Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.

The intracellular mechanisms underlying memory reconsolidation critically involve cAMP signaling. These events were originally attributed to PKA activation by cAMP, but the identification of Exchange Protein Activated by cAMP (Epac), as a distinct mediator of cAMP signaling, suggests that cAMP-regul...

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Autores principales:	Xun Wan, Mary M Torregrossa, Hayde Sanchez, Angus C Nairn, Jane R Taylor
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/57e8a695aaca4598a84aebf2203d48f3
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spelling	oai:doaj.org-article:57e8a695aaca4598a84aebf2203d48f32021-11-25T05:59:12ZActivation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.1932-620310.1371/journal.pone.0107359https://doaj.org/article/57e8a695aaca4598a84aebf2203d48f32014-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0107359https://doaj.org/toc/1932-6203The intracellular mechanisms underlying memory reconsolidation critically involve cAMP signaling. These events were originally attributed to PKA activation by cAMP, but the identification of Exchange Protein Activated by cAMP (Epac), as a distinct mediator of cAMP signaling, suggests that cAMP-regulated processes that subserve memory reconsolidation are more complex. Here we investigated how activation of Epac with 8-pCPT-cAMP (8-CPT) impacts reconsolidation of a memory that had been associated with cocaine self-administration. Rats were trained to lever press for cocaine on an FR-1 schedule, in which each cocaine delivery was paired with a tone+light cue. Lever pressing was then extinguished in the absence of cue presentations and cocaine delivery. Following the last day of extinction, rats were put in a novel context, in which the conditioned cue was presented to reactivate the cocaine-associated memory. Immediate bilateral infusions of 8-CPT into the basolateral amygdala (BLA) following reactivation disrupted subsequent cue-induced reinstatement in a dose-dependent manner, and modestly reduced responding for conditioned reinforcement. When 8-CPT infusions were delayed for 3 hours after the cue reactivation session or were given after a cue extinction session, no effect on cue-induced reinstatement was observed. Co-administration of 8-CPT and the PKA activator 6-Bnz-cAMP (10 nmol/side) rescued memory reconsolidation while 6-Bnz alone had no effect, suggesting an antagonizing interaction between the two cAMP signaling substrates. Taken together, these studies suggest that activation of Epac represents a parallel cAMP-dependent pathway that can inhibit reconsolidation of cocaine-cue memories and reduce the ability of the cue to produce reinstatement of cocaine-seeking behavior.Xun WanMary M TorregrossaHayde SanchezAngus C NairnJane R TaylorPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 9, p e107359 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xun Wan Mary M Torregrossa Hayde Sanchez Angus C Nairn Jane R Taylor Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.
description	The intracellular mechanisms underlying memory reconsolidation critically involve cAMP signaling. These events were originally attributed to PKA activation by cAMP, but the identification of Exchange Protein Activated by cAMP (Epac), as a distinct mediator of cAMP signaling, suggests that cAMP-regulated processes that subserve memory reconsolidation are more complex. Here we investigated how activation of Epac with 8-pCPT-cAMP (8-CPT) impacts reconsolidation of a memory that had been associated with cocaine self-administration. Rats were trained to lever press for cocaine on an FR-1 schedule, in which each cocaine delivery was paired with a tone+light cue. Lever pressing was then extinguished in the absence of cue presentations and cocaine delivery. Following the last day of extinction, rats were put in a novel context, in which the conditioned cue was presented to reactivate the cocaine-associated memory. Immediate bilateral infusions of 8-CPT into the basolateral amygdala (BLA) following reactivation disrupted subsequent cue-induced reinstatement in a dose-dependent manner, and modestly reduced responding for conditioned reinforcement. When 8-CPT infusions were delayed for 3 hours after the cue reactivation session or were given after a cue extinction session, no effect on cue-induced reinstatement was observed. Co-administration of 8-CPT and the PKA activator 6-Bnz-cAMP (10 nmol/side) rescued memory reconsolidation while 6-Bnz alone had no effect, suggesting an antagonizing interaction between the two cAMP signaling substrates. Taken together, these studies suggest that activation of Epac represents a parallel cAMP-dependent pathway that can inhibit reconsolidation of cocaine-cue memories and reduce the ability of the cue to produce reinstatement of cocaine-seeking behavior.
format	article
author	Xun Wan Mary M Torregrossa Hayde Sanchez Angus C Nairn Jane R Taylor
author_facet	Xun Wan Mary M Torregrossa Hayde Sanchez Angus C Nairn Jane R Taylor
author_sort	Xun Wan
title	Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.
title_short	Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.
title_full	Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.
title_fullStr	Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.
title_full_unstemmed	Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.
title_sort	activation of exchange protein activated by camp in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/57e8a695aaca4598a84aebf2203d48f3
work_keys_str_mv	AT xunwan activationofexchangeproteinactivatedbycampintheratbasolateralamygdalaimpairsreconsolidationofamemoryassociatedwithselfadministeredcocaine AT marymtorregrossa activationofexchangeproteinactivatedbycampintheratbasolateralamygdalaimpairsreconsolidationofamemoryassociatedwithselfadministeredcocaine AT haydesanchez activationofexchangeproteinactivatedbycampintheratbasolateralamygdalaimpairsreconsolidationofamemoryassociatedwithselfadministeredcocaine AT anguscnairn activationofexchangeproteinactivatedbycampintheratbasolateralamygdalaimpairsreconsolidationofamemoryassociatedwithselfadministeredcocaine AT janertaylor activationofexchangeproteinactivatedbycampintheratbasolateralamygdalaimpairsreconsolidationofamemoryassociatedwithselfadministeredcocaine
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Activation of exchange protein activated by cAMP in the rat basolateral amygdala impairs reconsolidation of a memory associated with self-administered cocaine.

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