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Caffeine is the most widely consumed psychostimulant drug which could affect learning and memory acting through central adenosine receptors. Although caffeine has been suggested to impair the acquisition and the expression of auditory fear conditioning, its effect on the extinction has not been elucidated. To address this issue, in the present study, we investigated whether caffeine affects the extinction of conditioned fear in an auditory fear conditioning paradigm. During conditioning, rats received pairings of auditory cues (conditioned stimulus, CS) and foot shocks (unconditioned stimulus). On the next day, the rats were intraperitoneally administrated saline or caffeine (5 or 10 mg/kg) and then subjected to the extinction training, in which CSs were repeatedly presented without the foot shocks. Twenty‐four hours later, the rats were re‐exposed to the presentations of CSs (retrieval test). We found an acute caffeine administration dose‐dependently decreased freezing rates during the presentations of CS in the extinction training. Furthermore, caffeine‐treated animals showed lower conditioned freezing responses in the retrieval test. These findings suggest that caffeine facilitates the extinction of conditioned fear. [ABSTRACT FROM AUTHOR]

We aimed to investigate the persistent trace of one traumatic event on neurocircuit controls in rats. Conditioning was reflected by reductions in rates of 'freezing' and 'other-than-freezing' motor activities, between which rats could alternate on delivery of pulsed footshocks of intensity 0.5 mA but not 1.0 mA. At the latter intensity, freezing began to suppress motor activity. The conditional responses evident during both the context and tone sessions persisted when the tests were repeated on post-conditioning days 7 and 8. Thus, difficulties with fear extinction/reduction remained. However, persistence was not evident on post-conditioning days 1 and 2. One day after the 1.0 mA pulsed footshock, ibotenate lesions and corresponding sham surgeries were performed in unilateral and bilateral hemispheres of the amygdala, hippocampus, and prefrontal cortex, as well as three different disconnections (one unilateral and another contralateral lesions out of three regions, a total of nine groups), and were tested on days 7-8. The drastic restoration of freezing following bilateral amygdala lesions was also evident in animals with three types of disconnection; however, this was not the case for hypoactivity. These results imply that a serious experience can drive different neurocircuits that all involve the amygdala, forming persistent concurrent memories of explicit (e.g., 'freezing') or implicit (e.g., 'other-than-freezing' motor activity) emotions, which may exhibit mutual interference. [ABSTRACT FROM AUTHOR]

Background and purpose: Neurobiological changes in memory processes seem to play a role in the pathophysiology of post-traumatic stress disorder (PTSD). Memory itself is influenced by PTSD, too. Histone deacetylase inhibitors (HDAIs) have shown promising results in the extinction of fear-related memories in animals and hence they seem to be important for the treatment of PTSD. Data are scarce about the effect of HDAIs in spatial memory formation/extinction in PTSD models. The main goal of the present work is to find the effect of sodium butyrate (NaBu), as an HDAI, on spatial memory and spatial memory extinction in rats exposed to single prolonged stress procedure (SPS). Experimental approach: Different doses of NaBu were administered subcutaneously for 7 days in different groups of rats after SPS procedure. Learning, memory, and extinction of memory were evaluated in the Morris water maze test of spatial memory in 6 consecutive days. Findings / Results: The results show that NaBu (0.5 mg/kg) alleviates impaired learning and memory in SPS rats. It also facilitates the extinction of newly formed memory in the animals. Conclusion and implications: Our data suggest that the administration of HDAIs after a traumatic experience can prevent the aversive effects of SPS on spatial memory. It also reinforces the notion that extinction of spatial memory involves the same or similar brain circuitry that is involved in the extinction of fear memories in PTSD patients. [ABSTRACT FROM AUTHOR]

Stress impairs extinction learning, and these deficits depend, in part, on stress-induced norepinephrine (NE) release in the basolateral amygdala (BLA). For example, systemic or intra-BLA administration of propranolol reduces the immediate extinction deficit (IED), an impairment in extinction learning that occurs when extinction trials are administered soon after fear conditioning. Here, we explored whether locus coeruleus (LC)-NE regulates stress-induced changes in spike firing in the BLA and consequent extinction learning impairments. Rats were implanted with recording arrays in the BLA and, after recovery from surgery, underwent a standard auditory fear conditioning procedure. Fear conditioning produced an immediate and dramatic increase in the spontaneous firing of BLA neurons that persisted (and in some units, increased further) up to an hour after conditioning. This stress-induced increase in BLA firing was prevented by systemic administration of propranolol. Conditioning with a weaker footshock caused smaller increases in BLA firing rate, but this could be augmented by chemogenetic activation of the LC. Conditioned freezing in response to a tone paired with a weak footshock was immune to the IED, but chemogenetic activation of the LC before the weak conditioning protocol increased conditioned freezing behavior and induced an IED; this effect was blocked with intra-BLA infusions of propranolol. These data suggest that stressinduced activation of the LC increases BLA spike firing and causes impairments in extinction learning. Stress-induced increases in BLA activity mediated by LC-NE may be a viable therapeutic target for individuals with stress- and trauma-related disorders. [ABSTRACT FROM AUTHOR]

Two experiments analyzed the role of extinction cues (EC) and stimuli associated to them in the reacquisition of conditioned ethanol tolerance. Ethanol-induced ataxia was measured in 80 rat subjects using a tilting plane, in a 5-phase procedure. The first experiment (which used 4 contexts and 40 rats) showed that the presentation of the extinction context by itself diminished the effectiveness of ECs in reducing response reacquisition. The second experiment (conducted in a single context with 40 rats and using 2 stimulus paired for some subjects or explicitly unpaired for others) showed that a secondary cue can reduce reacquisition, regardless of whether it was paired with the EC or not. The results of mixed and factor analyses of variance suggest that ECs affect response recovery through an association with the extinction context; however, a second-order cue associated to an EC appears to be unable to activate this association. [ABSTRACT FROM AUTHOR]

The neurobiological mechanisms that underlie the resistance of drug cue associations to extinction in addiction remain unknown. Fear extinction critically depends on the ventromedial prefrontal cortex (VMPFC). Here, we tested if this same region plays a role in extinction of non-fear, drug and pleasant cue associations. Eighteen chronic cocaine users and 15 matched controls completed three functional MRI scans. Participants first learned to associate an abstract cue (the conditioned stimulus, CS) with a drug-related (CSD+ ) or pleasant (CSP+ ) image. Extinction immediately followed where each CS was repeatedly presented without the corresponding image. Participants underwent a second identical session 24 hours later to assess retention of extinction learning. Results showed that like fear extinction, non-fear-based extinction relies on the VMPFC. However, extinction-related changes in the VMPFC differed by cue valence and diagnosis. In controls, VMPFC activation to the CSD+ (which was unpleasant for participants) gradually increased as in fear extinction, while it decreased to the CSP+ , consistent with a more general role of the VMPFC in flexible value updating. Supporting a specific role in extinction retention, we further observed a cross-day association between VMPFC activation and skin conductance, a classic index of conditioned responses. Finally, cocaine users showed VMPFC abnormalities for both CSs, which, in the case of the CSD+ , correlated with craving. These data suggest a global deficit in extinction learning in this group that may hinder extinction-based treatment efforts. More broadly, these data show that the VMPFC, when functionally intact, supports extinction learning in diverse contexts in humans. [ABSTRACT FROM AUTHOR]

It has been reported that in certain phenomena (spontaneous recovery, reacquisition, resurgence and contextual renewal) it is possible to observe the recovery of a previously extinguished response. Contextual renewal refers to the reappearance of an extinguished response that result from a change of context between the extinction and testing phase. The purpose of the present study was to evaluate contextual renewal, considering both the temporal distribution of the responses and the response rate. A recovery of the response rate was found, being a result consistent with those reported in the area of contextual renewal. In addition, a renewal of the temporal distribution of the responses could be identified. The results are discussed by recognizing that rate and temporal distribution are two behavioral dimensions that are modulated by contextual changes. [ABSTRACT FROM AUTHOR]

As basic units of neural networks, ensembles of synapses underlie cognitive functions such as learning and memory. These synaptic engrams show elevated synaptic density among engram cells following contextual fear memory formation. Subsequent analysis of the CA3-CA1 engram synapse revealed larger spine sizes, as the synaptic connectivity correlated with the memory strength. Here, we elucidate the synapse dynamics between CA3 and CA1 by tracking identical synapses at multiple time points by adapting two-photon microscopy and dual-eGRASP technique in vivo. After memory formation, synaptic connections between engram populations are enhanced in conjunction with synaptogenesis within the hippocampal network. However, extinction learning specifically correlated with the disappearance of CA3 engram to CA1 engram (E-E) synapses. We observed "newly formed" synapses near pre-existing synapses, which clustered CA3-CA1 engram synapses after fear memory formation. Overall, we conclude that dynamics at CA3 to CA1 E-E synapses are key sites for modification during fear memory states. • Hippocampal synaptic connections are tracked by two-photon imaging of dual-eGRASP • E-E synapses undergo synaptogenesis according to fear conditioning • Extinction learning significantly correlated with the disappearance of E-E synapses • Spatial distribution of new E-E synapses induces clustering of engram synapses Lee et al. use four-color two-photon imaging and dual-eGRASP system to enable longitudinal tracking of the synaptic connections between CA3 and CA1. From these data, they demonstrate a correlation between the dynamics of engram synapses and fear memory states. A particular distribution of newly formed synapses leads to clustering of E-E synapses. [ABSTRACT FROM AUTHOR]

Return of fear is a serious problem in exposure-based treatments of anxiety disorders. Renewal of the fear response may occur when re-encountering the conditioned stimulus within a novel context. Findings in rodents underpin the hippocampus' role in conditioned fear renewal in novel contexts, but it has yet to be investigated in humans. Forty-six healthy men took part in a 2-day, context-dependent, cued fear conditioning paradigm with fear acquisition, extinction learning (day 1) and extinction recall in the acquisition, extinction and a novel context one day later. Conditioned evaluative, skin conductance responses (SCRs) and blood-oxygen-level-dependent responses served as dependent variables. Context-dependent fear renewal was reflected in stronger conditioned SCRs. In the acquisition context, individuals with a higher renewal of conditioned SCRs showed stronger activation of the fear circuit. Hippocampal activation distinguished conditioned responding in the novel compared with the extinction context. Individuals with a stronger renewal of conditioned SCRs in the novel context showed increased effective connectivity of hippocampal activation foci with structures in the fear and extinction network. These results outline the pivotal role of the hippocampus and its connectivity in conditioned fear renewal in a novel context in humans and might have important implications for exposure therapy in anxiety disorders. [ABSTRACT FROM AUTHOR]

Background: Extinction of conditioned fear is an important brain function for animals to adapt to a new environment. Accumulating evidence suggests that innate immune cytokines are involved in the pathology of psychotic disorders. However, the involvement of cytokines in fear dysregulation remains less investigated. In the present study, we investigated how interferon (IFN)-α disrupts the extinction of conditioned fear and propose an approach to rescue IFN-α-induced neurologic impairment.Methods: We used a rat model of auditory fear conditioning to study the effect of IFN-α on the fear memory process. IFN-α was infused directly into the amygdala of rats and examined the rats' behavioral response (freezing) to fear-conditioned stimuli. Immunohistochemical staining was used to examine the glia activity status of glia in the amygdala. The levels of the proinflammatory cytokines interleukin (IL)-1β and tumor necrosis factor (TNF)-α in the amygdala were measured by enzyme-linked immunosorbent assay. We also administrated minocycline, a microglial activation inhibitor, before the IFN-α infusion to testify the possibility to reverse the IFN-α-induced effects.Results: Infusing the amygdala with IFN-α impaired the extinction of conditioned fear in rats and activated microglia and astrocytes in the amygdala. Administering minocycline prevented IFN-α from impairing fear extinction. The immunohistochemical and biochemical results show that minocycline inhibited IFN-α-induced microglial activation and reduced IL-1β and TNF-α production.Conclusions: Our findings suggest that IFN-α disrupts the extinction of auditory fear by activating glia in the amygdala and provides direction for clinical studies of novel treatments to modulate the innate immune system in patients with psychotic disorders. [ABSTRACT FROM AUTHOR]

The extinction of learned fear is a hippocampus-dependent process thought to embody new learning rather than erasure of the original fear memory, although it is unknown how these competing contextual memories are represented in the hippocampus. We previously demonstrated that contextual fear conditioning results in hippocampal place cell remapping and long-term stabilization of novel representations. Here we report that extinction learning also induces place cell remapping in C57BL/6 mice. Specifically, we observed cells that preferentially remapped during different stages of learning. While some cells remapped in both fear conditioning and extinction, others responded predominantly during extinction, whichmayserve to modify previous representations as well as encodenewsafe associations. Additionally, we found cells that remapped primarily during fear conditioning, which could facilitate reacquisition of the original fear association. Moreover, we also observed cells that were stable throughout learning, which may serve to encode the static aspects of the environment. The short-term remapping observed during extinction was not found in animals that did not undergo fear conditioning, or when extinction was conducted outside of the conditioning context. Finally, conditioning and extinction produced an increase in spike phase locking to the theta and gamma frequencies. However, the degree of remapping seen during conditioning and extinction only correlated with gamma synchronization. Our results suggest that the extinction learning is a complex process that involves both modification of pre-existing memories and formation of new ones, and these traces coexist within the same hippocampal representation. [ABSTRACT FROM AUTHOR]

Extinction and presentation of response-independent stimuli are two traditional procedures to suspend a response-consequence contingency. The goal of this review is to discuss some similarities and divergences in the behavioral effects of those procedures. Among the similarities, we found response-rate deceleration, stimulus control development, renewal, and increase in behavioral variability. Among the divergences, we observed the higher degree of response-rate deceleration, the occurrence of emotional responses and behavioral contrast effects under extinction; superstitious behavior and reinstatement under response-independent stimuli conditions. Such behavioral effects were discussed in light of the similarities (non-contingency) and differences (presence versus absence of reinforcing stimuli) in programming those conditions. [ABSTRACT FROM AUTHOR]

ABSTRACT Drug reinforcement learning is relevant for the development of addiction. The present study investigated how changes in the magnitude of drug-unconditioned stimulus during associative learning modulate the acquisition and extinction of cocaine-induced conditioned place preference (CPP). B6;129S F2 mice were conditioned by three dosing schedules of cocaine: (1) ascending, (2) fixed and (3) descending daily doses. Following acquisition of CPP, extinction was induced by (1) context re-exposure, (2) reconditioning by saline and (3) reconditioning by descending doses of cocaine. The magnitude of CPP following conditioning by daily ascending doses of cocaine (2, 4, 8 and 16 mg/kg) was significantly higher than that obtained from conditioning by either a fixed daily dose (16 mg/kg × 4 days) or daily descending doses (24, 12, 6 and 3 mg/kg). Extinction following context re-exposure showed persistent CPP in the 'ascending' group compared to the other two groups. However, extinction via reconditioning by saline was equally effective in all groups. Interestingly, reconditioning by descending doses of cocaine (1) extinguished CPP and (2) resulted in partial resistance to the reinstatement of conditioned response by cocaine priming. Results underscore the significance of daily changes in cocaine dosage in the development and extinction of drug-induced conditioned response. Increase and decrease in cocaine dosage strengthens and weakens cocaine-associated memory, respectively. Moreover, extinction by 'tapering down' drug reward may be superior to extinction by saline. [ABSTRACT FROM AUTHOR]

When a cue (X) and an outcome are paired, X comes to elicit responding similar to that elicited by the outcome. This potential is lessened if X is later presented by itself (i.e., experimental extinction). Extinction is interesting both for theoretical reasons and because it is a model for exposure therapy, which is used to treat numerous psychological disorders. Conventionally, extinction has been viewed as an isolated phenomenon unrelated to other response-attenuating treatments, whereas it is actually but one of several instances of associative interference that reduce conditioned responding. Although much has been learned about extinction from direct study, the larger associative-interference literature provides additional insight. Here we view extinction as new learning that is inconsistent with previously acquired knowledge (i.e., retroactive outcome interference). We provide an account of whether the acquisition or extinction memory will be expressed depending on the relative strengths of these two memories and the relative efficacies of their respective retrieval cues. [ABSTRACT FROM PUBLISHER]

During fear conditioning, animals learn an association between a previously neutral or conditioned stimulus (CS) and an aversive or unconditioned stimulus (US). Subsequent reexposure to the CS alone triggers two competing processes. Brief reexposure to the CS initiates reconsolidation processes that serve to stabilize or maintain the original CS-US memory. In contrast, more prolonged reexposure to the CS leads to the formation of an inhibitory extinction (CS-no US) memory. Previous studies have established that both reconsolidation and extinction require gene expression. Consistent with this, here we first show that genetic disruption of cAM-Presponsive element-binding protein (CREB)-mediated transcription blocks both reconsolidation and long-term extinction of contextual fear memory. We next asked whether reconsolidation and extinction engage CREB-mediated transcription in distinct brain regions. Accordingly, we used immunohistochemical approaches to characterize the activation of the transcription factor CREB [as well as the expression of the CREB-dependent gene Arc (activity-regulated cytoskeleton-associated protein)] after brief versus prolonged reexposure to a previously conditioned context. After brief reexposure, we observed significant activation of CREB-mediated gene expression in the hippocampus and amygdala. In contrast, after the prolonged reexposure, we observed significant activation of CREB-mediated gene expression in the amygdala and prefrontal cortex. Finally, we showed that blocking protein synthesis in either the hippocampus or the amygdala blocked reconsolidation of contextual fear memory, whereas similar blockade in the amygdala and prefrontal cortex prevented the formation of extinction memory. These experiments establish that reactivated contextual fear memories undergo CREB-dependent reconsolidation or extinction in distinct brain regions. [ABSTRACT FROM AUTHOR]

It is well established that the cerebellum and its associated circuitry are essential for classical conditioning of the eyeblink response and other discrete motor responses (e.g., limb flexion, head turn, etc.) learned with an aversive unconditioned stimulus. However, brain mechanisms underlying extinction of these responses are still relatively unclear. Behavioral studies have demonstrated extinction to be an active learning process distinct from acquisition. Accordingly, this current understanding of extinction has guided neural studies that have tried to identify possible brain structures that could support this new learning. However, whether extinction engages the same brain sites necessary for acquisition is not yet clear. This poses an overriding problem for understanding brain mechanisms necessary for extinction because such analysis cannot be done without first identifying brain sites and pathways involved in this phenomenon. Equally elusive is the validity of a behavioral theory of extinction that can account for the properties of extinction. In this study, we looked at the involvement of the interpositus and the red nucleus in extinction. Results show that, although inactivation of both nuclei blocks response expression, only inactivation of the interpositus has a detrimental effect on extinction. Moreover, this detrimental effect was completely removed when inactivation of the interpositus was paired with electrical stimulation of the red nucleus. These findings speak to the important role of cerebellar structures in the extinction of discrete motor responses and provide important insight as to the validity of a particular theory of extinction. [ABSTRACT FROM AUTHOR]

The motivational component of drug withdrawal may contribute to drug seeking and relapse through the negative reinforcement-based process. Here, we used conditioned place aversion (CPA) induced by naloxone-precipitated morphine withdrawal to measure the aversive effects. Using an unbiased conditioning paradigm, we treated rats with morphine hydrochloride [(10 mg/kg intraperitoneally (i.p.)] twice per day (at 08:00 and 20:00) for 6.5 days (from day 1 to day 7 morning), while gave them naloxone (0.3 mg/kg i.p.) on day 6, a precipitated withdrawal paired with a compartment that caused CPA to the side. Then, the rats exhibited CPA were received 12 extinction trials from days 7 to 13, by daily exposed to the two compartments for free exploration. On day 13, the rats with extinguished CPA were treated with a priming injection of morphine (10 mg/kg i.p.) followed by naloxone (0.3 mg/kg i.p.) that reliably reinstated CPA. These results demonstrated that repeatedly morphine-treated rats showed the formation, extinction and reinstatement of CPA. The present CPA model induced by these procedures may be useful for studying the biological mechanisms underlying the aversive motivational component of opiate withdrawal. [ABSTRACT FROM AUTHOR]

Functional analyses were conducted to identify reinforcers for noncompliance exhibited by 3 young children. Next, the effects of three antecedent-based interventions—noncontingent access to a preferred item, a warning, and a high-probability instructional sequence—were examined. The high-probability instructional sequence was effective for 1 child. Antecedent interventions were ineffective and extinction was necessary for the other 2 children. [ABSTRACT FROM AUTHOR]

The current study describes the assessment and treatment of the problem behavior of 3 individuals with autism for whom initial functional analysis results were inconclusive. Subsequent analyses revealed that the interruption of free-operant behavior using ‘do’ requests (Study 1) as well as ‘do’ and ‘don't’ requests (Study 2) occasioned problem behavior. Initially, treatment involved differential and noncontingent reinforcement without interruption. To make the intervention more sustainable in the natural environment (where interruptions are unavoidable), a two-component multiple-schedule arrangement was used to progressively increase the period of time in which ongoing activities would be interrupted. During generalization sessions, the intervention was applied across a variety of contexts and therapists. [ABSTRACT FROM AUTHOR]

Existing research suggests that there may be benefits to teaching signing to hearing infants who have not yet developed vocal communication. In the current study, each of 4 infants ranging in age from 6 to 10 months was taught a simple sign using delayed prompting and reinforcement. In addition, Experiment 1 showed that 2 children independently signed in a variety of novel stimulus conditions (e.g., in a classroom, with father) after participating in sign training under controlled experimental conditions. In Experiment 2, crying and whining were replaced with signing when sign training was implemented in combination with extinction. [ABSTRACT FROM AUTHOR]

The learning processes underlying the formation of drug–cue associations involve changes in synaptic transmission mediated by AMPA receptors. Here, we examine the consequences of targeted deletion of the gene encoding GluR1 subunits of AMPA receptors (gria1 knockouts (KO)) on cocaine self-administration and on the ability of cocaine-paired cues to affect cocaine-seeking in mice. Cocaine self-administration was unaffected by gria1 deletion, as was the ability of a cocaine-paired cue to reinstate responding following extinction, following either a 3 or a 66 day delay. However, gria1 KOs over-responded during extinction. The KOs were unable initially to learn a new response to access a cue previously conditioned to cocaine (conditioned reinforcement (CR)), although a second test 2 months later revealed that this was a transient deficit. These studies indicate that GluR1-containing AMPA-receptors are not involved in cocaine self-administration, cue-induced reinstatement of cocaine seeking, or incubation of the cocaine seeking response. In order to understand the specificity of the deficits in CR responding, a parallel study was performed with food reward. As with cocaine, there were no effects of gria1 deletion on food self-administration or cue-induced reinstatement, and KOs over-responded during extinction. However, even immediately after instrumental training for food, KO mice demonstrated responding for CR, suggesting that the CR deficit observed with a cocaine cue is specific to drug reward. These data indicate that GluR1-containing AMPA receptors are important in stimulus reward learning, though the method of cue-reward association formation, the reward class, and the behavioral end point are critical variables in determining their involvement.Neuropsychopharmacology (2007) 32, 343–353. doi:10.1038/sj.npp.1301045; published online 22 February 2006 [ABSTRACT FROM AUTHOR]

NMDA receptors are important for the acquisition, reconsolidation, and extinction of memories. NMDA receptor antagonists impair these memory processes, whereas the partial agonist D-cycloserine (DCS) potentiates both learning and extinction. Here,weusedDCSand the noncompetitive NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-SH-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) to investigate the effects of enhancing and blocking NMDA receptor-mediated glutamatergic transmission on the reconsolidation and extinction of a conditioned fear memory. Either long extinction training or short memory reactivation sessions were used to preferentially engage extinction and reconsolidation processes, respectively. MK-801 blocked extinction to maintain high levels of conditioned freezing, and DCS potentiated extinction to reduce freezing, when they were administered before a long extinction training session. However, the opposite behavioral outcome was observed when the brief memory reactivation session was used: MK-801 administration impaired, whereas DCS increased, freezing, likely reflecting impairment and enhancement of reconsolidation, respectively. Finally, by using localized intracerebral infusions, we showed that the basolateral amygdala is a primary locus of action of systemically administered DCS. Thus, intrabasolateral amygdala DCS potentiated both the extinction and the reconsolidation of fear conditioning, depending on the length of the extinction/memory reactivation session. Therefore, memory reconsolidation can be both disrupted and enhanced, and extinction can be both potentiated and impaired, either to reduce or increase conditioned fear. These results have important implications for the use of reconsolidation blockade and potentiation of extinction as treatment strategies for maladaptive memory disorders. [ABSTRACT FROM AUTHOR]

A sequence of behaviors consisting of appropriate responses, inappropriate responses, or a combination of both can be linked together in a behavior chain. Several operant processes may disrupt behavior chains. For example, one or more members of the behavior chain may be affected when reinforcement is withheld for the last response in the chain (extinction), when the last response is reinforced even if it occurs without the other responses in the chain (unchaining), or when access to the terminal reinforcer is available independent of responding (Satiation). However, few studies have examined the effects of these types of procedures on responding that occurs in the context of behavior chains. The purpose of this study was to examine the effects of three clinically relevant procedures and processes (i.e., extinction, satiation, and unchaining) on behaviors that occur as part of a behavior chain. Overall, extinction and satiation resulted in a decrease in both responses in the chain. During the unchaining procedure, decreases were observed in the first response in the chain but not in the second response. DESCRIPTORS: behavior chain, response chain, extinction, satiation [ABSTRACT FROM AUTHOR]

Conditioned taste aversion (CTA) is a form of aversive memory in which an association is made between a consumed substance and a subsequent malaise. CTA is a critical mechanism for the successful survival, and hence evolution, of most animal species. The role of excitatory neurotransmitters in the neurochemical mechanisms of CTA is well recognized; however, less is known about the involvement of inhibitory receptor systems. In particular, the potential functions of metabotropic GABAB receptors in CTA have not yet been fully explored. GABAB receptors are metabotropic GABA receptors that are comprised of two subunits, GABAB(1) and GABAB(2)) , which form heterodimers. The Gabbr1 gene is transcribed into two predominant isoforms, GABAB(1a) and GABAB(1b), which differ in sequence primarily by the inclusion of a pair of sushi domains (also known as short consensus repeats) in the GABA B(1a))N terminus. The behavioral function of mammalian GABA B(1)) receptor isoforms is currently unknown. Here, using a point mutation strategy in mice, we demonstrate that these two GABAB(1) receptor isoforms are differentially involved in critical components of CTA. In contrast to GABAB(1b))-/- and wild-type mice, GABAB(1a))-/-mice failed to acquire CTA. In contrast, GABAB(1b)-/- mice robustly acquired CTA but failed to show any extinction of this aversion. The data demonstrate that GABAB receptors are involved in both the acquisition and extinction of CTA; however, receptors containing the GABAB(1a) or the GABAB(1b) isoform differentially contribute to the mechanisms used to learn and remember the salience of aversive stimuli. [ABSTRACT FROM AUTHOR]

We attempted to isolate the evocative effects of the establishing operation for positively reinforced problem behavior with 2 participants. The study consisted of three phases. First, a functional analysis identified tangible items (Participant 1) and attention (Participant 2) as maintaining problem behavior. Second, access to tangible items and attention was systematically controlled (continuous access vs. no access) immediately prior to functional analysis sessions in which these consequences were delivered contingent on problem behavior. Results of this phase indicated that problem behavior occurred at higher levels when access to tangible items and attention was restricted. In the third phase, prior access was again controlled, but problem behavior produced no consequences. Results of this final phase indicated that problem behavior occurred at higher levels during extinction sessions when participants did not have prior access to the reinforcers. [ABSTRACT FROM AUTHOR]

Abstract: This paper analyses an interesting story, that of the physiologist Ivan Petrovitch Pavlov. While investigating the causes of salivary secretions in the waking, behaving dog, he discovered a class of causes that he called psychic, since they were associated with perceiving a visual, acoustic or other signal, delivered before food that normally created salivation. A temporary relationship was therefore established, between the secretory command and the cerebral site associated with an initially neutral stimulus that had become a signal. This gave rise to the “conditional reflex”. Pavlov was probably not the first who had observed this kind of association, but he very skilfully exploited these data to create a coherent conceptual system. In 23 “lectures”, he very precisely summarized his views and retraced the fundamental issues explaining the main features of the purely physiological cerebral command of behaviour. The Pavlovian system necessarily became, in the particular environment of the soviet regime, a kind of credo on physical-mental relationships based upon a generalized reflexology, not allowing any deviation, nor any dissidence, nor any concession to subjectivity. The notion of conditional reflex has indeed resisted to time, but number of subtelties of the Pavlovian thinking and many phenomena that he described now seem forgotten and to have lost much of their heuristic value. Most of the recent theories of learning have only rarely followed Pavlov''s line, to concentrate on more complex learning modalities. To cite this article: P. Buser, C. R. Biologies 329 (2006). [Copyright &y& Elsevier]

Cue-induced reinstatement of extinguished drug seeking is a preclinical model of relapse. However, relapse typically occurs after abstinence rather than explicit extinction training. We show that inactivation of the dorsolateral caudate-putamen, but not other structures previously implicated in reinstatement, attenuates cocaine seeking after abstinence. This suggests that there is limited overlap in the substrates of cocaine seeking after abstinence versus extinction, and that habit learning exerts greater control over drug seeking than regions implicated in stimulus-reward associations. [ABSTRACT FROM AUTHOR]

The feeding behaviors of a child diagnosed with failure to thrive were assessed using descriptive analysis methodology to identify the schedules of reinforcement provided by the child's parents. This analysis revealed that the child's appropriate feeding behaviors (i.e., bite acceptance, self-feeding) were on a lean schedule of positive reinforcement and that the child's refusal behaviors (e.g., non-acceptance, expulsion) were on a rich schedule of negative reinforcement. A treatment package consisting of differential positive reinforcement for bite acceptance with and without escape extinction was evaluated by manipulating the schedules of reinforcement that were identified to be used by the child's parents. The results showed a reduction of the child's inappropriate mealtime behaviors and increases in the child's acceptance of offered food items. The results also suggested that the differential reinforcement component appeared to be most responsible for ongoing effectiveness of the treatment. These results are discussed in terms of treating the food refusal behavior of children diagnosed with failure to thrive as a preventive measure for later development of developmental disabilities. [ABSTRACT FROM AUTHOR]

A demonstration of the effects of reinforcement requires comparison of response rates in the presence of a contingency with those in another condition that controls for the influence of extraneous variables. We describe several control conditions that have been used in evaluating the effects of positive and negative reinforcement. The methodological rigor and practical utility of each type of control condition are discussed, and recommendations for the use of these conditions are presented. [ABSTRACT FROM AUTHOR]

It is believed that de novo protein synthesis is fundamentally linked to synaptic changes in neuronal circuits involved in acquisition and extinction of conditioned responses. Recent studies show that neuronal plasticity may be also altered by cytoskeletal rearrangement independently of protein synthesis. We investigated the role of these processes in the hippocampus during acquisition and extinction of context-dependent conditioned fear in mice. Intrahippocampal injections of the protein synthesis inhibitors anisomycin and puromycin, or of the actin rearrangement inhibitors cytochalasin D and latrunculin A, prevented the acquisition of context-dependent fear. Unexpectedly, anisomycin and puromycin enhanced extinction without erasing the fear memory. In contrast, cytochalasin D and latrunculin A prevented extinction of context-dependent freezing. On the basis of these findings, it is suggested that certain hippocampal mechanisms mediating extinction of conditioned contextual fear are inhibited by protein synthesis and involve actin rearrangement. Such mechanisms might predominandy elicit modifications of hippocampal circuits that store the conditioning memory. [ABSTRACT FROM AUTHOR]

Operant conditioning with Betta splendens (Bettas) has been investigated extensively using males of the species. Ethological studies of female Bettas have revealed aggressive interactions that qualitatively parallel those between male Bettas. Given these similarities, four experiments were conducted with female Bettas to examine the generality of a widely reported finding with males: mirror-image reinforcement. Swimming through a ring was reinforced by a 10Đs mirror presentation. As with males, ring swimming was acquired and maintained when mirror presentations were immediate (Experiments 1, 2, and 3) and delayed (Experiment 4). The failure of conventional extinction (Experiments 1 and 2) and response-independent mirror presentations (Experiment 3) to maintain responding confirmed the reinforcing properties of mirror presentation. These results extend previous findings of mirror images as reinforcers in males of the same species and illustrate a complementarity between behavioral ecology and the experimental analysis of behavior. [ABSTRACT FROM AUTHOR]

Two experiments with rats examined the dynamics of well-learned response sequences when reinforcement sequence of lever presses until responding was stable. The contingencies then were shifted to a new reinforced sequence until responding was again stable. Extinction-induced resurgence of previously reinforced, and then extinguished, heterogeneous response sequences was observed in all subjects in both experiments. These sequences were demonstrated to be integrated behavioral units, controlled by processes acting at the level of the entire sequence. Response-level processes were also simultaneously operative. Errors in sequence production were strongly influenced by the terminal, not the initial, response in the currently reinforced sequence, but not by the previously reinforced sequence. These studies demonstrate that sequence-level and response-level processes can operate simultaneously in integrated behavioral units. Resurgence and the development of integrated behavioral units may be dissociated; thus the observation of one does not necessarily imply the other. [ABSTRACT FROM AUTHOR]