Literature DB >> 17072590

Glucocorticoid mechanisms may contribute to ECT-induced retrograde amnesia.

Nandakumar Nagaraja1, Chittaranjan Andrade, Suresh Sudha, Nagendra Madan Singh, J Suresh Chandra, B V Venkataraman.   

Abstract

RATIONALE: Cortisol levels rise sharply immediately after electroconvulsive therapy (ECT); the resultant stimulation of steroid receptors in the hippocampus may be beneficial or harmful to cognition, depending on the magnitude of the stimulation. Steroid mechanisms may therefore modulate ECT-induced amnesia.
OBJECTIVES: Using mifepristone (a glucocorticoid receptor antagonist) as a chemical probe, we sought to examine steroid mechanisms in an animal model of ECT-induced retrograde amnesia.
MATERIALS AND METHODS: Adult, male Wistar rats (n = 68) trained in a step-through passive-avoidance task were randomized to receive mifepristone (20 or 40 mg kg(-1) day(-1)) or vehicle (control). These treatments were administered 1 day before the electroconvulsive shock (ECS) course and, again, 1 h before each of five once-daily true (30 mC) or sham ECS. Recall of pre-ECS learning was tested 1 day after the last ECS.
RESULTS: Relative to sham ECS, true ECS resulted in significant retrograde amnesia in the vehicle group but not in either of the mifepristone groups. In sham ECS-treated animals, mifepristone did not significantly influence recall. In ECS-treated rats, the higher but not the lower dose of mifepristone was associated with significant protection against the retrograde amnesia evident in the vehicle group.
CONCLUSION: Mifepristone administered before the ECT seizure may attenuate ECT-induced retrograde amnesia. This suggests that glucocorticoid mechanisms may contribute to ECT-induced retrograde amnesia.

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Year:  2006        PMID: 17072590     DOI: 10.1007/s00213-006-0593-y

Source DB:  PubMed          Journal:  Psychopharmacology (Berl)        ISSN: 0033-3158            Impact factor:   4.530


  36 in total

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3.  Therapeutic and prophylactic role of cognitive enhancers in electroconvulsive therapy-induced cognitive deficits.

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4.  Celecoxib as an in vivo probe of cyclooxygenase-2 mechanisms underlying retrograde amnesia in an animal model of ECT.

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8.  Molecular mechanisms underlying electroconvulsive therapy-induced amnestic deficits: A decade of research.

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