Facets of Pavlovian and operant extinction

Lattal, K. Matthew; Lattal, Kennon A.

doi:10.1016/j.beproc.2012.03.009

Cited by 46 publications

(48 citation statements)

References 93 publications

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“…As this study and others [17-19] indicate, free operant responding is composed of multiple underlying components that change over the course of extinction. These changes may reflect the numerous processes implicated in extinction learning, such as reductions in arousal or incentive motivation [28-30], and learning new associations in an unreinforced context [31,32], among many others (see [31,33] for reviews). A precise mapping of these processes to changes in response-bout microstructure during extinction [18] would provide a foundation for inferences about the processes responsible for differences in performance between strains.…”

Section: Discussionmentioning

confidence: 99%

Extinction learning deficit in a rodent model of attention-deficit hyperactivity disorder

et al. 2012

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BackgroundDeficient operant extinction has been hypothesized to be constitutive of ADHD dysfunction. In order to elucidate the behavioral mechanisms underlying this deficit, the performance of an animal model of ADHD, the spontaneously hypertensive rat (SHR), was compared against the performance of a control strain, the Wistar-Kyoto rat (WKY) during extinction.MethodFollowing extensive training of lever pressing under variable interval schedules of food reinforcement (reported previously), SHR and WKY rats were exposed to two sessions of extinction training. Extinction data was analyzed using the Dynamic Bi-Exponential Refractory Model (DBERM) of operant performance. DBERM assumes that operant responses are organized in bouts separated by pauses; during extinction, bouts may decline across multiple dimensions, including frequency and length. DBERM parameters were estimated using hierarchical Bayesian modeling.ResultsSHR responded more than WKY during the first extinction session. DBERM parameter estimates revealed that, at the onset of extinction, SHR produced more response bouts than WKY. Over the course of extinction, response bouts progressively shortened for WKY but not for SHR.ConclusionsBased on prior findings on the sensitivity of DBERM parameters to motivational and schedule manipulations, present data suggests that (1) more frequent response bouts in SHR are likely related to greater incentive motivation, and (2) the persistent length of bouts in SHR are likely related to a slower updating of the response-outcome association. Overall, these findings suggest specific motivational and learning deficits that may explain ADHD-related impairments in operant performance.

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Section: Discussionmentioning

confidence: 99%

Extinction learning deficit in a rodent model of attention-deficit hyperactivity disorder

et al. 2012

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“…These experimental procedures incorporate aspects of both instrumental and classical conditioning to train animals to perform a behavior (e.g., lever pressing) to receive access to a drug and associate discrete cues (e.g., auditory and/or visual) with the drug’s reinforcing effects. Regardless of the type of reinforcer used (e.g., food or drug), extinction is defined in this review as the omission of a previously delivered unconditioned stimuli/reinforcers or the absence of a contingency between a response and reinforcer (Lattal and Lattal, 2012). In addition, while extinction behavior can be observed in both classical and instrumental conditioning paradigms, this review will not attempt to define the neural mechanisms associated with each form of learning.…”

Section: What Is Extinction Learning?mentioning

confidence: 99%

The Plasticity of Extinction: Contribution of the Prefrontal Cortex in Treating Addiction through Inhibitory Learning

Gass¹,

Chandler²

2013

Front. Psychiatry

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Theories of drug addiction that incorporate various concepts from the fields of learning and memory have led to the idea that classical and operant conditioning principles underlie the compulsiveness of addictive behaviors. Relapse often results from exposure to drug-associated cues, and the ability to extinguish these conditioned behaviors through inhibitory learning could serve as a potential therapeutic approach for those who suffer from addiction. This review will examine the evidence that extinction learning alters neuronal plasticity in specific brain regions and pathways. In particular, subregions of the prefrontal cortex (PFC) and their projections to other brain regions have been shown to differentially modulate drug-seeking and extinction behavior. Additionally, there is a growing body of research demonstrating that manipulation of neuronal plasticity can alter extinction learning. Therefore, the ability to alter plasticity within areas of the PFC through pharmacological manipulation could facilitate the acquisition of extinction and provide a novel intervention to aid in the extinction of drug-related memories.

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“…The extent of fear conditioning can be assessed by measuring the freezing responses to the cue or context, fear potentiated startle (FPS) responses, or suppression of ongoing operant behaviors. Additionally, in any of these procedures, subsequent nonreinforced exposure to the CS or context assesses the resistance of initial learning to change, as well as new inhibitory learning (extinction) that develops as animals learn that the cues are no longer associated with the US (Lattal & Lattal, 2012). …”

Section: Fear Conditioning As a Tool To Evaluate The Interaction Bmentioning

confidence: 99%

Substance abuse, memory, and post-traumatic stress disorder

Tipps

Raybuck

Lattal

2014

Neurobiology of Learning and Memory

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A large body of literature demonstrates the effects of abused substances on memory. These effects differ depending on the drug, the pattern of delivery (acute or chronic), and the drug state at the time of learning or assessment. Substance use disorders involving these drugs are often comorbid with anxiety disorders, such as post-traumatic stress disorder (PTSD). When the cognitive effects of these drugs are considered in the context of the treatment of these disorders, it becomes clear that these drugs may play a deleterious role in the development, maintenance, and treatment of PTSD. In this review, we examine the literature evaluating the cognitive effects of three commonly abused drugs: nicotine, cocaine, and alcohol. These three drugs operate through both common and distinct neurobiological mechanisms and alter learning and memory in multiple ways. We consider how the cognitive and affective effects of these drugs interact with the acquisition, consolidation, and extinction of learned fear, and we discuss the potential impediments that substance abuse creates for the treatment of PTSD.

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Facets of Pavlovian and operant extinction

Cited by 46 publications

References 93 publications

Extinction learning deficit in a rodent model of attention-deficit hyperactivity disorder

Extinction learning deficit in a rodent model of attention-deficit hyperactivity disorder

The Plasticity of Extinction: Contribution of the Prefrontal Cortex in Treating Addiction through Inhibitory Learning

Substance abuse, memory, and post-traumatic stress disorder

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