Showing papers on "Classical conditioning published in 2010"
TL;DR: Among a range of other findings, EC effects were stronger for high than for low contingency awareness, for supraliminal than for subliminal US presentation, for postacquisition than for postextinction effects, and for self-report than for implicit measures.
Abstract: This article presents a meta-analysis of research on evaluative conditioning (EC), defined as a change in the liking of a stimulus (conditioned stimulus; CS) that results from pairing that stimulus with other positive or negative stimuli (unconditioned stimulus; US). Across a total of 214 studies included in the main sample, the mean EC effect was d = .52, with a 95% confidence interval of .466-.582. As estimated from a random-effects model, about 70% of the variance in effect sizes were attributable to true systematic variation rather than sampling error. Moderator analyses were conducted to partially explain this variation, both as a function of concrete aspects of the procedural implementation and as a function of the abstract aspects of the relation between CS and US. Among a range of other findings, EC effects were stronger for high than for low contingency awareness, for supraliminal than for subliminal US presentation, for postacquisition than for postextinction effects, and for self-report than for implicit measures. These findings are discussed with regard to the procedural boundary conditions of EC and theoretical accounts about the mental processes underlying EC.
746 citations
TL;DR: Data suggest that mid regions of the dmPFC/dACC are part of a "core" fear network that is activated irrespective of how fear was learnt, and allow for maintaining the theory that the rostral dMPFC is involved in conscious threat appraisal.
378 citations
TL;DR: Human cerebellar lesion studies provide evidence that the cerebellum is involved in motor, emotional and cognitive associative learning and the posterolateral hemispheres appear to be of additional importance in fear conditioning in humans.
298 citations
TL;DR: Investigation of neural pathways that relay information about the UCS to the amygdala by recording neurons in the amygdala and periaqueductal gray of rats during fear conditioning found UCS-evoked responses in both amygdala and PAG were inhibited by expectation.
Abstract: A form of aversively motivated learning called fear conditioning occurs when a neutral conditioned stimulus is paired with an aversive unconditioned stimulus (UCS). UCS-evoked depolarization of amygdala neurons may instruct Hebbian plasticity that stores memories of the conditioned stimulus-unconditioned stimulus association, but the origin of UCS inputs to the amygdala is unknown. Theory and evidence suggest that instructive UCS inputs to the amygdala will be inhibited when the UCS is expected, but this has not been found during fear conditioning. We investigated neural pathways that relay information about the UCS to the amygdala by recording neurons in the amygdala and periaqueductal gray (PAG) of rats during fear conditioning. UCS-evoked responses in both amygdala and PAG were inhibited by expectation. Pharmacological inactivation of the PAG attenuated UCS-evoked responses in the amygdala and impaired acquisition of fear conditioning, indicating that PAG may be an important part of the pathway that relays instructive signals to the amygdala.
271 citations
TL;DR: Emerging data obtained by functional imaging procedures indicate that distinct memory traces form in different brain regions and correlate with different phases of memory, and indicate that cross talk between mushroom bodies and several other brain regions is critical for memory formation.
Abstract: Studies of olfactory learning in Drosophila have provided key insights into the brain mechanisms underlying learning and memory. One type of olfactory learning, olfactory classical conditioning, consists of learning the contingency between an odor with an aversive or appetitive stimulus. This conditioning requires the activity of molecules that can integrate the two types of sensory information, the odorant as the conditioned stimulus and the aversive or appetitive stimulus as the unconditioned stimulus, in brain regions where the neural pathways for the two stimuli intersect. Compelling data indicate that a particular form of adenylyl cyclase functions as a molecular integrator of the sensory information in the mushroom body neurons. The neuronal pathway carrying the olfactory information from the antennal lobes to the mushroom body is well described. Accumulating data now show that some dopaminergic neurons provide information about aversive stimuli and octopaminergic neurons about appetitive stimuli to the mushroom body neurons. Inhibitory inputs from the GABAergic system appear to gate olfactory information to the mushroom bodies and thus control the ability to learn about odors. Emerging data obtained by functional imaging procedures indicate that distinct memory traces form in different brain regions and correlate with different phases of memory. The results from these and other experiments also indicate that cross talk between mushroom bodies and several other brain regions is critical for memory formation.
179 citations
TL;DR: Results indicate that adult hippocampal neurogenesis is required for CFC in mice only when brief training is provided, and it is shown that the irradiation-induced deficit in single-trial CFC can be rescued by providing preexposure to the conditioning context.
Abstract: The role of adult hippocampal neurogenesis in contextual fear conditioning (CFC) is debated. Several studies demonstrated that blocking adult hippocampal neurogenesis in rodents impairs CFC, while several other studies failed to observe an impairment. We sought to determine whether different CFC methods vary in their sensitivity to the arrest of adult neurogenesis. Adult neurogenesis was arrested in mice using low-dose, targeted x-irradiation, and the effects of irradiation were assayed in conditioning procedures that varied in the use of a discrete conditioned stimulus, the number of trials administered, and the final level of conditioning produced. We demonstrate that irradiation impairs CFC in mice when a single-trial CFC procedure is used but not when multiple-trial procedures are used, regardless of the final level of contextual fear produced. In addition, we show that the irradiation-induced deficit in single-trial CFC can be rescued by providing preexposure to the conditioning context. These results indicate that adult hippocampal neurogenesis is required for CFC in mice only when brief training is provided.
162 citations
TL;DR: It is suggested that these contrasting results could depend on the contrasting influences of either: (1) occasion-setting contextual associations vs. direct context-CS associations formed as a consequence of the retrieval trial or (2) discrimination vs. generalization between the circumstances of conditioning and extinction.
Abstract: In six experiments we studied the effects of a single re-exposure to a conditioned stimulus (CS; "retrieval trial") prior to extinction training (extinction-reconsolidation boundary) on the development of and recovery from fear extinction. A single retrieval trial prior to extinction training significantly augmented the renewal and reinstatement of extinguished responding. Augmentation of recovery was not observed if the retrieval and extinction training occurred in different contexts. These results contrast with those reported in earlier papers by Monfils and coworkers in rats and by Schiller and coworkers in humans. We suggest that these contrasting results could depend on the contrasting influences of either: (1) occasion-setting contextual associations vs. direct context-CS associations formed as a consequence of the retrieval trial or (2) discrimination vs. generalization between the circumstances of conditioning and extinction.
150 citations
TL;DR: An alternative view based on the hypothesis that learning about the temporal relationships between events determines the speed of emergence, vigor and form of conditioned behavior is suggested, which depends on perceiving and encoding temporal regularities rather than stimulus contiguities.
Abstract: In a basic associative learning paradigm, learning is said to have occurred when the conditioned stimulus evokes an anticipatory response. This learning is widely believed to depend on the contiguous presentation of conditioned and unconditioned stimulus. However, what it means to be contiguous has not been rigorously defined. Here we examine the empirical bases for these beliefs and suggest an alternative view based on the hypothesis that learning about the temporal relationships between events determines the speed of emergence, vigor and form of conditioned behavior. This temporal learning occurs very rapidly and prior to the appearance of the anticipatory response. The temporal relations are learned even when no anticipatory response is evoked. The speed with which an anticipatory response emerges is proportional to the informativeness of the predictive cue (CS) regarding the rate of occurrence of the predicted event (US). This analysis gives an account of what we mean by "temporal pairing" and is in accord with the data on speed of acquisition and basic findings in the cue competition literature. In this account, learning depends on perceiving and encoding temporal regularities rather than stimulus contiguities.
139 citations
22 Oct 2010-Quarterly Journal of Experimental Psychology Section B-comparative and Physiological Psychology
TL;DR: Rats received Pavlovian pairings of conditioned stimuli with discriminably different unconditioned stimuli and the resulting CS-US associations were subjected to extinction and to interference by pairing the CSs with other USs.
Abstract: Rats received Pavlovian pairings of conditioned stimuli (CSs) with discriminably different unconditioned stimuli (USs). The resulting CS-US associations, indexed by magazine entry, were subjected t...
133 citations
TL;DR: The results demonstrate that processes of aging impact brain structures and associated behaviors differentially, with cerebellum showing earlier senescence than hippocampus.
Abstract: Cognitive functions show many alternative outcomes and great individual variation during normal aging. We examined learning over the adult life span in CBA mice, along with morphological and electrophysiological substrates. Our aim was to compare cerebellum-dependent delay eyeblink classical conditioning and hippocampus-dependent contextual fear conditioning in the same animals using the same conditioned and unconditioned stimuli for eyeblink and fear conditioning. In a subset of the behaviorally tested mice, we used unbiased stereology to estimate the total number of Purkinje neurons in cerebellar cortex and pyramidal neurons in the hippocampus. Several forms of synaptic plasticity were assessed at different ages in CBA mice: long-term depression (LTD) in both cerebellum and hippocampus and NMDA-mediated long-term potentiation (LTP) and voltage-dependent calcium channel LTP in hippocampus. Forty-four CBA mice tested at one of five ages (4, 8, 12, 18, or 24 months) demonstrated statistically significant age differences in cerebellum-dependent delay eyeblink conditioning, with 24-month mice showing impairment in comparison with younger mice. These same CBA mice showed no significant differences in contextual or cued fear conditioning. Stereology indicated significant loss of Purkinje neurons in the 18- and 24-month groups, whereas pyramidal neuron numbers were stable across age. Slice electrophysiology recorded from an additional 48 CBA mice indicated significant deficits in LTD appearing in cerebellum between 4 and 8 months, whereas 4- to 12-month mice demonstrated similar hippocampal LTD and LTP values. Our results demonstrate that processes of aging impact brain structures and associated behaviors differentially, with cerebellum showing earlier senescence than hippocampus.
114 citations
TL;DR: This work provides a more extensive review of the biological mechanisms supporting phasic DA firing and their relation to the spate of Pavlovian conditioning phenomena and their sensitivity to focal brain lesions, and extends the PVLV model by incorporating a new NV (novelty value) component reflecting the ability of novel stimuli to trigger phasIC DA firing.
TL;DR: It is shown that rats exposed to a novel tone in the presence of a cage-mate previously conditioned to that same tone selectively showed increased freezing to the stimulus the next day (fear conditioning by-proxy), which suggests that, during memory retrieval, fear of a stimulus can be socially transmitted to a Cage-mate.
TL;DR: Inappropriate activation of the midbrain in response to neutral stimuli during conditioning is associated with the severity of delusional symptoms in patients with schizophrenia.
Abstract: Context: Recent theories have suggested that the inappropriate activation of limbic motivational systems in response to neutral stimuli may underlie the development of delusions in schizophrenia.
Objective: To investigate the activation of the amygdala, midbrain, and ventral striatum during an aversive pavlovian conditioning task in patients with schizophrenia and healthy control participants using functional magnetic resonance imaging.
Design: Cross-sectional case-control functional neuroimaging study.
Setting: Academic medical center.
Participants: Twenty patients with DSM-IV–diagnosed schizophrenia or schizoaffective disorder and 20 healthy control participants.
Main Outcome Measures: Regional brain activation as assessed by functional magnetic resonance imaging blood oxygen level–dependent responses, and delusional symptom severity on the Positive and Negative Syndrome Scale.
Results: Patients with schizophrenia showed abnormal activation of the amygdala, midbrain, and ventral striatum during conditioning. Activation of the midbrain in response to neutral rather than aversive cues during conditioning was correlated with the severity of delusional symptoms in the patient group (corrected P = .04).
Conclusion: Inappropriate activation of the midbrain in response to neutral stimuli during conditioning is associated with the severity of delusional symptoms in patients with schizophrenia.
TL;DR: A role for the human amygdala in social learning is document and coarse regional dissociations in amygdala activity that are consistent with previous human and nonhuman animal data are revealed.
Abstract: The amygdala is consistently implicated in biologically relevant learning tasks such as Pavlovian conditioning. In humans, the ability to identify individual faces based on the social outcomes they have predicted in the past constitutes a critical form of associative learning that can be likened to “social conditioning.” To capture such learning in a laboratory setting, participants learned about faces that predicted negative, positive, or neutral social outcomes. Participants reported liking or disliking the faces in accordance with their learned social value. During acquisition, we observed differential functional magnetic resonance imaging activation across the human amygdaloid complex consistent with previous lesion, electrophysiological, and functional neuroimaging data. A region of the medial ventral amygdala and a region of the dorsal amygdala/substantia innominata showed signal increases to both Negative and Positive faces, whereas a lateral ventral region displayed a linear representation of the valence of faces such that Negative > Positive > Neutral. This lateral ventral locus also differed from the dorsal and medial loci in that the magnitude of these responses was more resistant to habituation. These findings document a role for the human amygdala in social learning and reveal coarse regional dissociations in amygdala activity that are consistent with previous human and nonhuman animal data.
TL;DR: It is concluded that NMDARs in dopamine neurons enhance but are not critical for phasic dopamine release to behaviorally relevant stimuli; furthermore, their contribution to phAsic dopamine signaling is not necessary for the development of cue-evoked dopamine or anticipatory activity in a D1R-dependent Pavlovian conditioning paradigm.
Abstract: During Pavlovian conditioning, phasic dopamine (DA) responses emerge to reward-predictive stimuli as the subject learns to anticipate reward delivery. This observation has led to the hypothesis that phasic dopamine signaling is important for learning. To assess the ability of mice to develop anticipatory behavior and to characterize the contribution of dopamine, we used a food-reinforced Pavlovian conditioning paradigm. As mice learned the cue–reward association, they increased their head entries to the food receptacle in a pattern that was consistent with conditioned anticipatory behavior. D1-receptor knockout (D1R-KO) mice had impaired acquisition, and systemic administration of a D1R antagonist blocked both the acquisition and expression of conditioned approach in wild-type mice. To assess the specific contribution of phasic dopamine transmission, we tested mice lacking NMDA-type glutamate receptors (NMDARs) exclusively in dopamine neurons (NR1-KO mice). Surprisingly, NR1-KO mice learned at the same rate as their littermate controls. To evaluate the contribution of NMDARs to phasic dopamine release in this paradigm, we performed fast-scan cyclic voltammetry in the nucleus accumbens of awake mice. Despite having significantly attenuated phasic dopamine release following reward delivery, KO mice developed cue-evoked dopamine release at the same rate as controls. We conclude that NMDARs in dopamine neurons enhance but are not critical for phasic dopamine release to behaviorally relevant stimuli; furthermore, their contribution to phasic dopamine signaling is not necessary for the development of cue-evoked dopamine or anticipatory activity in a D1R-dependent Pavlovian conditioning paradigm.
TL;DR: Results indicate that the relationship between poor fear conditioning and aggression occurs early in childhood, and enhanced electrodermal fear conditioning may protect children against future aggressive/violent behavior.
Abstract: Although deficits in fear conditioning have been found in adult psychopaths and criminals (Hare, 1978), little is known about how the development of conditioning is related to aggressive and disruptive behavior in childhood. To date only two prospective studies have been conducted, showing that poor classical conditioning at age 15 years is associated with both later delinquency at age 25 (Loeb & Mednick, 1977) and also crime by age 29 (Raine, Venables, & Williams, 1996). The poor fear conditioning – aggressive/antisocial relationship may reflect a stable, trait-like risk factor for later aggressive and antisocial behavior. Alternatively, it may reflect a neurodevelopmental abnormality whereby children who later become aggressive/antisocial show poor early fear conditioning, and also fail to manifest the age-related increase in conditioning found in normal children (Gao, Raine, Venables, Dawson, & Mednick, in press a). To date, there have been no developmental tests of these competing predictions. In the current study, these two hypotheses were tested using a longitudinal design.
It is unclear whether poor fear conditioning is specific to aggression or can also be observed for non-aggressive antisocial behavior. Studies have reported large body size, stimulation-seeking, fearlessness (Raine, Reynolds, Venables, Mednick, & Farrington, 1998), autonomic hyporeactivity (Babcock, Green, Webb, & Yerington, 2005; Raine, Venables, & Mednick, 1997), maternal smoking during pregnancy (Rasannen et al., 1999), and birth complications combined with early maternal rejection (Raine, Brennan, & Mednick, 1994) as risk factors for aggressive and violent, but not non-violent, antisocial behavior. Given that reduced fear conditioning is associated with antisocial behavior in adults and that childhood aggression has been found to be one of the best predictors for later aggressive, antisocial, and criminal behavior (Farrington, 1991; Huesmann, Eron, Lefkowitz, & Walder, 1984; Moffitt, 1990), it was hypothesized that reduced conditioning would be a specific correlate of childhood aggression. In contrast, relatively few studies have differentiated types of aggression/violence in their designs (Scarpa & Raine, 1997) or examined the physiological underpinnings of non-aggressive antisocial behavior. In the current study the association between fear conditioning and both non-aggressive and aggressive forms of antisocial behavior are explored.
Another unanswered question concerns whether the same psychophysiology – aggressive/antisocial behavior association is present in both males and females. Moffitt and colleagues (Moffitt & Caspi, 2001; Moffitt, Caspi, Rutter, & Silva, 2001) argue that the causes of life-course persistent antisocial behavior in females and males are essentially the same. However, other studies have argued for a significant sex difference (Silverthorn, Frick, & Reynolds, 2001) and several genetic studies have suggested a sex difference in gene -environment interactions predicting antisocial behavior (Langbehn, Cadoret, Yates, Troughton, & Stewarts, 1998). In the current study sex differences in the association between deficits in fear conditioning and aggressive/antisocial behavior were examined to test between these different perspectives.
Although the poor fear conditioning hypothesis of aggressive and antisocial behavior makes the prediction that those with poor fear conditioning should be aggressive/antisocial, very few if any studies have identified groups high or low in fear conditioning. Instead, almost all studies take a clinical grouping approach in which, for example, psychopaths are compared to non-psychopaths (Flor, Birbaumer, Hermann, Ziegler, & Patrick, 2002). Although this is understandably necessitated by the clinical design of most studies, an optimal design would be a community sample tested on conditioning, and grouped according to both their conditioning status and also their aggression status. Both analytic strategies were adopted here to assess the robustness of the autonomic fear conditioning – aggression association.
Given the significant comorbidity between aggressive behavior and attention-deficit/hyperactivity disorder (ADHD, American Psychiatric Association, 2002), it is of value to know whether hyperactivity-inattention is also associated with poor fear conditioning. Few studies have examined this association in children (Pliszka, Hatch, Borcherding, & Rogeness, 1993). Pliszka et al. compared 6–12-year-old children with ADHD and normal controls and reported no group differences in their electrodermal conditioned responses. It was therefore hypothesized that fear conditioning from ages 3 to 8 years would be unrelated to hyperactivity-inattention.
We previously found that electrodermal fear conditioning increases from ages 3 to 8 years (Gao et al., in press a). In the current study, latent class analyses were conducted on this sample to identify homogeneous groups based on conditioned responses across ages in relation to aggression. We hypothesized that: (1) compared to good conditioners, poor conditioners across ages 3 to 8 years would score higher on aggressive behavior at age 8; (2) the high aggression group would show poor electrodermal fear conditioning from ages 3 to 8 years; (3) no group differences would be observed for hyperactivity-inattention; and (4) no gender difference would be found in any observed fear conditioning - aggression associations. Finally, the association between fear conditioning and non-aggressive antisocial behavior is explored in the current study.
TL;DR: Data show that memory reconsolidation for a cocaine-paired stimulus is retrieval dependent and time limited and critically depends upon amygdalar PKA.
Abstract: Drug addiction is a chronic disorder associated with recurrent craving and relapse often precipitated by the presence of drug-associated stimuli. Pharmacological and behavioral treatments that disrupt drug-associated stimulus memories could be beneficial in the treatment of addictive disorders. Memory restabilization (or reconsolidation) following retrieval of drug-paired stimuli depends upon the amygdala. Here we assessed whether amygdalar PKA is required for the reconsolidation of an appetitive, cocaine-paired stimulus. Rats were trained to lever press for intravenous cocaine infusions paired with a light/tone conditioned stimulus. After 12 d of acquisition, rats either underwent lever extinction (8–12 d) followed by light/tone reactivation and subsequent cue-induced and cocaine-induced (15 mg/kg, i.p.) reinstatement testing or were subsequently tested to assess the ability of the light/tone stimulus to serve as a conditioned reinforcer in the acquisition of a new instrumental response (nose poking). Bilateral intra-amygdalar infusions of the PKA inhibitor Rp-cAMPS (18 μg per side) given immediately following light/tone stimulus reactivation decreased subsequent cue-induced reinstatement and responding with a conditioned reinforcer, while having no effect on cocaine-induced reinstatement. Intra-amygdalar infusions of Rp-cAMPS made 3 h following reactivation or immediately following no stimulus reactivation had no effect on subsequent cue-induced reinstatement. These data show that memory reconsolidation for a cocaine-paired stimulus is retrieval dependent and time limited and critically depends upon amygdalar PKA.
TL;DR: It is demonstrated that restoration of DA synthesis to both the basolateral amygdala (BLA) and nucleus accumbens (NAc) is required for long-term memory of FPS, providing crucial insight into the dopamine-dependent circuitry involved in the formation of fear-related memory.
Abstract: The neurotransmitter dopamine (DA) is essential for learning in a Pavlovian fear conditioning paradigm known as fear-potentiated startle (FPS). Mice lacking the ability to synthesize DA fail to learn the association between the conditioned stimulus and the fear-inducing footshock. Previously, we demonstrated that restoration of DA synthesis to neurons of the ventral tegmental area (VTA) was sufficient to restore FPS. Here, we used a target-selective viral restoration approach to determine which mesocorticolimbic brain regions receiving DA signaling from the VTA require DA for FPS. We demonstrate that restoration of DA synthesis to both the basolateral amygdala (BLA) and nucleus accumbens (NAc) is required for long-term memory of FPS. These data provide crucial insight into the dopamine-dependent circuitry involved in the formation of fear-related memory.
TL;DR: Observations support a dual process interpretation of classical conditioning whereby conditioning on an implicit level can occur without explicit knowledge about the contingencies.
Abstract: The role of contingency awareness in classical conditioning experiments using human subjects is currently under debate. This study took a novel approach to manipulating contingency awareness in a differential Pavlovian conditioning paradigm. Complex sine wave gratings were used as visual conditional stimuli (CS). By manipulating the fundamental spatial frequency of the displays, we were able to construct pairs of stimuli that varied in discriminability. One group of subjects was given an "easy" discrimination, and another was exposed to a "difficult" CS+ and CS-. A 3rd group was exposed to a stimulus that was paired with the unconditional stimulus (UCS) 50% of the time and served as a control. Skin conductance response (SCR) and continuous UCS expectancy data were measured concurrently throughout the experiment. Differential UCS expectancy was found only in the easy discrimination group. Differential SCRs were found in the easy discrimination group as well as in the difficult discrimination group, but not in the 50% contingency control. The difficult discrimination group did not exhibit differential UCS expectancy but did show clear differential SCR. These observations support a dual process interpretation of classical conditioning whereby conditioning on an implicit level can occur without explicit knowledge about the contingencies. The role of contingency awareness in classical conditioning experiments using human subjects is currently under debate. This study took a novel approach to manipulating contingency awareness in a differential Pavlovian conditioning paradigm. Complex sine wave gratings were used as visual conditional stimuli (CS). By manipulating the fundamental spatial frequency of the displays, we were able to construct pairs of stimuli that varied in discriminability. One group of subjects was given an "easy" discrimination, and another was exposed to a "difficult" CS+ and CS-. A 3rd group was exposed to a stimulus that was paired with the unconditional stimulus (UCS) 50% of the time and served as a control. Skin conductance response (SCR) and continuous UCS expectancy data were measured concurrently throughout the experiment. Differential UCS expectancy was found only in the easy discrimination group. Differential SCRs were found in the easy discrimination group as well as in the difficult discrimination group, but not in the 50% contingency control. The difficult discrimination group did not exhibit differential UCS expectancy but did show clear differential SCR. These observations support a dual process interpretation of classical conditioning whereby conditioning on an implicit level can occur without explicit knowledge about the contingencies.
TL;DR: Testing rats with 6-hydroxydopamine induced dopamine depletion of the NAc core for their sensitivity to outcome devaluation in a Pavlovian and an instrumental task indicates that 6-OHDA-lesioned animals were sensitive to outcome depreciation, providing support to the notion that NAccore dopamine may not be crucial in encoding action-outcome associations.
TL;DR: Supporting a propositional account of EC, evidence is found for intentional reliance on the contingency for the evaluation of stimuli and for contingency memory, which was based both on the actual contingency and on preexisting attitudes.
Abstract: Evaluative conditioning (EC) is a change in the valence of a stimulus that results from pairing the stimulus with an affective stimulus. Two high-powered studies (total N = 1,161) investigated the nature of the relationship between EC and contingency awareness measured as contingency memory. Stronger EC occurred among people with more accurate and more confident memory of the pairings. Awareness was a necessary condition for EC, but EC was not necessary for awareness. Supporting a propositional account of EC, we found evidence for intentional reliance on the contingency for the evaluation of stimuli. We also found evidence that contingency memory was based both on the actual contingency and on preexisting attitudes.
TL;DR: It is suggested that nicotine acts on different substrates to enhance trace versus contextual fear conditioning, and that nicotine-induced desensitization of nAChRs in the mPFC may contribute to the effects of nicotine on trace fear conditioning.
TL;DR: The findings suggest that the lemniscal pathway is important for discriminative learning, whereas the nonlemniscal isImportant for negatively regulating fear responses.
Abstract: The auditory system has two parallel streams in the brain that have been implicated in auditory fear learning. The lemniscal stream has selective neurons that are tonotopically organized and is thought to be important for sound discrimination. The nonlemniscal stream has less selective neurons, which are not tonotopically organized, and is thought to be important for multimodal processing and for several forms of learning. Therefore, it has been hypothesized that the lemniscal, but not the nonlemniscal, pathway supports discriminative fear to auditory cues. To test this hypothesis we assessed the effect of electrolytic lesions to the ventral, or medial, division of the medial geniculate nucleus (MGv or MGm, which correspond, respectively, to the lemniscal and the nonlemniscal auditory pathway to amygdala) on the acquisition, expression and extinction of fear responses in discriminative auditory fear conditioning, where one tone is followed by shock (conditioned stimulus, CS+), and another is not (CS−). Here we show that with single-trial conditioning control, MGv- and MGm-lesioned male rats acquire nondiscriminative fear of both the CS+ and the CS−. However, after multiple-trial conditioning, control rats discriminate between the CS+ and CS−, whereas MGv- and MGm-lesioned do not. Furthermore, post-training lesions of MGm, but not MGv, lead to impaired expression of discriminative fear. Finally, MGm-lesioned rats display high levels of freezing to both the CS+ and CS− even after an extinction session to the CS+. In summary, our findings suggest that the lemniscal pathway is important for discriminative learning, whereas the nonlemniscal is important for negatively regulating fear responses.
TL;DR: MaLER conditioning allows full control of the stimulation sequence, inter-stimulus and inter-trial intervals and satiety, which is crucial for any further study on associative learning in ants.
TL;DR: Findings support the view that mirror system development depends on associative learning and indicate that this learning is not purely Hebbian and could be used to explain, predict, and intervene in Mirror system development.
Abstract: The associative sequence learning model proposes that the development of the mirror system depends on the same mechanisms of associative learning that mediate Pavlovian and instrumental conditioning To test this model, two experiments used the reduction of automatic imitation through incompatible sensorimotor training to assess whether mirror system plasticity is sensitive to contingency (ie, the extent to which activation of one representation predicts activation of another) In Experiment 1, residual automatic imitation was measured following incompatible training in which the action stimulus was a perfect predictor of the response (contingent) or not at all predictive of the response (noncontingent) A contingency effect was observed: There was less automatic imitation indicative of more learning in the contingent group Experiment 2 replicated this contingency effect and showed that, as predicted by associative learning theory, it can be abolished by signaling trials in which the response occurs in the absence of an action stimulus These findings support the view that mirror system development depends on associative learning and indicate that this learning is not purely Hebbian If this is correct, associative learning theory could be used to explain, predict, and intervene in mirror system development
TL;DR: Adult mice placed in different enriched environments presented similar increases in the strength of field EPSPs evoked at the hippocampal CA3-CA1 synapse across classical conditioning sessions, with no significant differences between groups.
Abstract: We have studied the motor abilities and associative learning capabilities of adult mice placed in different enriched environments. Three-month-old animals were maintained for a month alone (AL), alone in a physically enriched environment (PHY), and, finally, in groups in the absence (SO) or presence (SOPHY) of an enriched environment. The animals' capabilities were subsequently checked in the rotarod test, and for classical and instrumental learning. The PHY and SOPHY groups presented better performances in the rotarod test and in the acquisition of the instrumental learning task. In contrast, no significant differences between groups were observed for classical eyeblink conditioning. The four groups presented similar increases in the strength of field EPSPs (fEPSPs) evoked at the hippocampal CA3-CA1 synapse across classical conditioning sessions, with no significant differences between groups. These trained animals were pulse-injected with bromodeoxyuridine (BrdU) to determine hippocampal neurogenesis. No significant differences were found in the number of NeuN/BrdU double-labeled neurons. We repeated the same BrdU study in one-month-old mice raised for an additional month in the above-mentioned four different environments. These animals were not submitted to rotarod or conditioned tests. Non-trained PHY and SOPHY groups presented more neurogenesis than the other two groups. Thus, neurogenesis seems to be related to physical enrichment at early ages, but not to learning acquisition in adult mice.
TL;DR: D-cycloserine facilitates extinction of morphine withdrawal-associated place aversion and this effect is qualitatively similar to the effect of DCS on extinction of conditioned fear, raising the possibility of common neural mechanisms.
TL;DR: Four appetitive Pavlovian conditioning experiments with rats examined the rate at which the discrimination between compounds AY and AX was solved relative to the discriminationbetween compounds Ay and BY, showing that the AY/BY discrimination was solved more readily than the Ay/AX discrimination.
Abstract: Four appetitive Pavlovian conditioning experiments with rats examined the rate at which the discrimination between compounds AY and AX was solved relative to the discrimination between compounds AY and BY. In Experiments 1 and 2, these discriminations were preceded by training in which A and B were continuously reinforced and X and Y were partially reinforced. Consistent with the Pearce and Hall (1980) model, the results showed that the AY/AX discrimination was solved more readily than the AY/BY discrimination. In Experiments 3 and 4, the discriminations were preceded by feature-positive training in which trials with AX and BY signaled food but trials with X and Y did not. Consistent with the Mackintosh (1975) model, the results showed that the AY/BY discrimination was solved more readily than the AY/AX discrimination. These results are discussed with respect to a hybrid model of conditioning and attention.
TL;DR: A role for dorsomedial PFC (dmPFC), and a thalamic → dmPFC pathway, is suggested in signaling whether or not aversive events are expected or unexpected and so whether they are to be learned about.
Abstract: Pavlovian fear conditioning depends on prediction error, or the discrepancy between actual and expected outcomes. We used immunohistochemistry, neuronal tract tracing, and reversible inactivation to study the role of prefrontal cortex and thalamocortical pathways in predictive fear learning. Unexpected, but not expected, conditioned stimulus (CS)-unconditioned stimulus (US) presentations caused increased c-Fos expression in the prefrontal cortex (PFC), midline thalamus, lateral amygdala, as well as retrograde labeled midline thalamic afferents to PFC. Reversible inactivation of dorsomedial PFC, but not infralimbic PFC, prevented the associative blocking of fear learning. These results suggest a role for dorsomedial PFC (dmPFC), and a thalamic → dmPFC pathway, in signaling whether or not aversive events are expected or unexpected and so whether they are to be learned about.
TL;DR: This study provides an example of how animal experiments can be used to inform and target human studies, which in turn can corroborate results obtained in experimental animals.
Abstract: Background. Learned safety is established by negatively correlating the occurrence of a neutral stimulus and a noxious stimulus, which renders the previously neutral stimulus a ‘safety signal’. While the neurophysiological and molecular mechanisms have been characterized in mice, it is currently not known how the neural substrates involved compare between mice and people. Methods. Here we attempt to adapt the original animal protocol to humans and use functional magnetic resonance imaging to examine neural responses to the conditioned stimulus in safety conditioned and fear conditioned subjects. Diffusion tensor imaging (DTI) was used in a parallel group of subjects as a fi rst approach to delineate the underlying neural circuitry. Results. Learned safety is associated with dampened amygdala and increased dorsolateral prefrontal cortex and caudate responses and paralleled by pupillary constriction. A neural connection between the amygdala and the dorsolateral prefrontal cortex is suggested by DTI. Conclusion. We present a translational bridge between mouse and human models of learned safety in which cellular and molecular insights from animal experiments are extended to the human neural circuitry. This study provides an example of how animal experiments can be used to inform and target human studies, which in turn can corroborate results obtained in experimental animals.