Nimodipine Counteracts Corticosterone-Induced Habituation Impairments

Dachir, Shlomit; Robinzon, B.; Grauer, Esther; Levy, Aharon

doi:10.1006/nlme.1995.1028

Cited by 9 publications

(2 citation statements)

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“…Studies that have found spatial learning and memory deficits after chronic glucocorticoid exposure differ from the present research. These studies used a protocol that may have produced neuron loss, and/or glucocorticoid treatment continued during training and testing, which combines the chronic and acute actions of glucocorticoids on performance (Bardgett et al, 1994(Bardgett et al, , 1996Dachir et al, 1995;Endo et al, 1996;McLay et al, 1998;Ramos-Remus et al, 2002). Indeed, CoburnLitvak et al (2003) found spatial memory deficits when chronic glucocorticoid treatment extended to 56 d. These findings support the interpretation that CA3 dendritic retraction is not responsible for spatial learning and memory deficits (Conrad, 2006).…”

Section: Discussionmentioning

confidence: 86%

Chronic Glucocorticoids Increase Hippocampal Vulnerability to Neurotoxicity under Conditions That Produce CA3 Dendritic Retraction But Fail to Impair Spatial Recognition Memory

Conrad¹,

McLaughlin²,

Harman³

et al. 2007

J. Neurosci.

128

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We previously found that chronic stress conditions producing CA3 dendritic retraction and spatial memory deficits make the hippocampus vulnerable to the neurotoxin ibotenic acid (IBO). The purpose of this study was to determine whether exposure to chronic corticosterone (CORT) under conditions that produce CA3 dendritic retraction would enhance CA3 susceptibility to IBO. Male Sprague Dawley rats were chronically treated for 21 d with CORT in drinking water (400 g/ml), and half were given daily injections of phenytoin (40 mg/kg), an antiepileptic drug that prevents CA3 dendritic retraction. Three days after treatments stopped, IBO was infused into the CA3 region. Conditions producing CA3 dendritic retraction (CORT and vehicle) exacerbated IBO-induced CA3 damage compared with conditions in which CA3 dendritic retraction was not observed (vehicle and vehicle, vehicle and phenytoin, CORT and phenytoin). Additionally, spatial recognition memory was assessed using the Y-maze, revealing that conditions producing CA3 dendritic retraction failed to impair spatial recognition memory. Furthermore, CORT levels in response to a potentially mild stressor (injection and Y-maze exposure) stayed at basal levels and failed to differ among key groups (vehicle and vehicle, CORT and vehicle, CORT and phenytoin), supporting the interpretations that CORT levels were unlikely to have been elevated during IBO infusion and that the neuroprotective actions of phenytoin were not through CORT alterations. These data are the first to show that conditions with prolonged glucocorticoid elevations leading to structural changes in hippocampal dendritic arbors can make the hippocampus vulnerable to neurotoxic challenges. These findings have significance for many disorders with elevated glucocorticoids that include depression, schizophrenia, Alzheimer's disease, and Cushing's disease.

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Section: Discussionmentioning

confidence: 86%

Chronic Glucocorticoids Increase Hippocampal Vulnerability to Neurotoxicity under Conditions That Produce CA3 Dendritic Retraction But Fail to Impair Spatial Recognition Memory

Conrad¹,

McLaughlin²,

Harman³

et al. 2007

J. Neurosci.

128

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“…As is the case for other stress-related hormones like ACTH and vasopressin, epinephrine has an inverted U-shaped dose-response curve: low doses facilitate memory while high doses impair retention (3,4). Moreover, many studies have provided evidence that glucocorticoids regulate learning and memory (5,(7)(8)(9)(10). It has also been shown that stress impairs hippocampal long-term potentiation (LTP) (11,12), a long-lasting increase in synaptic excitability that might be involved in the mechanism of memory storage (13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Effect of repeated restraint stress on memory in different tasks

Gamaro

Michalowski

Catelli

et al. 1999

Braz J Med Biol Res

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The present study investigated the effect of repeated stress applied to female rats on memory evaluated by three behavioral tasks: two-way shuttle avoidance, inhibitory avoidance and habituation to an open field. Repeated stress had different effects on rat behavior when different tasks were considered. In the two-way active avoidance test the stressed animals presented memory of the task, but their memory scores were impaired when compared to all other groups. In the habituation to the open field, only the control group showed a significant difference in the number of rearings between training and testing sessions, which is interpreted as an adequate memory of the task. In the handled and chronically stressed animals, on the other hand, no memory was observed, suggesting that even a very mild repeated stress would be enough to alter habituation to this task. The performance in the inhibitory avoidance task presented no significant differences between groups. The findings suggest that repeated restraint stress might induce cognitive impairments that are dependent on the task and on stress intensity.

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