Verapamil enhances acute stress or glucocorticoid-induced deficits in retrieval of long-term memory in rats

• Published in: Behavioural brain research 2009-10, Vol.203 (1), p.76-80
• Main Authors: Rashidy-Pour, Ali, Vafaei, Abbas Ali, Taherian, Abbas Ali, Miladi-Gorji, Hossein, Sadeghi, Hassan, Fathollahi, Yaghoub, Bandegi, Ahmad Reza
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Avoidance Learning - drug effects; Behavioral psychophysiology; Biological and medical sciences; Calcium Channel Blockers - administration & dosage; Calcium Channel Blockers - pharmacology; Corticosterone - blood; Electroshock; Fundamental and applied biological sciences. Psychology; Glucocorticoids; Glucocorticoids - blood; Male; Memory - drug effects; Memory - physiology; Memory Disorders - chemically induced; Memory Disorders - drug therapy; Memory retrieval; Motor Activity - drug effects; Motor Activity - physiology; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Random Allocation; Rats; Rats, Wistar; Restraint stress; Restraint, Physical; Stress, Psychological - drug therapy; Time Factors; Verapamil; Verapamil - administration & dosage; Verapamil - pharmacology; Voltage-dependent calcium channels
• ISSN: 0166-4328; 1872-7549
• DOI: 10.1016/j.bbr.2009.04.018

This study was designed to investigate an interaction between acute restraint stress and corticosterone with verapamil, a blocker of L-type voltage-dependent calcium (VDC) channels on retrieval of long-term memory. Young adult male rats were trained in one trial inhibitory avoidance task (0.5mA, 3s footshock). On retention test given 48h after training, the latency to re-enter dark compartment of the apparatus was recorded. In Experiment 1, verapamil pretreatment (5, 10, or 20mg/kg) enhanced the impairing effects of acute stress (which was applied for 10min in a Plexiglass tube 30min before the retention test) on memory retrieval. The applied stress increased circulating corticosterone levels as assessed immediately after the retention test, indicating that stress-induced impairment of memory retrieval is mediated, in part, by increased plasma levels of glucocorticoids. Verapamil did not change this response. In Experiment 2, pretreatment of an intermediate dose of verapamil also enhanced corticosterone-induced impairment of memory retrieval. In Experiments 3 and 4, acute stress or corticosterone did not change motor activity with or without prior treatment of verapamil, suggesting that stress or glucocorticoid-induced impairment of memory retrieval is not due to any gross disturbances in motor performance of animals. These findings indicate that blockade of L-type VDC channels enhances stress or glucocorticoid-induced impairment of memory retrieval, and provide evidence for the existence of an interaction between glucocorticoids and L-type VDC channels on memory retrieval.