Showing papers on "Classical conditioning published in 2004"
TL;DR: The authors review the literature on the 2 main models of the placebo effect: expectancy theory and classical conditioning and suggest that classical conditioning procedures are one shaping factor but that verbal information can also shape placebo effects.
Abstract: The authors review the literature on the 2 main models of the placebo effect: expectancy theory and classical conditioning. A path is suggested to dissolving the theoretical impasse that has long plagued this issue. The key is to make a clear distinction between 2 questions: What factors shape placebo effects? and What learning mediates the placebo effect? The reviewed literature suggests that classical conditioning procedures are one shaping factor but that verbal information can also shape placebo effects. The literature also suggests that conditioning procedures and other sources of information sometimes shape conscious expectancies and that these expectancies mediate some placebo effects; however, in other cases conditioning procedures appear to shape placebo effects that are not mediated by conscious cognition. The placebo effect is a topic of interest to psychologists and health practitioners in a wide variety of areas, and the question of the mechanisms underlying this effect is gaining increasing attention. In this article, we review the literature related to the two main approaches to the placebo phenomenon: expectancy theory and classical conditioning. According to expectancy theory, placebo effects are mediated by explicit (consciously accessible) expectancies. In contrast, according to the classical conditioning approach, they are conditioned responses (CRs). We begin with the problematic issue of defining placebos and placebo effects, and we then turn to the question of whether these effects actually exist. Having established that they do, we shift the focus to the main task of the article: determining the roles of expectancy and conditioning in the placebo effect. This task is divided into two parts. The first has the aim of clearing up the confusion that exists in the placebo literature concerning the relationship between conditioning and expectancy. These approaches are often pitted against one another, under the assumption that either expectancy theory or classical conditioning accounts for the placebo effect. We reject this view, arguing that the two approaches are compatible. One stumbling block is the assumption that classical conditioning is a particular form of learning, necessarily distinct from expectancy learning. However, conditioning is defined in terms of stimulus inputs and their subsequent effects. Specifically, an organism has been classically conditioned when exposure to a contingency between a conditioned stimulus (CS) and an unconditioned stimulus (US) results in a relevant change in the organism’s state or behavior. This leaves open the question of what mechanisms mediate conditioning. In some cases, conditioning procedures lead to nonconscious learning, and the effects of conditioning are not cognitively mediated. In other cases, though, conditioning effects are mediated by conscious expectancies. Thus, expectancy theory provides an explanation for some examples of classical conditioning. Furthermore, expectancies are not shaped only by conditioning procedures, but also by factors such
694 citations
TL;DR: It is shown that neural activity in the ventral striatum and the anterior insula displays a marked correspondence to the signals for sequential learning predicted by temporal difference models, revealing a flexible aversive learning process ideally suited to the changing and uncertain nature of real-world environments.
Abstract: The ability to use environmental stimuli to predict impending harm is critical for survival. Such predictions should be available as early as they are reliable. In pavlovian conditioning, chains of successively earlier predictors are studied in terms of higher-order relationships, and have inspired computational theories such as temporal difference learning. However, there is at present no adequate neurobiological account of how this learning occurs. Here, in a functional magnetic resonance imaging (fMRI) study of higher-order aversive conditioning, we describe a key computational strategy that humans use to learn predictions about pain. We show that neural activity in the ventral striatum and the anterior insula displays a marked correspondence to the signals for sequential learning predicted by temporal difference models. This result reveals a flexible aversive learning process ideally suited to the changing and uncertain nature of real-world environments. Taken with existing data on reward learning, our results suggest a critical role for the ventral striatum in integrating complex appetitive and aversive predictions to coordinate behaviour.
655 citations
TL;DR: The aim of this review is to clarify the complex actions of dopamine in fear conditioning with respect to the wide-spread distribution of dopaminergic innervation over structures constituting the fear related circuitry.
540 citations
TL;DR: It is argued that the mechanisms (conjunctive representations and pattern completion) that mediate the contribution the hippocampus makes to contextual fear conditioning are the same ones that enable the hippocampus to support declarative memory in humans.
482 citations
TL;DR: The present study showed that IL stimulation inhibits freezing if given 0.1 s after tone onset (the latency of tone-evoked responses) but has no effect if given either 1 s before or 1 s aftertone onset, suggesting that IL gates the response of downstream structures such as the amygdala to fear stimuli.
Abstract: The authors recently showed that extinction of auditory fear conditioning leads to potentiation of tone-evoked activity of neurons in the infralimbic (IL) subregion of the medial prefrontal cortex, suggesting that IL inhibits fear after extinction (M. R. Milad, & G. J. Quirk, 2002). In support of this finding, pairing conditioned tones with brief (300-ms) electrical stimulation of IL reduces conditioned freezing. The present study showed that IL stimulation inhibits freezing if given 0.1 s after tone onset (the latency of tone-evoked responses) but has no effect if given either 1 s before or 1 s after tone onset. This suggests that IL gates the response of downstream structures such as the amygdala to fear stimuli.
394 citations
TL;DR: Functional magnetic resonance imaging was used to measure human brain activity evoked during olfactory aversive conditioning and extinction learning and showed that a CS+ retains access to representations of UCS value in distinct regions of ventral prefrontal cortex, even as extinction proceeds.
Abstract: In extinction, an animal learns that a previously conditioned stimulus (CS+) no longer predicts delivery of a salient reinforcer (unconditioned stimulus, UCS). Rodent studies indicate that extinction relies on amygdala-prefrontal interactions and involves formation of memories that inhibit, without actually erasing, the original conditioning trace. Whether extinction learning in humans follows similar neurobiological principles is unknown. We used functional magnetic resonance imaging to measure human brain activity evoked during olfactory aversive conditioning and extinction learning. Neural responses in orbitofrontal cortex and amygdala were preferentially enhanced during extinction, suggesting potential cross-species preservation of learning mechanisms that oppose conditioning. Moreover, by manipulating UCS aversiveness via reinforcer inflation, we showed that a CS+ retains access to representations of UCS value in distinct regions of ventral prefrontal cortex, even as extinction proceeds.
369 citations
TL;DR: As in previous studies, participants also displayed a significant learning response to masked stimuli following Pavlovian conditioning, however, whereas the observational-learning group also showed this effect, the instructed- learning group did not.
Abstract: This study compared fear learning acquired through direct experience (Pavlovian conditioning) and fear learning acquired without direct experience via either observation or verbal instruction We examined whether these three types of learning yielded differential responses to conditioned stimuli (CS+) that were presented unmasked (available to explicit awareness) or masked (not available to explicit awareness) In the Pavlovian group, the CS+ was paired with a mild shock, whereas the observational-learning group learned through observing the emotional expression of a confederate receiving shocks paired with the CS+ The instructed-learning group was told that the CS+ predicted a shock The three groups demonstrated similar levels of learning as measured by the skin conductance response to unmasked stimuli As in previous studies, participants also displayed a significant learning response to masked stimuli following Pavlovian conditioning However, whereas the observational-learning group also showed this
355 citations
TL;DR: It is demonstrated that implicit self-esteem can be increased using a computer game that repeatedly pairs self-relevant information with smiling faces, establishing the associative and interpersonal nature of implicit selfesteem and demonstrating the potential benefit of applying basic learning principles in this domain.
Abstract: Implicit self-esteem is the automatic, nonconscious aspect of self-esteem. This study demonstrated that implicit self-esteem can be increased using a computer game that repeatedly pairs self-relevant information with smiling faces. These findings, which are consistent with principles of classical conditioning, establish the associative and interpersonal nature of implicit self-esteem and demonstrate the potential benefit of applying basic learning principles in this domain.
285 citations
TL;DR: Neurons in the VH are importantly involved in the acquisition of auditory fear conditioning and the expression of auditory and contextual fear under some conditions.
Abstract: The authors compared the effects of pharmacological inactivation of the dorsal hippocampus (DH) or ventral hippocampus (VH) on Pavlovian fear conditioning in rats. Freezing behavior served as the measure of fear. Pretraining infusions of muscimol, a GABAA receptor agonist, into the VH disrupted auditory, but not contextual, fear conditioning; DH infusions did not affect fear conditioning. Pretesting inactivation of the VH or DH did not affect the expression of conditional freezing. Pretraining electrolytic lesions of the VH reproduced the effects of muscimol infusions, whereas posttraining VH lesions disrupted both auditory and contextual freezing. Hence, neurons in the VH are importantly involved in the acquisition of auditory fear conditioning and the expression of auditory and contextual fear under some conditions. An abundance of evidence indicates that the hippocampus is importantly involved in associative learning and memory (Anagnostaras, Gale, & Fanselow, 2001; Douglas, 1967; Eichenbaum,
270 citations
01 Apr 2004-Quarterly Journal of Experimental Psychology Section B-comparative and Physiological Psychology
TL;DR: This paper reviews the behavioural and neuroscience literatures on extinction in Pavlovian conditioning and concludes that both levels of analysis can benefit the other in the pursuit of a more comprehensive understanding of extinction.
Abstract: This paper reviews the behavioural and neuroscience literatures on extinction in Pavlovian conditioning with a view towards finding possible points of contact between these two often independent li...
266 citations
TL;DR: The present data show learning-related amygdala and hippocampal activity during human Pavlovian fear conditioning and suggest that the amygdala is particularly important for forming new associations as relationships between stimuli change.
Abstract: Previous functional magnetic resonance imaging (fMRI) studies have characterized brain systems involved in conditional response acquisition during Pavlovian fear conditioning. However, the functional neuroanatomy underlying the extinction of human conditional fear remains largely undetermined. The present study used fMRI to examine brain activity during acquisition and extinction of fear conditioning. During the acquisition phase, participants were either exposed to light (CS) presentations that signaled a brief electrical stimulation (paired group) or received light presentations that did not serve as a warning signal (control group). During the extinction phase, half of the paired group subjects continued to receive the same treatment, whereas the remainder received light alone. Control subjects also received light alone during the extinction phase. Changes in metabolic activity within the amygdala and hippocampus support the involvement of these regions in each of the procedural phases of fear conditioning. Hippocampal activity developed during acquisition of the fear response. Amygdala activity increased whenever experimental contingencies were altered, suggesting that this region is involved in processing changes in environmental relationships. The present data show learning-related amygdala and hippocampal activity during human Pavlovian fear conditioning and suggest that the amygdala is particularly important for forming new associations as relationships between stimuli change.
TL;DR: Results demonstrate overlapping patterns of activation within the anterior cingulate, medial thalamus, and visual cortex during delay and trace procedures, with additional recruitment of the hippocampus, SMA, frontal operculum, middle frontal gyrus, and inferior parietal lobule during trace conditioning.
Abstract: Previous functional magnetic resonance imaging (fMRI) studies with human subjects have explored the neural substrates involved in forming associations in Pavlovian fear conditioning. Most of these studies used delay procedures, in which the conditioned stimulus (CS) and unconditioned stimulus (UCS) coterminate. Less is known about brain regions that support trace conditioning, a procedure in which an interval of time (trace interval) elapses between CS termination and UCS onset. Previous work suggests significant overlap in the neural circuitry supporting delay and trace fear conditioning, although trace conditioning requires recruitment of additional brain regions. In the present event-related fMRI study, skin conductance and continuous measures of UCS expectancy were recorded concurrently with whole-brain blood oxygenation level-dependent (BOLD) imaging during direct comparison of delay and trace discrimination learning. Significant activation was observed within the visual cortex for all CSs. Anterior cingulate and medial thalamic activity reflected associative learning common to both delay and trace procedures. Activations within the supplementary motor area (SMA), frontal operculum, middle frontal gyri, and inferior parietal lobule were specifically associated with trace interval processing. The hippocampus displayed BOLD signal increases early in training during all conditions; however, differences were observed in hippocampal response magnitude related to the accuracy of predicting UCS presentations. These results demonstrate overlapping patterns of activation within the anterior cingulate, medial thalamus, and visual cortex during delay and trace procedures, with additional recruitment of the hippocampus, SMA, frontal operculum, middle frontal gyrus, and inferior parietal lobule during trace conditioning. These data suggest that the hippocampus codes temporal information during trace conditioning, whereas brain regions supporting working memory processes maintain the CS-UCS representation during the trace interval.
TL;DR: It is demonstrated that inhibition of extracellular signal-regulated kinase (Erk) cascade in the rat medial prefrontal cortex did not interfere with memory encoding for trace fear conditioning but impaired memory retention, indicating a direct role for the prefrontal cortex in associative memory storage for temporally separated events as well as in memory storage of relevancy.
Abstract: The prefrontal cortex has been shown to participate in the association of events separated by time. However, it is not known whether the prefrontal cortex stores the memory for these relationships. Trace conditioning is a form of classical conditioning in which a time gap separates the conditioned stimulus (CS) from the unconditioned stimulus (US), the association of which has been shown to depend on prefrontal activity. Here we demonstrate that inhibition of extracellular signal-regulated kinase (Erk) cascade (a biochemical pathway involved in long-term memory storage) in the rat medial prefrontal cortex did not interfere with memory encoding for trace fear conditioning but impaired memory retention. In addition, animals displayed impaired memory for the irrelevancy of the training context. Hippocampal Erk phosphorylation was found to have a later time course than prefrontal Erk phosphorylation after trace fear conditioning, indicating a direct role for the prefrontal cortex in associative memory storage for temporally separated events as well as in memory storage of relevancy.
TL;DR: Data suggest that although conditioning to a synthetic predator odor, trimethylthiazoline, has been difficult to demonstrate, conditioning can occur by modifying by the environment and the relevance of the animal studies to human anxiety disorders is discussed.
Abstract: A neurobehavioral system approach to conditioned and unconditioned fear is presented. By employing reproducible fear behaviors in Pavlovian conditioning and unconditioned fear paradigms, it has been possible to delineate some differences in neural circuitry and cellular biology for conditioned and unconditioned fear. It is suggested that the basolateral complex of the amygdala and the central nucleus of the amygdala are part of the neural circuitry for fear conditioning but not for unconditioned fear to a predator odor. Furthermore, changes in expression of the transcription factor early growth response gene 1 in the lateral nucleus of the amygdala are shown to be important for contextual fear conditioning but not for unconditioned fear to a predator odor. In addition, data suggest that although conditioning to a synthetic predator odor, trimethylthiazoline, has been difficult to demonstrate, conditioning can occur by modifying by the environment. Finally, the relevance of the animal studies to human anxiety disorders is discussed.
TL;DR: The role of context, interference, and retrieval in a number of classical conditioning phenomena (e.g. extinction), and an overview of how long-term and short-term memory processes influence behavior as it is studied in classical conditioning are reviewed.
TL;DR: In this article, the data pertaining to the role of higher-order cognition in conditioning is reviewed, and a theoretical synthesis is proposed that provides a role for both automatic and cognitively mediated processes.
Abstract: For the past 35 years, learning theorists have been providing models that depend on mental representations, even in their most simple, deterministic, and mechanistic approaches. Hence, cognitive involvement (typically thought of as expectancy) is assumed for most instances of classical and operant conditioning, with current theoretical differences concerning the level of cognition that is involved (e.g., simple association vs. rule learning), rather than its presence. Nevertheless, many psychologists not in the mainstream of learning theory continue to think of cognitive and conditioning theories as rival families of hypotheses. In this article, the data pertaining to the role of higher-order cognition in conditioning is reviewed, and a theoretical synthesis is proposed that provides a role for both automatic and cognitively mediated processes.
TL;DR: The present study suggests that BDNF plays a critical role in fear conditioning and infusing BDNF protein into the hippocampus appeared to partially restore contextual fear learning of BDNF+/- mice.
Abstract: In this study, brain-derived neurotrophic factor (BDNF) heterozygous knock-outs were tested on fear conditioning, and their wild-type littermates were used as controls Results showed that BDNF(+/-) mice are impaired in contextual learning, whereas tone learning remains intact Because BDNF is involved in synaptic transmission and contextual learning is hippocampal dependent, we hypothesized that this deficit is attributable to abnormal BDNF-modulated synaptic plasticity in the hippocampus A "gain-of-function" experiment was performed next by infusing recombinant BDNF protein into the hippocampal formation to investigate whether this deficit can be rescued Infusion of BDNF protein into the hippocampus appeared to partially restore contextual fear learning of BDNF(+/-) mice In conclusion, the present study suggests that BDNF plays a critical role in fear conditioning Loss of one copy of the BDNF gene leads to impairment of contextual fear learning in BDNF(+/-) This deficit can be partially rescued by infusing BDNF protein into the hippocampus Other brain regions interacting with the hippocampus in the context conditioned stimulus pathway, for example, the amygdala, may also require normal BDNF expression levels to fully rescue this impairment
TL;DR: The authors' data indicate that the formation of a lasting representation of the context or shock engages protein synthesis‐dependent processes, and it is shown that disrupting either NMDA or calcium/calmodulin‐dependent kinase II (CaMKII) function impairs consolidation of context memories.
Abstract: Much attention has been paid to the associative processes that are necessary to fuse together representations of the various compo- nents of an episodic memory. In the present study, we focus on the processes involved in the formation of lasting representations of the individual components that make up a fear-conditioning episode. In one- trial contextual fear conditioning experiments, weak conditioning to con- text occurs if the shock is delivered immediately following placement of the animal in a novel conditioning apparatus, a phenomenon known as the immediate shock deficit. We show that the immediate shock deficit in mice may be alleviated by pre-exposure to either the context or shock. In using this approach to temporally dissect a contextual fear-conditioning task into its constituent representational and associative processes, we are able to examine directly the processes that are important for formation of lasting representations of the context conditioned stimulus (CS) or uncon- ditioned stimulus (US). Our data indicate that the formation of a lasting representation of the context or shock engages protein synthesis-depen- dent processes. Furthermore, genetic disruption of cAMP-responsive ele- ment binding protein (CREB), a transcription factor that regulates the synthesis of new proteins required for long-term memory, disrupts the formation of lasting context memories. We go on to show that the stress hormone epinephrine modulates the consolidation of a context memory, and reverses consolidation deficits in the CREB-deficient mice. Finally we show that disrupting either NMDA or calcium/calmodulin-dependent kinase II (CaMKII) function impairs consolidation of context memories. Together, these data suggest that this approach is particularly suited for the characterization of molecular and cellular processes underlying the formation of stimulus representations. © 2004 Wiley-Liss, Inc.
TL;DR: The results indicate that fear conditioning is partially disrupted with unilateral amygdalar lesions, but that the right amygdala has greater involvement than the left amygdala when conditioning occurs under a normal brain state.
Abstract: The relative contribution of left and right amygdalae in the acquisition and retention of fear conditioning was investigated in rats. Pretraining bilateral electrolytic lesions blocked the acquisition of conditioned fear to tone and context, whereas unilateral lesions induced partial impairments with no left-right amygdala differences. In contrast, posttraining bilateral and unilateral lesions produced significant deficits in the retention of conditioned fear to tone and context. Although no left-right difference was observed to tone, the right amygdala lesions generated greater deficits in contextual fear than the left amygdala lesions. These results indicate that fear conditioning is partially disrupted with unilateral amygdalar lesions, but that the right amygdala has greater involvement than the left amygdala when conditioning occurs under a normal brain state.
TL;DR: The level of spontaneous recovery between the first extinction session and a second, 24 h later, was increased in IL-lesioned rats relative to sham animals, and reinstatement of the CR following unsignaled delivery of the US was also increased inilsioned rats.
Abstract: The prefrontal cortex (PFC) has a well-established role in the inhibition of inappropriate responding, and evidence suggests that the infralimbic (IL) region of the rat medial PFC (MPFC) may be involved in some aspects of extinction of conditioned fear. MPFC lesions including, but not those sparing the IL cortex increase spontaneous recovery of extinguished conditioned fear when tested 24 h after an initial extinction session. The current experiment extended these findings by use of appetitive rather than aversive conditioning. Ten IL-lesioned and 11 sham-operated rats were trained on a Pavlovian task in which a conditioned stimulus (CS) was followed by food pellets (the unconditioned stimulus or US). IL lesions had no effect on extinction of the conditioned response (CR, magazine entries) during the first extinction session. However, the level of spontaneous recovery between the first extinction session and a second, 24 h later, was increased in IL-lesioned rats relative to sham animals. In contrast, evidence of savings measured between the extinction sessions did not differ between groups. Furthermore, reinstatement of the CR following unsignaled delivery of the US was also increased in IL-lesioned rats.
TL;DR: The adaptive advantage of cognition is increased response flexibility, however, it must be capable of overriding the influence of simpler automatic processes, and the higher up the phylogenetic scale, the smaller the role of nonconscious conditioning processes and the larger the roles of cognition.
Abstract: Classical conditioning is included as a component in the response expectancy model of placebo responding. Though introspectable when attention is drawn to them, expectancies need not be in awareness while guiding behavior. Most placebo effects are linked to expectancies, and classical conditioning is one factor (but not the only factor) by which these expectancies can be produced and altered. Conditioned placebo effects without expectancies exist but are relatively rare in humans. The adaptive advantage of cognition is increased response flexibility. For it to convey that benefit, however, it must be capable of overriding the influence of simpler automatic processes. Thus, the higher up the phylogenetic scale, the smaller the role of nonconscious conditioning processes and the larger the role of cognition.
TL;DR: The results show for the first time that the midbrain PAG contributes to fear extinction and specifically identify a role for vlPAG opioid receptors in the acquisition but not the expression of such extinction.
Abstract: Four experiments studied the role of opioid receptors in the midbrain periaqueductal gray matter (PAG), an important structure eliciting conditioned fear responses, in the extinction of Pavlovian fear. Rats received pairings of an auditory conditioned stimulus (CS) with a foot shock unconditioned stimulus (US). The freezing conditioned response (CR) elicited by the CS was then extinguished via nonreinforced presentations of the CS. Microinjection of the opioid receptor antagonist naloxone into the ventrolateral PAG (vlPAG) before nonrein-forced CS presentations impaired development of extinction, but such microinjections at the end of extinction did not reinstate an already extinguished freezing CR. This role for opioid receptors in fear extinction was specific to the vlPAG because infusions of naloxone into the dorsal PAG did not impair fear extinction. Finally, the impairment of fear extinction produced by vlPAG infusions of naloxone was dose-dependent. These results show for the first time that the midbrain PAG contributes to fear extinction and specifically identify a role for vlPAG opioid receptors in the acquisition but not the expression of such extinction. Taken together with our previous findings, we suggest that, during fear conditioning, activation of vlPAG opioid receptors contributes to detection of the discrepancy between the actual and expected outcome of the conditioning trial. vlPAG opioid receptors regulate the learning that accrues to the CS and other stimuli present on a trial because they instantiate an associative error correction process influencing US information reaching the site of CS-US convergence in the amygdala. During nonreinforcement, this vlPAG opioid receptor contribution signals extinction.
TL;DR: This work shows that Pavlovian conditioning produced a net recruitment of responsive neural units across the AL that persisted after conditioning and provides evidence that the basis of the learning-dependent changes in the AL is not simply an increase in activity in the neural network representing an odorant.
Abstract: Recent evidence suggests that odor-driven responses in the insect antennal lobe (AL) can be modified by associative and nonassociative processes, as has been shown in the vertebrate olfactory bulb. However, the specific network changes that occur in response to olfactory learning remain unknown. To characterize changes in AL network activity during learning, we developed an in vivo protocol in Manduca sexta that allows continuous monitoring of neural ensembles and feeding behavior over the course of olfactory conditioning. Here, we show that Pavlovian conditioning produced a net recruitment of responsive neural units across the AL that persisted after conditioning. Recruitment only occurred when odor reliably predicted food. Conversely, when odor did not predict food, a net loss of responsive units occurred. Simultaneous measures of feeding responses indicated that the treatment-specific patterns of neural recruitment were positively correlated with changes in the insect's behavioral response to odor. In addition to recruitment, conditioning also produced consistent and profound shifts in the temporal responses of 16% of recorded units. These results show that odor representations in the AL are dynamic and related to olfactory memory consolidation. We furthermore provide evidence that the basis of the learning-dependent changes in the AL is not simply an increase in activity in the neural network representing an odorant. Rather, learning produces a restructuring of spatial and temporal components of network responses to odor in the AL.
TL;DR: Clear evidence is established for reinstatement of conditioned responses in humans by using a differential Pavlovian conditioning procedure and for the role of negative stimulus valence in the return of conditioned responding after extinction.
Abstract: The present study investigated reinstatement of conditioned responses in humans by using a differential Pavlovian conditioning procedure. Evidence for reinstatement was established in a direct (fear rating) and in an indirect measure (secondary reaction time task) of conditioning. Moreover, the amount of reinstatement in the secondary reaction time task was significantly correlated with the difference in valence between the conditioned stimulus (CS)+ and the CS- after extinction. These data provide clear evidence for reinstatement and for the role of negative stimulus valence in the return of conditioned responding after extinction.
TL;DR: A role for 5- HT(1A) and 5-HT(7) receptors in memory formation is confirmed and the hypothesis that serotonergic, cholinergic, and glutamatergic systems interact in cognitively impaired animals is supported.
TL;DR: The results provide behavioural evidence that REM/non‐REM sleep deprivation has neuroanatomically selective actions, differentially interfering with the neural systems underlying contextual learning and cued learning, and support the involvement of the hippocampus in both foreground and background contextual conditioning.
Abstract: Prolonged sleep deprivation results in cognitive deficits. In rats, for example, sleep deprivation impairs spatial learning and hippocampal long-term potentiation. We tested the effects of sleep deprivation on learning in a Pavlovian fear conditioning paradigm, choosing a sleep deprivation paradigm in which REM sleep was completely prevented and non-REM sleep was strongly decreased. During conditioning, rats were given footshocks, either alone or paired with a tone, and tested 24 h later for freezing responses to the conditioning context, and to the tone in a novel environment. Whereas control animals had robust contextual learning in both background and foreground contextual conditioning paradigms, 72 h of sleep deprivation before conditioning dramatically impaired both types of contextual learning (by more than 50%) without affecting cued learning. Increasing the number of footshocks did not overcome the sleep deprivation-induced deficit. The results provide behavioural evidence that REM/non-REM sleep deprivation has neuroanatomically selective actions, differentially interfering with the neural systems underlying contextual learning (i.e. the hippocampus) and cued learning (i.e. the amygdala), and support the involvement of the hippocampus in both foreground and background contextual conditioning.
TL;DR: Startle was potentiated by the CS+ in both rooms, which suggests generalization of fear across contexts and supports the future use of virtual reality to design new conditioning experiments to study both fear and anxiety.
TL;DR: This is the first study to compare the effects of a subliminal and conscious CS and to find classical conditioning of sexual arousal in women, and women showed the opposite effect, conditioned arousal to the sexually irrelevant rather than to the relevant CS.
Abstract: Classical conditioning of sexual arousal has previously been demonstrated in human males but not in females. This study explored the role of classical (Pavlovian) conditioning in the activation of genital sexual arousal in both women and men, and assessed the effects of varying conditioned stimulus (CS) duration (subliminal/conscious) and relevance (sexually relevant/irrelevant). Twenty-seven female and 29 male participants received either subliminal or conscious presentations of a photograph of either a sexually relevant (abdomen of the opposite sex) or irrelevant (gun) CS+, which was followed by the unconditioned stimulus (US-erotic film clip). A CS-, a stimulus not paired with the US, was also included in the 11 conditioning trials. Ten participants were assigned to a control group that received unpaired presentations of the CS+, CS-, and the US. Both women and men showed more evidence of conditioning to the abdomen than to the gun when the CS was presented subliminally. When consciously perceived CSs were used, however, gender differences emerged. Men again showed the expected cue-to-consequence specificity but women showed the opposite effect, that is, conditioned arousal to the sexually irrelevant rather than to the relevant CS. The latter finding may be due to increased autonomic nervous system arousal associated with the irrelevant CS (gun). Skin conductance responses indicated more general arousal to the gun than to the male abdomen in women. This is the first study to compare the effects of a subliminal and conscious CS and to find classical conditioning of sexual arousal in women.
TL;DR: Chronic exposure to corticosteroids alters BLA functioning in a non-linear fashion and that contextual conditioning is influenced more than tone conditioning by chronic corticosterone and BLA glucocorticoid receptor stimulation is suggested.
TL;DR: The idea that the hippocampus is needed to form simple inhibitory associations between events that are concurrently embedded in simple excitatory associations is considered.