Activation of amygdaloid PKC pathway is necessary for conditioned cues-provoked cocaine memory performance

Lai, Yu Ting; Fan, Hsin Yi; Cherng, Chianfang G.; Chiang, Chih Yuan; Kao, Gour Shenq; Yu, Lung

doi:10.1016/j.nlm.2008.03.006

Cited by 35 publications

(19 citation statements)

References 33 publications

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“…Cycloheximide is a less commonly used protein synthesis inhibitor than anisomycin, but it is sometimes preferred as it is easier to keep in solution. There is no evidence to suggest that it is less effective than other protein synthesis inhibitors (e.g., Milekic et al 2006;Lai et al 2008), and it has been successfully used in the amygdala as an amnesic agent in a number of studies (e.g., Berman et al 1978;Duvarci et al 2005;Pedroso et al 2013), including the present study.…”

Section: Discussionmentioning

confidence: 66%

The amygdala is critical for trace, delay, and contextual fear conditioning

et al. 2015

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Numerous investigations have definitively shown amygdalar involvement in delay and contextual fear conditioning. However, much less is known about amygdala contributions to trace fear conditioning, and what little evidence exists is conflicting as noted in previous studies. This discrepancy may result from selective targeting of individual nuclei within the amygdala. The present experiments further examine the contributions of amygdalar subnuclei to trace, delay, and contextual fear conditioning. Rats were trained using a 10-trial trace, delay, or unpaired fear conditioning procedure. Pretraining lesions targeting the entire basolateral amygdala (BLA) resulted in a deficit in trace, delay, and contextual fear conditioning. Immediate post-training infusions of the protein synthesis inhibitor, cycloheximide, targeting the basal nucleus of the amygdala (BA) attenuated trace and contextual fear memory expression, but had no effect on delay fear conditioning. However, infusions targeting the lateral nucleus of the amygdala (LA) immediately following conditioning attenuated contextual fear memory expression, but had no effect on delay or trace fear conditioning. In follow-up experiments, rats were trained using a three-trial delay conditioning procedure. Immediate post-training infusions targeting the LA produced deficits in both delay tone and context fear, while infusions targeting the BA produced deficits in context but not delay tone fear. These data fully support a role for the BLA in trace, delay, and contextual fear memories. Specifically, these data suggest that the BA may be more critical for trace fear conditioning, whereas the LA may be more critical for delay fear memories.Pavlovian fear conditioning is one of the most extensively studied systems for investigating the neural mechanisms mediating learning and memory processes. It is a behavioral paradigm in which an organism learns to anticipate an aversive event by pairing that event (i.e., unconditioned stimulus; US) with a particular place or predictive stimulus (i.e., conditioned stimulus; CS). The amygdala serves a critical role in this fear learning; it receives both unimodal and multimodal sensory information and projects to a number of individual response circuits allowing for a coordinated fear response (e.g

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Section: Discussionmentioning

confidence: 66%

The amygdala is critical for trace, delay, and contextual fear conditioning

et al. 2015

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“…10 ). Moreover, these 3 groups of mice exhibited comparable food-induced CPP magnitude in test 1 (F (2,14) = 0.3282, p = 0.7265). Likewise, 3 groups of mice exhibited comparable food-induced CPP magnitude in test 2 approximately 48 h after the intra-accumbal infusion (F (2,14) = 1.56, p = 0.2499).…”

Section: Expression Of Accumbal 14-3-3 Protein Did Notmentioning

confidence: 85%

“…In this model, cocaine-conditioned cue/context induces animals' preference to the cocaine-associated place for a period of time even when cocaine is not provided any longer after conditioning. Previously, we demonstrated that newly synthesized proteins are involved in the consolidation, expression and reconsolidation of this cocaine-conditioned memory [13][14][15] . However, the roles of specific proteins in mediating the retrieval of this cocaine memory remain unexplored.…”

Section: Introductionmentioning

confidence: 94%

“…Pretest, cocaine-induced CPP training, test and cocaine priming test were all conducted in commercial chambers designed for mice (MedAssociates Inc., Georgia, Vt., USA) as described in our previous reports [13,14] . Mice of the paired and unpaired groups were placed in the center of any randomly chosen chamber and their time spent in each compartment of the chamber was measured for unconditioned preference in a 15-min pretest on day 1.…”

Section: Cocaine-induced Cpp Training Test and Cocaine-priming Testmentioning

confidence: 99%

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Accumbal 14-3-3ζ Protein Downregulation Is Associated with Cocaine-Conditioned Memory

et al. 2011

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Cocaine-conditioned memory has been known to cause cocaine craving and relapse, while its underlying mechanisms remain unclear. We explored accumbal protein candidates responsible for a cocaine-conditioned memory, cocaine-induced conditioned place preference (CPP). Two-dimensional gel electrophoresis in conjunction with liquid chromatography mass spectrometry analysis was utilized to identify accumbal protein candidates involved in the retrieval of cocaine-induced CPP. Among the identified candidate proteins, a downregulated 14-3-3ζ protein was chosen and confirmed by Western immunoblotting. A polymer-mediated plasmid DNA delivery system was then used to overexpress 14-3-3 protein in mouse nucleus accumbens before the CPP retrieval tests. Overexpression of accumbal 14-3-3ζ protein was found to diminish conditioned cue/context-mediated cocaine-induced CPP. In contrast, another isoform of 14-3-3 protein, 14-3-3ε protein, did not affect conditioned cue/context-mediated cocaine-induced CPP. Overexpression of accumbal 14-3-3ζ protein did not produce motor activity-impairing effect or alter local dopamine metabolism. Moreover, overexpression of accumbal 14-3-3ζ protein did not affect food-induced CPP. These results, taken together, indicated that overexpressed accumbal 14-3-3ζ protein specifically decreased conditioned cue/context-mediated cocaine memory. Further understanding of the function of accumbal 14-3-3ζ protein may shed light on the treatment of cocaine craving and relapse.

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“…During acquisition, animals receive the drug or saline in an appropriate, distinctive chamber and then form memories about the drug and cues. In the retrieval phase, cues previously associated with the receipt of drugs strongly induce animals to reinstate drug-seeking and drug-taking behavior ( Lai et al, 2008). Afterward, the reconsolidation phase that follows memory retrieval begins once a previously consolidated memory is activated by conditioned cues, causing memory to enter a labile state that is vulnerable to disruption (Nade, 2003).…”

mentioning

confidence: 99%

Blockage of glucocorticoid receptors during memory acquisition, retrieval and reconsolidation prevents the expression of morphine-induced conditioned place preferences in mice

Yang¹,

Niu²,

Huma³

et al. 2013

Zoological Research

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Association between the reward caused by consuming drugs and the context in which they are consumed is essential in the formation of morphine-induced conditioned place preference (CPP). Glucocorticoid receptor (GRs) activation in different regions of the brain affects reward-based reinforcement and memory processing. A wide array of studies have demonstrated that blockage of GRs in some brain areas can have an effect on reward-related memory; however, to date there have been no systematic studies about the involvement of glucocorticoids (GCs) in morphine-related reward memory. Here, we used the GR antagonist RU38486 to investigate how GRs blockage affects the sensitization and CPP behavior during different phases of reward memory included acquisition, retrieval and reconsolidation. Interestingly, our results showed RU38486 has the ability to impair the acquisition, retrieval and reconsolidation of reward-based memory in CPP and sensitization behavior. But RU38486 by itself cannot induce CPP or conditioned place aversion (CPA) behavior. Our data provide a much more complete picture of the potential effects that glucocorticoids have on the reward memory of different phases and inhibit the sensitization behavior.

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Activation of amygdaloid PKC pathway is necessary for conditioned cues-provoked cocaine memory performance

Cited by 35 publications

References 33 publications

The amygdala is critical for trace, delay, and contextual fear conditioning

The amygdala is critical for trace, delay, and contextual fear conditioning

Accumbal 14-3-3ζ Protein Downregulation Is Associated with Cocaine-Conditioned Memory

Blockage of glucocorticoid receptors during memory acquisition, retrieval and reconsolidation prevents the expression of morphine-induced conditioned place preferences in mice

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