Spermidine-induced improvement of reconsolidation of memory involves calcium-dependent protein kinase in rats.

Autor:	Girardi BA; Graduate Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil., Ribeiro DA; Graduate Program in Biological Sciences: Toxicological Biochemistry, Center of Exact and Natural Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil., Signor C; Graduate Program in Biological Sciences: Toxicological Biochemistry, Center of Exact and Natural Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil., Muller M; Undergraduate in Pharmacy, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil., Gais MA; Undergraduate in Pharmacy, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil., Mello CF; Graduate Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil., Rubin MA; Graduate Program in Pharmacology, Center of Health Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil Graduate Program in Biological Sciences: Toxicological Biochemistry, Center of Exact and Natural Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil maribel.rubin@gmail.com.
Jazyk:	angličtina
Zdroj:	Learning & memory (Cold Spring Harbor, N.Y.) [Learn Mem] 2015 Dec 15; Vol. 23 (1), pp. 21-8. Date of Electronic Publication: 2015 Dec 15 (Print Publication: 2016).
DOI:	10.1101/lm.039396.115
Abstrakt:	In this study, we determined whether the calcium-dependent protein kinase (PKC) signaling pathway is involved in the improvement of fear memory reconsolidation induced by the intrahippocampal administration of spermidine in rats. Male Wistar rats were trained in a fear conditioning apparatus using a 0.4-mA footshock as an unconditioned stimulus. Twenty-four hours after training, animals were re-exposed to the apparatus in the absence of shock (reactivation session). Immediately after the reactivation session, spermidine (2-200 pmol/site), the PKC inhibitor 3-[1-(dimethylaminopropyl)indol-3-yl]-4-(indol-3-yl) maleimide hydrochloride (GF 109203X, 0.3-30 pg/site), the antagonist of the polyamine-binding site at the NMDA receptor, arcaine (0.2-200 pmol/site), or the PKC activator phorbol 12-myristate 13-acetate (PMA, 0.02-2 nmol/site) was injected. While the post-reactivation administration of spermidine (20 and 200 pmol/site) and PMA (2 nmol/site) improved memory reconsolidation, GF 109203X (1, 10, and 30 pg/site) and arcaine (200 pmol/site) impaired it. GF 109203X (0.3 pg/site) impaired memory reconsolidation in the presence of spermidine (200 pmol/site). PMA (0.2 nmol/site) prevented the arcaine (200 pmol/site)-induced impairment of memory reconsolidation. Anisomycin (2 µg/site) also impaired memory reconsolidation in the presence of spermidine (200 pmol/site). Drugs had no effect when they were administered in the absence of reactivation. These results suggest that the spermidine-induced enhancement of memory reconsolidation involves PKC activation. (© 2015 Girardi et al.; Published by Cold Spring Harbor Laboratory Press.)
Databáze:	MEDLINE
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