Nonconscious perception, conscious awareness and attention

Because it is unclear how a nonconscious stimulus is cognitively processed, there is uncertainty concerning variables that modulate the processing. In this context recent findings of a set of neuroimaging experiments are important. These findings suggest that conscious and nonconscious stimuli activate same areas of the brain during performance of a similar task. Further, different areas are activated when a task is performed with or without awareness of processing. It appears that the neural network involved in cognitive processing depends on the awareness of processing rather than awareness of perception. Since conscious and nonconscious cognitive processing use separate neural networks, each processing is modulated by different variables. Attention modulates most conscious cognitive processing and most, but not all, nonconscious processing is attention dependent. Nonconscious tasks that require attentional resources, with or without conscious awareness, are processed using the attention dependent system. Further, because attention dependent and attention independent tasks are processed by separate neural networks, the cognitive processing and modulating variables can be understood better if cognitive tasks are defined as attention dependent or attention independent, rather than conscious or nonconscious.     

Conjunctive representations,the hippocampus,and contextual fear conditioning

The context in which events occur can be represented as both (1) a set of independent features, the feature representation view, and (2) a set of features bound into a unitary representation, the conjunction representation view. It is assumed that extrahippocampal (e.g., neocortical) areas provide a basis for feature representations, but the hippocampal formation makes an essential contribution to the automatic storage of conjunctive representations. We develop this dual-representation view and explore its implications for hippocampal contributions to contextual fear conditioning processes. To this end, we discuss how our framework can resolve some of the conflicts in the recent literature relating the hippocampus to contextual fear conditioning. We also present new data supporting the role of a key mechanism afforded by conjunctive representations—pattern completion (the ability of a subset of a memory pattern to activate the complete memory)—in contextual fear conditioning. As is implied by this mechanism, we report that fear can be conditioned to the memory representation of a context that is not actually present at the time of shock. Moreover, this result is predicted by our computational model of cortical and hippocampal function. We suggest that pattern completion demonstrated in animals and by our model provides a mechanistic bridge to human declarative memory.     

Covariation bias,classical conditioning,and phobic fear

The present study investigated whether phobics show an illusory correlation (IC) between phobia-relevant stimuli and aversive events. Nineteen treated and 19 untreated spider phobics were exposed to a series of 72 slides. Three different categories were used: Phobia-relevant slides (spiders), alternative fear-relevant slides (weapons), and neutral slides (flowers). Slides were randomly paired with either a shock, a siren, or nothing at all. All slide/outcome combinations occurred equally frequently. A posteriori recorded contingency estimates indicated that untreated phobics dramatically overestimate the covariation of spiders and shock. On-line recorded outcome expectancies revealed that the bias to overestimate the spider-shock contingency is highly resistant to extinction. The covariation bias was accompanied by differentially heightened electrodermal first interval responses (FIR) and unconditioned electrodermal responses (third interval responses: TIR) on phobia-relevant trials. Treated phobics did not show a covariation bias, indicating that such bias can be modulated by behavioral treatment. The present findings sustain the hypothesis that phobic subjects process information in a fear-confirming way.     

Bodily expressions,feelings, and the direct perception account of social cognition

Phenomenology and the Cognitive Sciences - In this paper, I will argue in favor of a direct perception account of social cognition (DP), focusing on the idea that we can directly grasp at least...     

Naloxone and Pavlovian fear conditioning

Previous research has shown that pretreating rats with the opiate antagonist naloxone increases the freezing that follows painful electric shock. Three experiments, using freezing behavior as a dependent variable, were carried out to determine whether the drug might cause this effect by enhancing fear conditioning. Two of the studies employed a differential context fear-conditioning paradigm. Naloxone did not affect freezing behavior during the preshock adaptation period. In Experiment 1, naloxone was found to increase resistance to extinction in the S+ context. In Experiment 2, naloxone was found to increase freezing in the S+ context. This effect was dependent upon administering naloxone during training but not dependent on administering it during testing. The third study employed a generalization paradigm. It was found that naloxone's effect on postshock freezing was dependent on the place of testing; as the contextual cues of the test chamber were changed from those of the conditioning chamber, the effect of naloxone on freezing was reduced. The results of these experiments lend strong support to the hypothesis that naloxone increases freezing by enhancing the conditioning of fear to contextual stimuli associated with shock.     

The development of cued versus contextual conditioning in a predictable and an unpredictable human fear conditioning preparation

In this human fear conditioning study, the online development of conditioned US-expectancy to discrete cues and background contexts was measured in two groups. In the paired group (n=30), the CS was systematically followed by an aversive shock (US). In the unpaired group (n=30), CS and US were presented explicitly unpaired. Using US-expectancy ratings, we replicated the basic finding already illustrated in humans with startle modulation. In the paired group, the CS elicited more US-expectancy than the context, whereas in the unpaired group, the context elicited more US-expectancy than the CS. Interestingly, we also observed a trial-by-trial development of conditioning to the context in the unpaired group as indicated by a significant linear trend. This gradual development and the evidence for the role of US-expectancy in contextual fear add to the idea that cued and contextual fear rely on the same basic associative processes.     

Macromolecular synthesis, distributed synaptic plasticity, and fear conditioning

Recent work from a number of laboratories has provided new and important insights about how gene expression is altered by experience and how these molecular changes may provide a substrate for the long-term storage of new memories. Here, we review a series of recent studies using aversive Pavlovian conditioning in rats as a well characterized model system in which experience-dependent alterations in gene expression can be manipulated and quantified within a specific neural circuit. We highlight some of the issues involved in using broad-spectrum inhibitors of mRNA and protein synthesis to study cellular changes underlying the formation and long-term stability of memory and discuss the idea that these changes occur over widespread, behaviorally-defined, networks of cells. We also discuss the idea that the maintenance of memory and its susceptibly to disruption after retrieval may relate to local protein synthesis in dendrites. Finally, a series of recent experiments from our laboratory studying the role of a specific signaling pathway (mTOR) which regulates translational processes and memory formation in the amygdala and hippocampus during fear conditioning are reviewed.     

Coantagonism of glutamate receptors and nicotinic acetylcholinergic receptors disrupts fear conditioning and latent inhibition of fear conditioning

The present study investigated the hypothesis that both nicotinic acetylcholinergic receptors (nAChRs) and glutamate receptors (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPARs) and N-methyl-d-aspartate glutamate receptors (NMDARs)) are involved in fear conditioning, and may modulate similar processes. The effects of the nAChR antagonist mecamylamine administered alone, the AMPAR antagonist NBQX administered alone, and the NMDAR antagonist MK-801 administered alone on cued fear conditioning, contextual fear conditioning, and latent inhibition of cued fear conditioning were examined. In addition, the effects of coadministration of either mecamylamine and NBQX or mecamylamine and MK-801 on these behaviors were examined. Consistent with previous studies, neither mecamylamine nor NBQX administered alone disrupted any of the tasks. However, coadministration of mecamylamine and NBQX disrupted both contextual fear conditioning and latent inhibition of cued fear conditioning. In addition, coadministration of mecamylamine with a dose of MK-801 subthreshold for disrupting either task disrupted both contextual fear conditioning and latent inhibition of cued fear conditioning. Coadministration of mecamylamine and NBQX, and coadministration of mecamylamine with a dose of MK-801 subthreshold for disrupting fear conditioning had little effect on cued fear conditioning. These results suggest that nAChRs and glutamate receptors may support similar processes mediating acquisition of contextual fear conditioning and latent inhibition of fear conditioning.     

The development of an attentional bias for angry faces following Pavlovian fear conditioning

Although it is well documented that fear responses develop following aversive Pavlovian conditioning, it is unclear whether fear learning also manifests in the form of attentional biases for fear-related stimuli. Boschen, Parker, and Neumann (Boschen, M. J., Parker, I., & Neumann, D. L. (2007). Changes in implicit associations do not occur simultaneously to Pavlovian conditioning of physiological anxiety responses. Journal of Anxiety Disorders, 21, 788-803.) showed that despite the acquisition of differential skin conductance conditioned responses to angry faces paired (CS+) and unpaired (CS−) with an aversive shock, development of implicit associations was not subsequently observed on the Implicit Association Test. In the present study, participants (N = 76) were assigned either to a Shock or NoShock group and completed a similar aversive Pavlovian conditioning procedure with angry face CS+ and CS− stimuli. Participants next completed a visual probe task in which the angry face CS+ and CS− stimuli were paired with angry face control stimuli and neutral faces. Results confirmed that differential fear conditioning was observed in the Shock group but not in the NoShock group, and that the Shock group subsequently showed a selective attentional bias for the angry face CS+ compared with the CS− and control stimuli during the visual probe task. The findings confirm the interplay between learning-based mechanisms and cognitive processes, such as attentional biases, in models of fear acquisition and have implications for treatment of the anxiety disorders.     

Histone acetylation rescues contextual fear conditioning in nNOS KO mice and accelerates extinction of cued fear conditioning in wild type mice

Epigenetic regulation of chromatin structure is an essential molecular mechanism that contributes to the formation of synaptic plasticity and long-term memory (LTM). An important regulatory process of chromatin structure is acetylation and deacetylation of histone proteins. Inhibition of histone deacetylase (HDAC) increases acetylation of histone proteins and facilitate learning and memory. Nitric oxide (NO) signaling pathway has a role in synaptic plasticity, LTM and regulation of histone acetylation. We have previously shown that NO signaling pathway is required for contextual fear conditioning. The present study investigated the effects of systemic administration of the HDAC inhibitor sodium butyrate (NaB) on fear conditioning in neuronal nitric oxide synthase (nNOS) knockout (KO) and wild type (WT) mice. The effect of single administration of NaB on total H3 and H4 histone acetylation in hippocampus and amygdala was also investigated. A single administration of NaB prior to fear conditioning (a) rescued contextual fear conditioning of nNOS KO mice and (b) had long-term (weeks) facilitatory effect on the extinction of cued fear memory of WT mice. The facilitatory effect of NaB on extinction of cued fear memory of WT mice was confirmed in a study whereupon NaB was administered during extinction. Results suggest that (a) the rescue of contextual fear conditioning in nNOS KO mice is associated with NaB-induced increase in H3 histone acetylation and (b) the accelerated extinction of cued fear memory in WT mice is associated with NaB-induced increase in H4 histone acetylation. Hence, a single administration of HDAC inhibitor may rescue NO-dependent cognitive deficits and afford a long-term accelerating effect on extinction of fear memory of WT mice.