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UBC Theses and Dissertations

Sex-specific effects of prenatal ethanol exposure on hippocampal synaptic plasticity in adolescent rats Titterness, Andrea Kay


The hippocampus is a brain region intimately involved with learning and memory. Long-term depression (LTD) and long-term potentiation (LTP) are putative mechanisms behind learning and memory. Prenatal and postnatal events that alter LTP and/or LTD also impair hippocampal-dependent learning and memory. Prenatal stress and prenatal ethanol exposure (PNEE) can both independently reduce LTP in male offspring; acute postnatal stress enhances LTD in males. It remains to be determined how these events alter synaptic plasticity in adolescent females. Stress-induced changes to LTD might be more pronounced following PNEE due to a heightened stress response in ethanol-exposed offspring. In Chapter 2, it was found that acute stress was required for the expression of LTD in control males but blocked LTD in females. Acute stress was required for LTD in males following PNEE but LTD was not apparent in females. The experiments in Chapter 3 were designed to investigate how combined exposure to stress and ethanol in utero affect LTP in the hippocampus of adolescent males and females. PNEE reduced LTP in males but enhanced LTP in females. In animals not exposed prenatally to ethanol, prenatal stress significantly reduced LTP in males but not females. On the other hand, LTP was reduced in males exposed both ethanol and stress in utero but the magnitude of LTP was not significantly different from that of ethanol-exposed males. In females, however, prenatal stress reduced the ethanol-induced enhancement of LTP. These findings indicate that synaptic plasticity in adolescent males and females is differentially affected by prenatal and postnatal events. Putative mechanisms behind the observed plasticity will be discussed in Chapter 4. Specifically, PNEE can delay the onset of puberty, which might alter the influence of the depressant effect of estradiol on synaptic plasticity in adolescent females. PNEE has previously been shown to “masculinize” the female brain and “feminize” the male brain, which might influence synaptic plasticity during adolescence. The expression of the placental barrier to CORT is also altered by prenatal stress and PNEE and might also contribute to observed changes in synaptic plasticity. Potential pitfalls of the experiments and future directions will be presented.

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