• W2897688507 creator A5026143344 @default.
• W2897688507 creator A5041564370 @default.
• W2897688507 creator A5079430064 @default.
• W2897688507 creator A5089790860 @default.
• W2897688507 date "2018-12-01" @default.
• W2897688507 modified "2023-09-27" @default.
• W2897688507 title "Sex-specific deficits in biochemical but not behavioral responses to delay fear conditioning in prenatal alcohol exposure mice" @default.
• W2897688507 cites W1503193875 @default.
• W2897688507 cites W1512733937 @default.
• W2897688507 cites W1532900970 @default.
• W2897688507 cites W1544853593 @default.
• W2897688507 cites W1568806114 @default.
• W2897688507 cites W1592661589 @default.
• W2897688507 cites W1768069588 @default.
• W2897688507 cites W1876061808 @default.
• W2897688507 cites W1951547560 @default.
• W2897688507 cites W1964605298 @default.
• W2897688507 cites W1969388849 @default.
• W2897688507 cites W1971626420 @default.
• W2897688507 cites W1971940677 @default.
• W2897688507 cites W1972618119 @default.
• W2897688507 cites W1972816782 @default.
• W2897688507 cites W1979732884 @default.
• W2897688507 cites W1981361333 @default.
• W2897688507 cites W1983738080 @default.
• W2897688507 cites W1984853374 @default.
• W2897688507 cites W1987375729 @default.
• W2897688507 cites W1989085266 @default.
• W2897688507 cites W1989896761 @default.
• W2897688507 cites W1991246134 @default.
• W2897688507 cites W1992339013 @default.
• W2897688507 cites W1992374003 @default.
• W2897688507 cites W1992533568 @default.
• W2897688507 cites W1992811119 @default.
• W2897688507 cites W1993095204 @default.
• W2897688507 cites W1995288330 @default.
• W2897688507 cites W1995933145 @default.
• W2897688507 cites W1996741148 @default.
• W2897688507 cites W1997374959 @default.
• W2897688507 cites W1998426079 @default.
• W2897688507 cites W2000209446 @default.
• W2897688507 cites W2000721883 @default.
• W2897688507 cites W2002644740 @default.
• W2897688507 cites W2002665203 @default.
• W2897688507 cites W2003509522 @default.
• W2897688507 cites W2003627321 @default.
• W2897688507 cites W2003895990 @default.
• W2897688507 cites W2004316996 @default.
• W2897688507 cites W2013048655 @default.
• W2897688507 cites W2015706391 @default.
• W2897688507 cites W2015757113 @default.
• W2897688507 cites W2018389826 @default.
• W2897688507 cites W2018956566 @default.
• W2897688507 cites W2021335702 @default.
• W2897688507 cites W2024417488 @default.
• W2897688507 cites W2024983072 @default.
• W2897688507 cites W2027120715 @default.
• W2897688507 cites W2027374885 @default.
• W2897688507 cites W2029931657 @default.
• W2897688507 cites W2031875570 @default.
• W2897688507 cites W2031885286 @default.
• W2897688507 cites W2032629419 @default.
• W2897688507 cites W2034398750 @default.
• W2897688507 cites W2034764820 @default.
• W2897688507 cites W2035856041 @default.
• W2897688507 cites W2036608908 @default.
• W2897688507 cites W2037276920 @default.
• W2897688507 cites W2039891360 @default.
• W2897688507 cites W2040310712 @default.
• W2897688507 cites W2044959710 @default.
• W2897688507 cites W2046299324 @default.
• W2897688507 cites W2046960533 @default.
• W2897688507 cites W2050726283 @default.
• W2897688507 cites W2051185092 @default.
• W2897688507 cites W2051859809 @default.
• W2897688507 cites W2053184611 @default.
• W2897688507 cites W2055380229 @default.
• W2897688507 cites W2057909143 @default.
• W2897688507 cites W2058877345 @default.
• W2897688507 cites W2060819923 @default.
• W2897688507 cites W2061897214 @default.
• W2897688507 cites W2063836304 @default.
• W2897688507 cites W2063990250 @default.
• W2897688507 cites W2064425630 @default.
• W2897688507 cites W2065764124 @default.
• W2897688507 cites W2070125500 @default.
• W2897688507 cites W2071141381 @default.
• W2897688507 cites W2071456539 @default.
• W2897688507 cites W2071715920 @default.
• W2897688507 cites W2072126247 @default.
• W2897688507 cites W2073564837 @default.
• W2897688507 cites W2074165127 @default.
• W2897688507 cites W2074802748 @default.
• W2897688507 cites W2075361934 @default.
• W2897688507 cites W2075643640 @default.

• next