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Open AccessArticle

Cognitive Deficits Following a Post-Myocardial Infarct in the Rat Are Blocked by the Serotonin-Norepinephrine Reuptake Inhibitor Desvenlafaxine

1
Research Center, Hôpital du Sacré-Coeur de Montréal, Montréal, QC H4J 1C5, Canada
2
Department of Pharmacology and Physiology, Université de Montréal, Montréal, QC H3C 3J7, Canada
3
Department of Psychiatry, Université de Montréal, Montréal, QC H3C 3J7, Canada
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(12), 3748; https://doi.org/10.3390/ijms19123748
Received: 12 October 2018 / Revised: 13 November 2018 / Accepted: 22 November 2018 / Published: 26 November 2018
Myocardial infarction (MI) in animal models induces cognitive deficits as well as the activation of caspase in the limbic system; both can be blocked by 2 weeks of treatment following MI using tricyclic antidepressants or selective serotonin uptake blockers. Here we used three different treatment schedules to test the short- and long-term effects of the combined serotonin-norepinephrine reuptake inhibitor desvenlafaxine on post-MI-associated cognitive deficits and caspase activation. MI was induced in 39 young adult rats, and 39 rats served as sham-operated controls. Desvenlafaxine (3 mg/kg/day, i.p.) or saline was administered according to one of three schedules: (1) for 2 weeks, starting right after surgery; (2) for 16 weeks, starting 2 weeks after surgery; (3) for 16 weeks, starting right after surgery. Behavior was tested 2 weeks (social interaction, passive avoidance) and 16 weeks (forced swimming, Morris water maze) after surgery. Caspase-3 and caspase-6 activities were measured 16 weeks after surgery. At 2 and 16 weeks post-surgery, saline-treated MI rats displayed performance deficits compared to desvenlafaxine-treated rats, regardless of the treatment schedule. Caspase-3 activity was higher in the amygdala (medial and lateral) and hippocampal CA3 region in untreated MI rats, whereas caspase-6 activity was higher in the CA1 region. Caspase-6 activity correlated positively with deficits in the Morris water maze. These results indicate that, independently of treatment schedules, various treatment schedules with desvenlafaxine can prevent MI-associated cognitive deficits and decrease caspase activities in the limbic system. View Full-Text
Keywords: desvenlafaxine; myocardial infarction; caspase-3; caspase-6; behavior; limbic system; memory desvenlafaxine; myocardial infarction; caspase-3; caspase-6; behavior; limbic system; memory
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Malick, M.; Gilbert, K.; Brouillette, J.; Godbout, R.; Rousseau, G. Cognitive Deficits Following a Post-Myocardial Infarct in the Rat Are Blocked by the Serotonin-Norepinephrine Reuptake Inhibitor Desvenlafaxine. Int. J. Mol. Sci. 2018, 19, 3748.

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