Morris water maze performance deficit produced by intermittent swim stress is partially mediated by norepinephrine

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Abstract

Intermittent swim stress (ISS) exposes a rat to cold water and the effects of the procedure produce detrimental results on activity measures 24 h later. The ISS model can be used with the Morris water maze (MWM) to investigate the impact of stress on a spatial learning and memory task, known to involve the hippocampus. We investigated if the ISS model produced performance deficits in the MWM (experiments 1 and 2). We also investigated the role of norepinephrine by using an alpha-2 adrenergic agonist (i.e., clonidine) to exacerbate ISS-induced deficits (experiment 3), and using antidepressants (i.e., desipramine and reboxetine) that enhance the synaptic availability of norepinephrine to reduce ISS-induced deficits (experiments 4 and 5). Results indicated a main effect for stress in all experiments, with the exception of experiment 2, as ISS did induce performance deficits in the MWM. Clonidine enhanced ISS-induced deficits only in the learning trials, while desipramine and reboxetine reduced ISS-induced deficits in the learning trials. Additionally, only reboxetine reduced memory deficits in the MWM. These findings provide evidence that norepinephrine may act as a partial mediator of ISS-induced deficits in MWM performance.

Highlights

▸ Intermittent swim stress (ISS) did produce performance deficits in the MWM. ▸ Desipramine reduced ISS-induced deficits only in the learning trials of the MWM. ▸ Reboxetine reduced ISS-induced deficits in acquisition and retrieval in the MWM. ▸ Clonidine enhanced ISS-induced deficits only in the learning trials of the MWM. ▸ NE may act as a partial mediator of ISS-induced deficits in MWM performance.

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