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J Neural Transm (Vienna). 2008 Jul;115(7):1063-70. doi: 10.1007/s00702-008-0063-2. Epub 2008 Jun 4.

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

Author information

1
Department of Psychopharmacology, National Institute of Mental Health and Neurosciences, Bangalore 560 029, India. andrade@nimhans.kar.nic.in

Abstract

BACKGROUND:

Cyclooxygenase-2 (COX-2) mechanisms are involved in glutamate-mediated learning and memory as well as in glutamatergic excitotoxicity. Electroconvulsive therapy (ECT)-induced amnesia may arise from glutamatergic excitotoxicity; if so, COX-2 inhibition may attenuate retrograde amnesia with ECT.

METHODS:

Wistar rats which received celecoxib (15 mg/kg per day) or vehicle for 18 days were trained for 3 days on a passive avoidance task. On each of the next 3 days, rats which showed perfect learning (n=51) received true or sham suprathreshold electroconvulsive shocks (ECS; 60 mC) in a factorial design; daily dosing with drug or vehicle was continued. One day after the last ECS, recall of pre-ECS learning was tested.

RESULTS:

ECS-treated rats showed impaired recall in the vehicle but not celecoxib group. Celecoxib significantly protected against ECS-induced retrograde amnesia; this benefit was independent of the drug-induced attenuation of ECS seizure duration.

CONCLUSIONS:

Celecoxib may protect against ECS-induced retrograde amnesia by attenuating ECS-induced, COX-2-mediated glutamatergic excitotoxicity.

PMID:
18523723
DOI:
10.1007/s00702-008-0063-2
[Indexed for MEDLINE]

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