In CPP, the place preference is extinguished by repeated exposure to the previously drug-paired context in the absence of reinforcement, while in the self-administration/extinction/reinstatement model, the operant response required to produce a drug infusion is extinguished by withholding the reinforcer after a response (Tzschentke, 2007; Shaham et al., 2003).
Full Answer
Does extinction enhance efficacy of pharmacological and behavioral treatments for addiction?
Clinical use of extinction and reconsolidation based therapies. Several researchers have attempted to use extinction learning, known as cue exposure therapy clinically, to treat addiction to a variety of drugs of abuse (Conklin and Tiffany, 2002). Cue exposure therapy (CET) is based on the assumption that when environmental stimuli are repeatedly associated with a drug, the …
What is extinction in behavior therapy?
The ultimate goal of these interventions, extinction of the original conditioned response, is a new learning process that results in a decrease in frequency or intensity of conditioned responses to drug or fear cues. This review explores extinction approaches in …
What is extinction of the original conditioned response?
Extinction involves the formation of new inhibitory memories rather than memory erasure; thus, it should be possible to facilitate the extinction of cue-drug memories to reduce relapse. We propose that context-dependency of extinction might be altered by mnemonic agents, thereby enhancing the efficacy of cue-exposure therapy as treatment strategy.
What are extinction therapy counter measures?
Jan 01, 2011 · Such an extinction based treatment is cue exposure treatment (CET). CET is a manualized presentation of drug-related cues and it has been shown to reduce cue activated emotional responses. This extinction treatment approach reduces craving and relapse but has been only partially effective in clinical trials.
How does extinction therapy work?
Extinction therapy countermeasures seek to reduce conditioned responses using a set of techniques in which patients are repeatedly exposed to conditioned appetitive or aversive stimuli using imaginal imagery, in vivo exposure, or written scripts. Such interventions allow patients to rehearse more adaptive responses to conditioned stimuli. The ultimate goal of these interventions, extinction of the original conditioned response, is a new learning process that results in a decrease in frequency or intensity of conditioned responses to drug or fear cues. This review explores extinction approaches in conditioned drug reward and fear responses. The behavioral, neuroanatomical and neurochemical mechanisms of conditioned reward and fear responses and their extinction are derived from our understanding of the animal literature. Extensive neuroscience research shows that even though many mechanisms differ in conditioned fear and reward, converging prefrontal cortical glutamatergic pathways underlie extinction learning. Efficacy of pharmacological and behavioral treatment approaches in addiction and anxiety disorders may be optimized by enhancing extinction and weakening the bond between the original conditioned stimuli and conditioned responses. Adjunctive pharmacotherapy approaches using agents which alter glutamate or γ-aminobutyric acid signaling or epigenetic mechanisms in prefrontal cortical pathways can enhance extinction learning. A comparative study of extinction processes and its neural mechanisms can be translated into more effective behavioral and pharmacological treatment approaches in substance abuse and anxiety.
Which part of the brain is responsible for fear conditioning?
Fear related sensory information is transmitted to the amygdala through its basal and lateral (BLA) nuclei. PTSD can be conceptualized as a cue- and context-associated fear conditioning process that results from amygdalar hyperresponsivity and an inability to extinguish these neural responses. The hippocampus is critical in associative learning, memory consolidation and in the retrieval of episodic memories. The sites of extinction learning may be distributed across several structures, especially the PFC and its corticolimbic projections to the amygdala ( Fig. 2 ). Glutamatergic excitatory projections from the PL extend to the sites of fear memory storage in the BLA and central nucleus of the amyg dala (CNA) and activate downstream fear circuitry. Projections from the BLA to the CNA are thought to activate fear responses through outputs to the hypothalamus and brainstem. The IL cortex appears to be the primary candidate key pathway to suppress fear responses via extinction learning. Single unit recordings have shown that IL neurons respond to conditioned stimuli only after extinction learning has developed ( Milad et al., 2006 ). Agents that activate IL pathways suppress conditioned fear ( Vidal-Gonzalez et al, 2006 ). The IL projects to GABAergic neurons between the BLA and CNA called the intercalated cell masses (ITC) positioned between these two amygdalar subregions. Activation of the ITC inhibits output from the CNA and reduces fear responses. It has been hypothesized that fear extinction entails an increase in excitatory drive to the ITC and produces reductions in output from the CNA ( Peters et al., 2009 ).
How do drugs interact with stimuli?
Drugs of abuse interact with stimuli in the drug-taking environment via classical and instrumental conditioning to alter motivational responses and self-administration behaviors ( Robbins et al., 2008 ). Pavlovian conditioning mechanisms link unconditioned drug responses to associated contextual cues, allowing the drug responses to be elicited by these non-drug stimuli. For example, drug cue exposure in heroin and cocaine abusing individuals results in real-time drug craving and consequent drug use ( Epstein et al., 2009 ). The temporal and spatial relatedness of these contextual stimuli to motivational responses produces powerful conditioned effects ( O'Brien et al., 1993 ). When these stimuli are encountered in an abstinent state, they can induce memories of prior drug experience, or drug craving, which can result in drug taking and relapse ( Weiss, 2005 ). Cue-induced craving is predictive of relapse in addiction. Any improvements in our understanding of mechanisms of craving or conditioned reward will lead to a better development of treatment approaches ( Sinha and Li, 2007 ).
What are the components of the neural circuitry for cue and context induced reward and relapse?
The major components of the neural circuitry for cue and context induced reward and relapse include the prefrontal cortex, which includes prelimbic (PL) and infralimbic (IL) subregions, the basolateral amygdala (BLA), hippocampus, nucleus accumbens (NAc), ventral pallidum, and ventral tegmental area (VTA) as highlighted in Fig. 1. Drugs of abuse produce direct motivational effects by activating dopaminergic neurons originating in the VTA which project to the amygdala, NAc, anterior cingulate cortex and PFC ( Hammer, 2002 ). Exposures to conditioned drug cue and context exposures also activate the mesolimbic dopaminergic system. In support of dopamine's role, cocaine dependent humans viewing drug cues demonstrate craving with correlated increases striatal dopamine levels ( Volkow et al., 2006 ). In conditioned drug reward, classically conditioned cue and contextual responses are established via activation of neurons in the medial PFC ( Taylor et al., 2009 ). Glutamatergic neurons from the prelimbic cortex (PL) of the PFC and from the basolateral amygdala (BLA) project to the NAc core region and to the VTA ( Kauer and Malenka, 2007) and are hypothesized to activate drug-seeking behavior ( McFarland et al., 2003, Di Ciano and Everitt, 2004 ). Inactivation of these PL cortical neurons reduces relapse in rat models ( LaLumiere and Kalivas, 2008 ). In contrast, glutamatergic projections from the infralimbic cortex (IL) to the NAc shell subregion are hypothesized to extinguish drug-seeking behavior ( Peters et al., 2008, LaLumiere et al., 2010 ).
How to understand extinction?
Understand the definition of extinction Understand how to implement extinction based on behavior function Understand the effect of extinction on rate of behavior Understand generalization and maintenance as it relates to behavior reduction
What is spontaneous recovery?
Spontaneous Recovery The behavior that diminished during the extinction process recurs even though the behavior does not produce reinforcement Short-lived and limited if the extinction procedure remains in effect.
What does "extinction" mean?
Extinction is formally defined as “the omission of previously delivered unconditioned stimuli or reinforcers, ” but it can also describe the “absence of a contingency between response and reinforcer.” Essentially, this means that learned behaviors will gradually disappear if they are not reinforced.
What are the three forms of extinction?
In order for extinction to occur, target behaviors need to be identified, and new ones need to be established, and procedures typically take on one of three different forms based on: Negative Reinforcement. Positive Reinforcement. Automatic Reinforcement.
What is the purpose of behavior modification?
Behavior Modification For Reducing Problematic Behaviors. Extinction, in psychology, has a different meaning than the traditional sense of the word. However, to an extent, they are also similar in some ways.
Can extinction behavior be done without professional assistance?
Using extinction behavior to help bring about change despite the sideeffects can be done without professional assistance in many cases, but others find the help of a therapist useful and might decide to meet with one who specializes in applied behavior analysis.
What is spontaneous recovery?
Spontaneous recovery is a term coined by Pavlov that means that if time is able to elapse after extinction, it can also return. Renewal refers to the return of extinguished responding when the conditioned stimulus is removed from the extinction context and tested in another one.
What is automatic reinforcement?
Automatic reinforcement, also known as sensory extinction, is slightly more straightforward but can be used in certain scenarios. For instance, if someone is fascinated by the feel and sound of clicking a pen, the act of doing so is stimulating and a form of automatic reinforcement.
What is ABA therapy?
ABA is a common therapy for individuals who have a disability, such as autism or Down syndrome, that may have challenging behaviors . ABA is not a typical form of psychotherapy, and it is not a one-size-fits-all approach, but with some trial and error and data collection, behavioral change can occur. Source: rawpixel.com.