Article

The neuroscience of mammalian associative learning. Annu Rev Psychol

Department of Psychology and Brain Research Institute, University of California-Los Angeles, Los Angeles, CA 90095-1563, USA.
Annual Review of Psychology (Impact Factor: 20.53). 02/2005; 56:207-34. DOI: 10.1146/annurev.psych.56.091103.070213
Source: PubMed

ABSTRACT Mammalian associative learning is organized into separate anatomically defined functional systems. We illustrate the organization of two of these systems, Pavlovian fear conditioning and Pavlovian eyeblink conditioning, by describing studies using mutant mice, brain stimulation and recording, brain lesions and direct pharmacological manipulations of specific brain regions. The amygdala serves as the neuroanatomical hub of the former, whereas the cerebellum is the hub of the latter. Pathways that carry information about signals for biologically important events arrive at these hubs by circuitry that depends on stimulus modality and complexity. Within the amygdala and cerebellum, neural plasticity occurs because of convergence of these stimuli and the biologically important information they predict. This neural plasticity is the physical basis of associative memory formation, and although the intracellular mechanisms of plasticity within these structures share some similarities, they differ significantly. The last Annual Review of Psychology article to specifically tackle the question of mammalian associative learning ( Lavond et al. 1993 ) persuasively argued that identifiable "essential" circuits encode memories formed during associative learning. The next dozen years saw breathtaking progress not only in detailing those essential circuits but also in identifying the essential processes occurring at the synapses (e.g., Bi & Poo 2001, Martinez & Derrick 1996 ) and within the neurons (e.g., Malinow & Malenka 2002, Murthy & De Camilli 2003 ) that make up those circuits. In this chapter, we describe the orientation that the neuroscience of learning has taken and review some of the progress made within that orientation.

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Available from: Michael Fanselow, Aug 21, 2015
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    • "Learning to avoid physically harmful situations is critical for the survival of organisms. Aversive learning is formed when a certain neutral situation (conditioned stimulus or CS) is associated with the physically harmful situation (unconditioned stimulus or US) (Fanselow and Poulos, 2005; LeDoux, 2000). In rodents, fear (which does not mean the conscious feeling of fear, but instead, a defensive response to a threat) manifests as immobility or ''freezing'' under environmental conditions that predict pain—the major sensory modality of the physical harm (Herry and Johansen, 2014; Pape and Pare, 2010). "
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    ABSTRACT: Animals learn to avoid harmful situations by associating a neutral stimulus with a painful one, resulting in a stable threat memory. In mammals, this form of learning requires the amygdala. Although pain is the main driver of aversive learning, the mechanism that transmits pain signals to the amygdala is not well resolved. Here, we show that neurons expressing calcitonin gene-related peptide (CGRP) in the parabrachial nucleus are critical for relaying pain signals to the central nucleus of amygdala and that this pathway may transduce the affective motivational aspects of pain. Genetic silencing of CGRP neurons blocks pain responses and memory formation, whereas their optogenetic stimulation produces defensive responses and a threat memory. The pain-recipient neurons in the central amygdala expressing CGRP receptors are also critical for establishing a threat memory. The identification of the neural circuit conveying affective pain signals may be pertinent for treating pain conditions with psychiatric comorbidities. Copyright © 2015 Elsevier Inc. All rights reserved.
    Cell 07/2015; 162(2):363. DOI:10.1016/j.cell.2015.05.057 · 33.12 Impact Factor
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    • "We first explored the role of CPEB3 in a form of associative memory that requires the integrity of the hippocampus, contextual fear conditioning (Fanselow and Poulos, 2005; LeDoux, 2000). Following habituation on day 1, mice were trained using a one-trial protocol on day 2 and tested for memory retention on day 3. "
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    ABSTRACT: Consolidation of long-term memories depends on de novo protein synthesis. Several translational regulators have been identified, and their contribution to the formation of memory has been assessed in the mouse hippocampus. None of them, however, has been implicated in the persistence of memory. Although persistence is a key feature of long-term memory, how this occurs, despite the rapid turnover of its molecular substrates, is poorly understood. Here we find that both memory storage and its underlying synaptic plasticity are mediated by the increase in level and in the aggregation of the prion-like translational regulator CPEB3 (cytoplasmic polyadenylation element-binding protein). Genetic ablation of CPEB3 impairs the maintenance of both hippocampal long-term potentiation and hippocampus-dependent spatial memory. We propose a model whereby persistence of long-term memory results from the assembly of CPEB3 into aggregates. These aggregates serve as functional prions and regulate local protein synthesis necessary for the maintenance of long-term memory. Copyright © 2015 Elsevier Inc. All rights reserved.
    Neuron 06/2015; 86(6). DOI:10.1016/j.neuron.2015.05.021 · 15.98 Impact Factor
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    • "It offers an analogue model to study processes that play a role in the pathogenesis and treatment of anxiety disorders (Mineka & Zinbarg, 2006). Over the past decennia, fear conditioning research in animals and humans has unraveled key processes involved in the formation, consolidation and expression of associative fear memories (e.g., see Craske, Hermans, & Vansteenwegen, 2006; Fanselow & Poulos, 2005; LeDoux, 2000), which are supposed to lie at the root of anxiety disorders. "
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    ABSTRACT: We argue that the stimuli used in traditional fear conditioning paradigms are too simple to model the learning and unlearning of complex fear memories. We therefore developed and tested an adapted fear conditioning paradigm, specifically designed for the study of complex associative memories. Second, we explored whether manipulating the meaning and complexity of the CS-UCS association strengthened the learned fear association.Methods In a two-day differential fear conditioning study, participants were randomly assigned to two experimental conditions. All participants were subjected to the same CSs (i.e., pictures) and UCS (i.e., 3 sec film clip) during fear conditioning. However, in one of the conditions (negative-relevant context), the reinforced CS and UCS were meaningfully connected to each other by a 12 min aversive film clip presented prior to fear acquisition. Participants in the other condition (neutral context) were not able to make such meaningful connection between these stimuli, as they viewed a neutral film clip.ResultsFear learning and unlearning were observed on fear-potentiated startle data and distress ratings within the adapted paradigm. Moreover, several group differences on these measures indicated increased UCS valence and enhanced associative memory strength in the negative-relevant context condition compared to the neutral context condition.LimitationsDue to technical equipment failure, skin conductance data could not be interpreted.Conclusions The fear conditioning paradigm as presented in the negative-relevant context condition holds considerable promise for the study of complex associative fear memories and therapeutic interventions for such memories.
    Journal of Behavior Therapy and Experimental Psychiatry 11/2014; DOI:10.1016/j.jbtep.2014.11.007 · 2.23 Impact Factor
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