Literature DB >> 11031131

Impaired memory consolidation in rats produced with beta-adrenergic blockade.

L Cahill1, C A Pham, B Setlow.   

Abstract

Despite abundant evidence that systemic administration of adrenergic drugs and hormones can produce retrograde memory enhancement, the literature contains no clear demonstration that postlearning systemic administration of adrenergic antagonists produces retrograde amnesia. Here we demonstrate retrograde amnesia for a stressful learning task (a spatial water maze) with systemic administration of the beta-adrenergic antagonist propranolol (5 mg/kg). The amnesic effect of the drug depended on the degree of learning in the subjects: Propranolol caused a robust retrograde amnesia in "good learners," but did not significantly affect memory in "poor learners." The findings provide critical additional support for the hypothesis that postlearning adrenergic activation modulates memory consolidation processes after emotionally stressful events and help explain previous failures to detect memory impairment after systemic administration of adrenergic blocking drugs. Copyright 2000 Academic Press.

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Year:  2000        PMID: 11031131     DOI: 10.1006/nlme.1999.3950

Source DB:  PubMed          Journal:  Neurobiol Learn Mem        ISSN: 1074-7427            Impact factor:   2.877


  39 in total

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3.  Post-retrieval propranolol treatment does not modulate reconsolidation or extinction of ethanol-induced conditioned place preference.

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Authors:  K Kühlmeyer; R J Jox
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7.  Adrenergic manipulation inhibits pavlovian conditioned approach behaviors.

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8.  Memory enhancing effects of nicotine, cocaine, and their conditioned stimuli; effects of beta-adrenergic and dopamine D2 receptor antagonists.

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Journal:  Psychopharmacology (Berl)       Date:  2021-06-26       Impact factor: 4.530

Review 9.  A memory-based model of posttraumatic stress disorder: evaluating basic assumptions underlying the PTSD diagnosis.

Authors:  David C Rubin; Dorthe Berntsen; Malene Klindt Bohni
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10.  Environmental novelty activates β2-adrenergic signaling to prevent the impairment of hippocampal LTP by Aβ oligomers.

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