Candesartan prevents impairment of recall caused by repeated stress in rats

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Abstract

Rationale

Deleterious effects of psychological stress on memory are increasingly important. Overexpression of the AT ₁ angiotensin receptors in brain has been found to participate in several negative effects of chronic stress including hypertension and a cognitive impairment.

Objective

In this study, we searched for the protective effects the AT ₁ angiotensin receptor blockade with candesartan against the adverse effects of repeated stress on recall of aversively and appetitively motivated behaviours in rats.

Methods

Two groups of male Wistar rats were repeatedly stressed by keeping them daily (2 h/21 days) in tight plastic tubes. The subjects of the group 1 received candesartan (0.1 mg/kg, orally) each day before the stressing procedure. The rats of the group 2 received vehicle. Another two groups of rats (3 and 4) receiving candesartan and vehicle, respectively, were appropriately handled but not stressed. Next day, after ending the repeated stress procedure, all rats were tested in two cognitive paradigms: inhibitory avoidance (IA) and object recognition (OR).

Results

Stressed animals displayed decreased recall of the IA behaviour ( p < 0.01) and decreased OR ( p < 0.05). These effects were not seen in the animals stressed and concomitantly treated with candesartan. The auxiliary tests designed to control for the possible unspecific contribution of motor (open field) and emotional (elevated “plus” maze) effects of the experimental procedures to results of the cognitive tests showed no such contribution.

Conclusion

These data strongly suggest that the AT ₁ angiotensin receptor blockade effectively counteracts deleterious effects of stress on recall of aversively and appetitively motivated memories in rats.

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Most cited references 58

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This article presents a new formulation of the relationship between stress and the processes leading to disease. It emphasizes the hidden cost of chronic stress to the body over long time periods, which act as a predisposing factor for the effects of acute, stressful life events. It also presents a model showing how individual differences in the susceptibility to stress are tied to individual behavioral responses to environmental challenges that are coupled to physiologic and pathophysiologic responses. Published original articles from human and animal studies and selected reviews. Literature was surveyed using MEDLINE. Independent extraction and cross-referencing by us. Stress is frequently seen as a significant contributor to disease, and clinical evidence is mounting for specific effects of stress on immune and cardiovascular systems. Yet, until recently, aspects of stress that precipitate disease have been obscure. The concept of homeostasis has failed to help us understand the hidden toll of chronic stress on the body. Rather than maintaining constancy, the physiologic systems within the body fluctuate to meet demands from external forces, a state termed allostasis. In this article, we extend the concept of allostasis over the dimension of time and we define allostatic load as the cost of chronic exposure to fluctuating or heightened neural or neuroendocrine response resulting from repeated or chronic environmental challenge that an individual reacts to as being particularly stressful. This new formulation emphasizes the cascading relationships, beginning early in life, between environmental factors and genetic predispositions that lead to large individual differences in susceptibility to stress and, in some cases, to disease. There are now empirical studies based on this formulation, as well as new insights into mechanisms involving specific changes in neural, neuroendocrine, and immune systems. The practical implications of this formulation for clinical practice and further research are discussed.

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A novel test for the selective identification of anxiolytic and anxiogenic drug effects in the rat is described, using an elevated + -maze consisting of two open arms and two enclosed arms. The use of this test for detecting such drug effects was validated behaviourally, physiologically, and pharmacologically. Rats made significantly fewer entries into the open arms than into the closed arms, and spent significantly less time in open arms. Confinement to the open arms was associated with the observation of significantly more anxiety-related behaviours, and of significantly greater plasma corticosterone concentrations, than confinement to the closed arms. Neither novelty nor illumination was a significant contributor to the behaviour of the rats on the + -maze. A significant increase in the percentage of time spent on the open arms and the number of entries into the open arms was observed only within clinically effective anxiolytics (chlordiazepoxide, diazepam and, less effectively, phenobarbitone). Compounds that cause anxiety in man significantly reduced the percentage of entries into, and time spent on, the open arms (yohimbine, pentylenetetrazole, caffeine, amphetamine). Neither antidepressants nor major tranquilisers had a specific effect. Exposure to a holeboard immediately before placement on the + -maze showed that behaviour on the maze was not clearly correlated either with exploratory head-dipping or spontaneous locomotor activity.

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Stress and glucocorticoids impair retrieval of long-term spatial memory.

B Roozendaal, D. de Beer, James McGaugh (1998)

Extensive evidence from animal and human studies indicates that stress and glucocorticoids influence cognitive function. Previous studies have focused exclusively on glucocorticoid effects on acquisition and long-term storage of newly acquired information. Here we report that stress and glucocorticoids also affect memory retrieval. We show that rats have impaired performance in a water-maze spatial task after being given footshock 30 min before retention testing but are not impaired when footshock is given 2 min or 4 h before testing. These time-dependent effects on retention performance correspond to the circulating corticosterone levels at the time of testing, which suggests that the retention impairment is directly related to increased adrenocortical function. In support of this idea, we find that suppression of corticosterone synthesis with metyrapone blocks the stress-induced retention impairment. In addition, systemic corticosterone administered to non-stressed rats 30 min before retention testing induces dose-dependent retention impairment. The impairing effects of stress and glucocorticoids on retention are not due to disruption of spatial navigation per se. Our results indicate that besides the well described effects of stress and glucocorticoids on acquisition and consolidation processes, glucocorticoids also affect memory retrieval mechanisms.

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Author and article information

Contributors

Jan Józef Braszko: +48-85-7450647 , +48-85-7450647 , braszko@umb.edu.pl

Journal

Journal ID (nlm-ta): Psychopharmacology (Berl)

Journal ID (iso-abbrev): Psychopharmacology (Berl.)

Title: Psychopharmacology

Publisher: Springer-Verlag (Berlin/Heidelberg )

ISSN (Print): 0033-3158

ISSN (Electronic): 1432-2072

Publication date (Electronic): 14 August 2012

Publication date PMC-release: 14 August 2012

Publication date (Print): January 2013

Volume: 225

Issue: 2

Pages: 421-428

Affiliations

Department of Clinical Pharmacology, Medical University of Bialystok, Waszyngtona 15a, 15-274 Bialystok, Poland

Article

Publisher ID: 2829

DOI: 10.1007/s00213-012-2829-3

PMC ID: 3537078

PubMed ID: 22890474

SO-VID: a8b81758-6f78-4bb0-ae56-073855346ca3

History

Date received : 14 March 2012

Date accepted : 26 July 2012

Custom metadata

ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine

Keywords: angiotensin,antagonist,avoidance,memory,rat,receptor,recognition,stress

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ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine

Keywords: angiotensin, antagonist, avoidance, memory, rat, receptor, recognition, stress

Candesartan prevents impairment of recall caused by repeated stress in rats

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Abstract

Rationale

Objective

Methods

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Conclusion

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Most cited references 58

Stress and the individual. Mechanisms leading to disease.

Validation of open:closed arm entries in an elevated plus-maze as a measure of anxiety in the rat.

Stress and glucocorticoids impair retrieval of long-term spatial memory.

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