Endocrine Abstracts (2007) 13 P238

The effect of exogenous estradiol administration on working memory in the ovariectomised female hooded-lister rat

Jane Sutcliffe, Jo Neill & Kay Marshall


University of Bradford, Bradford, United Kingdom.


The aim of the investigation was to evaluate the effect exogenous of 17-β-estradiol propionate (E2) on working memory as assessed by the novel object recognition (NOR) paradigm following intermittent or delayed E2 regimens.

15 rats were ovariectomised under anaesthesia and were divided into 3 groups namely: (1) vehicle (2) intermittent E2 dosing weeks 1–6 and 13–18, with no treatment weeks 7–12 and (3) delayed (no treatment in weeks 1–12) E2 treatment dosing weeks 13–18. The hormone regime included vehicle (v) (1 ml/kg olive oil) or E2 (450 μg/kg weekly) s.c. 5 regularly cycling animals were also included which were tested during pro-oestrus (group 4). On week 15, all animals were tested in the NOR task. Testing consisted of a 3-minute acquisition phase where 2 identical objects were presented, followed by a 1 hour inter-trial interval (ITI) where objects and test arena were cleaned and rats returned to the home cage. In the final 3-minute retention trial, rats explored a duplicate of an object from the first trial and one novel object. Data were analysed by paired samples t-test, n=5 for each group.

GroupFamiliar objectNovel object
119.6±6.013.7±3.0
2 10.0±1.031.0±3.0***
313.4±4.021.0±1.0
47.3±1.724.3±4.8**

Table1. Exploration times (s) for each group during the retention trial of the NOR following a 1 hour ITI (P<0.001***, P<0.01** paired samples t-test familiar vs novel object exploration for each group).

The primary finding of this study was that E2 replacement appears to loose its ability to positively affect working memory after a hormone deprived period. E2 has been shown to regulate many neural systems in the brain and the mechanism by which E2 looses its ability to affect working memory after a hormone deprived period is unknown, although hippocampal morphology (specifically, CA1) and NMDA receptor levels have been implicated in recent years.

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