Article

Role of amygdala central nucleus in aversive learning produced by shock or by unexpected omission of food.

Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, Maryland 21218, USA.
Journal of Neuroscience (Impact Factor: 6.91). 02/2012; 32(7):2461-72. DOI: 10.1523/JNEUROSCI.5090-11.2012
Source: PubMed

ABSTRACT Many psychological learning theories have noted commonalities between aversive states produced by presentation of negative reinforcers, such as electric shock, and the omission of expected positive reinforcers, such as food. Here, three groups of rats received training with one auditory cue paired with shock and another with the omission of expected food, a shock-paired cue and a food-omission control cue, or a food-omission cue and a shock control cue. Food-omission cues were established by contrast with food delivery; after extensive light-food pairings, the light was followed by the food-omission cue instead of food. Aversiveness of the food-omission cue was assessed with a conditioned punishment procedure, in which presentation of that cue was made contingent on performance of one previously trained instrumental response, whereas a second response had no consequences. We found that rats with lesions of amygdala central nucleus (CeA) showed impaired acquisition of freezing to the cue paired with shock and no evidence for acquisition of aversive properties by the cue that accompanied the omission of expected food. Furthermore, analyses of Arc and Homer1a mRNAs after rats were exposed to a two-epoch test procedure that allowed assessment of gene expression produced by two different test stimuli showed that both food-omission and shock-paired cues generated more neuronal activity in CeA than appropriate control cues. However, the number of neurons that were activated by both shock and food-omission cues was not significantly greater than expected by chance. Thus, under these test conditions, different subsets of CeA neurons represented these two aversive states.

0 Bookmarks
 · 
55 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: To make appropriate decisions, organisms must evaluate the risks and benefits of action selection. The nucleus accumbens (NAc) has been shown to be critical for this processing and is necessary for appropriate risk-based decision-making behavior. However, it is not clear how NAc neurons encode this information to promote appropriate behavioral responding. Here, rats (n = 17) were trained to perform a risky decision-making task in which discrete visual cues predicted the availability to respond for a smaller certain (safer) or larger uncertain (riskier) reward. Electrophysiological recordings were made in the NAc core and shell to evaluate neural activity during task performance. At test, animals exhibited individual differences in risk-taking behavior; some displayed a preference for the risky option, some the safe option, and some did not have a preference. Electrophysiological analysis indicated that NAc neurons differentially encoded information related to risk versus safe outcomes. Further, during free choice trials, neural activity during reward-predictive cues reflected individual behavioral preferences. In addition, neural encoding of reward outcomes was correlated with risk-taking behavior, with safe-preferring and risk-preferring rats showing differential activity in the NAc core and shell during reward omissions. Consistent with previously demonstrated alterations in prospective reward value with effort and delay, NAc neurons encode information during reward-predictive cues and outcomes in a risk task that tracked the rats' preferred responses. This processing appears to contribute to subjective encoding of anticipated outcomes and thus may function to bias future risk-based decisions.
    Biological psychiatry 10/2013; · 8.93 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Relapse to alcohol abuse is an important clinical issue that is frequently caused by cue-induced drug craving. Therefore, disruption of the memory for the cue-alcohol association is expected to prevent relapse. It is increasingly accepted that memories become labile and erasable soon after their reactivation through retrieval during a memory reconsolidation process that depends on protein synthesis. Here we show that reconsolidation of alcohol-related memories triggered by the sensory properties of alcohol itself (odor and taste) activates mammalian target of rapamycin complex 1 (mTORC1) in select amygdalar and cortical regions in rats, resulting in increased levels of several synaptic proteins. Furthermore, systemic or central amygdalar inhibition of mTORC1 during reconsolidation disrupts alcohol-associated memories, leading to a long-lasting suppression of relapse. Our findings provide evidence that the mTORC1 pathway and its downstream substrates are crucial in alcohol-related memory reconsolidation and highlight this pathway as a therapeutic target to prevent relapse.
    Nature Neuroscience 06/2013; · 15.25 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Correlational data suggest that learned associations are encoded within neuronal ensembles. However, it has been difficult to prove that neuronal ensembles mediate learned behaviours because traditional pharmacological and lesion methods, and even newer cell type-specific methods, affect both activated and non-activated neurons. In addition, previous studies on synaptic and molecular alterations induced by learning did not distinguish between behaviourally activated and non-activated neurons. Here, we describe three new approaches - Daun02 inactivation, FACS sorting of activated neurons and Fos-GFP transgenic rats - that have been used to selectively target and study activated neuronal ensembles in models of conditioned drug effects and relapse. We also describe two new tools - Fos-tTA transgenic mice and inactivation of CREB-overexpressing neurons - that have been used to study the role of neuronal ensembles in conditioned fear.
    Nature Reviews Neuroscience 10/2013; · 31.38 Impact Factor