Characterization of Fear Memory Reconsolidation

Duvarci, Sevil; Nader, Karim

doi:10.1523/jneurosci.2971-04.2004

Cited by 352 publications

(327 citation statements)

References 37 publications

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“…Thus, our data confirm that the effects of Zif268 ASO on the impairment of appetitive and aversive memory reconsolidation are reactivation dependent (Lee et al, 2005(Lee et al, , 2006Debiec et al, 2006). Some studies have demonstrated a recovery from amnesia after reconsolidation blockade with repeated testing (Lattal and Abel, 2004;Power et al 2006), whereas others have found no evidence of recovery (Duvarci and Nader, 2004;Lee et al, 2004). Although the current study did not test for persistent impairments in heroin seeking, previous data from our laboratory using Zif268 ASOs to explore both appetitive and aversive memory reconsolidation deficits have never observed any indication of a recovery, suggesting a persistent amnesia after this manipulation (Lee et al, 2004(Lee et al, , 2005(Lee et al, , 2006.…”

Section: Discussionsupporting

confidence: 85%

Disrupting Reconsolidation of Conditioned Withdrawal Memories in the Basolateral Amygdala Reduces Suppression of Heroin Seeking in Rats

Hellemans¹,

Everitt²

2006

J. Neurosci.

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Recent data from our laboratory have demonstrated that appetitive drug memories undergo protein synthesis-dependent reconsolidation in the basolateral amygdala (BLA), an area important in the formation of emotional memories. We here investigated the importance of the BLA in the reconsolidation of opiate conditioned withdrawal memories. Rats with bilateral cannulas implanted in the BLA were trained to respond for heroin (0.12 mg/kg, i.v.) under a seeking-taking schedule, which required responding on a seeking lever to gain the opportunity to self-administer heroin by a single response on a taking lever. After induction of opiate dependence with subcutaneously implanted, heroin-filled osmotic minipumps (3 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 heroin), rats received five consecutive pairings of a conditioned stimulus (CS) (tone, light, and odor compound) paired with naloxone (0.10 mg/kg, s.c.)-precipitated withdrawal. We replicated our previous findings that heroin seeking is suppressed in the presence of the withdrawal-associated CS. However, infusion of Zif268 antisense oligodeoxynucleotide into the BLA before reactivation of the CS-withdrawal association abolished this conditioned suppression in a reactivation-dependent manner. We also report that reconsolidation of CS-withdrawal memories upregulates Zif268 protein in the basolateral but not central nucleus of the amygdala and that Zif268 knockdown occurs selectively in the BLA. These results demonstrate that drug withdrawal memories undergo protein synthesis-dependent reconsolidation in the BLA and suggest a common mechanism for the reconsolidation of both appetitive and aversive drug memories.

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Section: Discussionsupporting

confidence: 85%

Disrupting Reconsolidation of Conditioned Withdrawal Memories in the Basolateral Amygdala Reduces Suppression of Heroin Seeking in Rats

Hellemans¹,

Everitt²

2006

J. Neurosci.

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“…Accumulated experimental data support the argument that after retrieval, consolidated memory may become temporarily vulnerable to disruption for a limited period of time (Przybyslawski and Sara, 1997;Przybyslawski et al, 1999;Nader, 2003;Debiec and Ledoux, 2004;Duvarci and Nader, 2004). Such vulnerability is followed by a stabilization processFusually referred to as reconsolidationFthat requires de novo protein synthesis.…”

Section: Introductionmentioning

confidence: 70%

Disruptive Effect of Midazolam on Fear Memory Reconsolidation: Decisive Influence of Reactivation Time Span and Memory Age

Bustos

Maldonado

Molina

2008

Neuropsychopharmacol

136

128

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Benzodiazepine (BDZ) administered shortly after retrieval disrupts the reconsolidation of fear memory. In this research, we explored the way in which different factors that limit the emergence of such process may affect BDZ's disruptive effect on fear memory reconsolidation. Animals were conditioned in a contextual fear paradigm; the consolidated memory was reactivated by exposure to the associated context for different periods of time that were followed by midazolam (MDZ) administration. We also studied MDZ amnesic effect after reactivating fear memories of several ages. We finally analyzed the effectiveness of different MDZ doses in preventing the reconsolidation of different age fear memories. The memory trace was disrupted following MDZ when the reactivation session lasted 3-5 min but it was not after a briefer 1-min reactivation period. Over a 10-min reactivation session, all animals gradually reduced their fear response, which indicates the emergence of the extinction process. When tested, MDZ rats exhibited a robust fear, suggesting that MDZ impaired the consolidation of extinction. In a 3-min reactivation session, MDZ (1-1.5 mg/kg) prevented the reconsolidation of recently acquired memories. A 21-day-old fear memory was only vulnerable to MDZ at a 1.5 mg/kg dose with a reactivation session of 5 and not 3 min, whereas a 36-day-old memory was only disrupted with a higher MDZ dose (3 mg/kg) regardless of the reactivation trial's duration. This study demonstrated MDZ's interference on fear-memory reconsolidation within a relatively short reactivation period in recently acquired memories. Over longer reexposure, MDZ disrupts the consolidation of extinction. A longer duration of the reexposure session, as well as higher MDZ doses, is required to prevent the reconsolidation process of remote fear memories.

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“…Extinction is a process by which a new inhibitory association is formed following a longer exposure to a CS, resulting in a reduced fear response (Myers and Davis, 2002). Previous studies suggest that the basolateral nucleus of the amygdala (BLA) is mainly involved in reconsolidation (Nader et al, 2000;Duvarci and Nader, 2004;Baldi et al, 2008), and that the amygdala, hippocampus, and medial prefrontal cortex (mPFC) form a circuit necessary for extinction in rodents (for review, see Corcoran and Quirk, 2007;Sotres-Bayon et al, 2004;Quirk and Mueller, 2008).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological Discrimination of Extinction and Reconsolidation of Contextual Fear Memory by a Potentiator of AMPA Receptors

Yamada

Zushida

Wada

et al. 2009

Neuropsychopharmacol

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Conditioned fear memory, once formed through fear conditioning, is modulated by reexposure of individuals to a conditioned stimulus. The reexposure reactivates the fear memory, which induces reconsolidation of the memory first, and then extinction of the fear response. Both attenuating the former and facilitating the latter are effective in reducing the fear response, and these findings are potentially translatable to the enhancement of exposure therapy for complex anxiety disorders. Currently, there is no drug that is established to modulate either reconsolidation or extinction selectively, which are thought to be independent processes. Here, we report that an extinction-facilitating AMPA potentiator, 4-[2-(phenylsulfonylamino)ethylthio]-2,6-difluoro-phenoxyacetamide (PEPA), does not act on the reconsolidation of fear memory formed by contextual fear conditioning in mice. The freezing rates observed in contextually conditioned mice following short reexposure (3 min) to the context were not influenced by intraperitoneal or intra-amygdala administration of PEPA. The same short reexposure to the context enhanced freezing responses in mice that were similarly administered D-cycloserine (DCS), a drug that facilitates both extinction and reconsolidation, and this enhancement of freezing responses in mice intraperitoneally administered DCS was abolished by propranolol, a drug that suppresses reconsolidation. At the same doses used in the short reexposure experiments, PEPA and DCS facilitated extinction of the fear response induced by long reexposure to the context and suppressed reinstatement of the conditioned fear memory. PEPA and DCS did not affect reextinction. These results suggest that PEPA acts on extinction of contextual fear memory without having detectable influences on its reconsolidation.

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Characterization of Fear Memory Reconsolidation

Cited by 352 publications

References 37 publications

Disrupting Reconsolidation of Conditioned Withdrawal Memories in the Basolateral Amygdala Reduces Suppression of Heroin Seeking in Rats

Disrupting Reconsolidation of Conditioned Withdrawal Memories in the Basolateral Amygdala Reduces Suppression of Heroin Seeking in Rats

Disruptive Effect of Midazolam on Fear Memory Reconsolidation: Decisive Influence of Reactivation Time Span and Memory Age

Pharmacological Discrimination of Extinction and Reconsolidation of Contextual Fear Memory by a Potentiator of AMPA Receptors

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