Compound tests for excitation in early acquisition and after prolonged extinction of conditioned suppression

Reberg, Douglas

doi:10.1016/0023-9690(72)90021-5

Cited by 111 publications

(113 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The data of primary interest are presented in Figure 2d, which illustrates responding during the final extinction trials and test for spontaneous recovery of responding conducted 4 weeks later. As predicted by the work of Reberg (1972), data shown in Figure 2d, the final extinction day, responding to the single stimulus (Y) remained low, whereas responding to the compound (AX) was higher. Critically, the pattern reversed at test where responding to the stimulus that had been presented as part of the compound (X) was low and responding to the stimulus extinguished alone (Y) increased.…”

Section: Compound Stimulus Extinction Reduces Spontaneous Recovery Ofsupporting

confidence: 70%

“…These data are illustrated in Figure 2b as the mean response rates for the stimuli that would subsequently be presented as either single or compound during extinction. Reberg (1972) noted that even when two stimuli have themselves been extinguished individually, presenting them Mean lever presses performed per 30 s stimulus or in the 30 s pre-stimulus interval on the final acquisition day for rats in the saline or atomoxetine groups; note that atomoxetine was given 45 min prior to the third extinction session. *Responding during the stimuli was significantly greater than during the pre-stimulus interval and^responding during the stimuli was not different between groups.…”

Section: Compound Stimulus Extinction Reduces Spontaneous Recovery Ofmentioning

confidence: 99%

See 1 more Smart Citation

Compound Stimulus Presentation and the Norepinephrine Reuptake Inhibitor Atomoxetine Enhance Long-Term Extinction of Cocaine-Seeking Behavior

Janak

Bowers²,

Corbit

2011

Neuropsychopharmacol

View full text Add to dashboard Cite

Drug abstinence is frequently compromised when addicted individuals are re-exposed to environmental stimuli previously associated with drug use. Research with human addicts and in animal models has demonstrated that extinction learning (non-reinforced cue-exposure) can reduce the capacity of such stimuli to induce relapse, yet extinction therapies have limited long-term success under real-world conditions (Bouton, 2002;O'Brien, 2008). We hypothesized that enhancing extinction would reduce the later ability of drugpredictive cues to precipitate drug-seeking behavior. We, therefore, tested whether compound stimulus presentation and pharmacological treatments that augment noradrenergic activity (atomoxetine; norepinephrine reuptake inhibitor) during extinction training would facilitate the extinction of drug-seeking behaviors, thus reducing relapse. Rats were trained that the presentation of a discrete cue signaled that a lever press response would result in cocaine reinforcement. Rats were subsequently extinguished and spontaneous recovery of drug-seeking behavior following presentation of previously drug-predictive cues was tested 4 weeks later. We find that compound stimulus presentations or pharmacologically increasing noradrenergic activity during extinction training results in less future recovery of responding, whereas propranolol treatment reduced the benefit seen with compound stimulus presentation. These data may have important implications for understanding the biological basis of extinction learning, as well as for improving the outcome of extinction-based therapies.

show abstract

Section: Compound Stimulus Extinction Reduces Spontaneous Recovery Ofsupporting

confidence: 70%

Section: Compound Stimulus Extinction Reduces Spontaneous Recovery Ofmentioning

confidence: 99%

Compound Stimulus Presentation and the Norepinephrine Reuptake Inhibitor Atomoxetine Enhance Long-Term Extinction of Cocaine-Seeking Behavior

Janak

Bowers²,

Corbit

2011

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…During reacquisition training, savings is apparent because relearning occurs much faster than original learning (Frey and Ross, 1968;Napier et al, 1992). The existence of savings is among the evidence supporting the notion that extinction training leaves behind residual excitatory strength (Reberg, 1972;Schactman et al, 1985;Kehoe, 1988). Here we present evidence for this residual-plasticity hypothesis in eyelid conditioning and characterize basic mechanisms involved in the savings observed with this form of motor learning.…”

mentioning

confidence: 53%

A Mechanism for Savings in the Cerebellum

2001

View full text Add to dashboard Cite

The phenomenon of savings (the ability to relearn faster than the first time) is a familiar property of many learning systems. The utility of savings makes its underlying mechanisms of special interest. We used a combination of computer simulations and reversible lesions to investigate mechanisms of savings that operate in the cerebellum during eyelid conditioning, a well characterized form of motor learning. The results suggest that a site of plasticity outside the cerebellar cortex (possibly in the cerebellar nucleus) can be protected from the full consequences of extinction and that the residual plasticity that remains can later contribute to the savings seen during relearning.Key words: plasticity; learning; memory; eyelid conditioning; simulation; LTD; LTP; extinction Riding a bicycle, playing the piano, and typing are examples of motor skills that illustrate our capacity for relearning that is much more rapid than the original learning. In the laboratory, this rapid relearning is known as savings and has been frequently studied in the context of Pavlovian conditioning of motor responses. During conditioning of eyelid responses for example, paired presentations of a tone [the conditioned stimulus (CS)] and a reinforcing unconditioned stimulus (US), such as periorbital electrical stimulation, promote the acquisition of a conditioned motor response (closing the eyelid in response to the tone). These conditioned responses can be unlearned during extinction training in which the CS is not paired with the US (Schneiderman et al., 1962). During reacquisition training, savings is apparent because relearning occurs much faster than original learning (Frey and Ross, 1968;Napier et al., 1992). The existence of savings is among the evidence supporting the notion that extinction training leaves behind residual excitatory strength (Reberg, 1972;Schactman et al., 1985;Kehoe, 1988). Here we present evidence for this residual-plasticity hypothesis in eyelid conditioning and characterize basic mechanisms involved in the savings observed with this form of motor learning.A variety of evidence indicates that the cerebellum is a necessary component of the neural pathways that mediate eyelid conditioning (Thompson, 1986;Thompson and Krupa, 1994;Raymond et al., 1996;Kim and Thompson, 1997). This evidence, combined with the well characterized synaptic organization and physiology of the cerebellum (Eccles et al., 1967;Llinas, 1981;Ito, 1984;Voogd and Glickstein, 1998), makes it possible to build large-scale computer simulations of the cerebellum and to test their capacity to display eyelid conditioning. We have shown previously that, by incorporating the evidence for plasticity at two sites (one in the cerebellar cortex and one in the cerebellar interpositus nucleus), these simulations can emulate the acquisition and extinction of conditioned responses (Medina et al., 2000). Here we report that these same simulations also display savings, even after extensive extinction training. In the simulations, the rules for plasticity combine...

show abstract

“…27,28 Thus, reinstatement seems to depend on context conditioning and is likely to involve summation of two fear-inducing tendencies, each behaviorally subthreshold when considered independently, but suprathreshold when combined (cf. Hendry 29 and Reberg 30 ): weak conditioning to context and residual net excitation to the extinguished CS. Other context-dependent mechanisms may contribute as well.…”

Section: Behavioral and Theoretical Considerationsmentioning

confidence: 99%

Mechanisms of fear extinction

2006

View full text Add to dashboard Cite

Excessive fear and anxiety are hallmarks of a variety of disabling anxiety disorders that affect millions of people throughout the world. Hence, a greater understanding of the brain mechanisms involved in the inhibition of fear and anxiety is attracting increasing interest in the research community. In the laboratory, fear inhibition most often is studied through a procedure in which a previously fear conditioned organism is exposed to a fear-eliciting cue in the absence of any aversive event. This procedure results in a decline in conditioned fear responses that is attributed to a process called fear extinction. Extensive empirical work by behavioral psychologists has revealed basic behavioral characteristics of extinction, and theoretical accounts have emphasized extinction as a form of inhibitory learning as opposed to an erasure of acquired fear. Guided by this work, neuroscientists have begun to dissect the neural mechanisms involved, including the regions in which extinction-related plasticity occurs and the cellular and molecular processes that are engaged. The present paper will cover behavioral, theoretical and neurobiological work, and will conclude with a discussion of clinical implications. Molecular Psychiatry (2007) 12, 120-150.

show abstract

Compound tests for excitation in early acquisition and after prolonged extinction of conditioned suppression

Cited by 111 publications

References 13 publications

Compound Stimulus Presentation and the Norepinephrine Reuptake Inhibitor Atomoxetine Enhance Long-Term Extinction of Cocaine-Seeking Behavior

Compound Stimulus Presentation and the Norepinephrine Reuptake Inhibitor Atomoxetine Enhance Long-Term Extinction of Cocaine-Seeking Behavior

A Mechanism for Savings in the Cerebellum

Mechanisms of fear extinction

Contact Info

Product

Resources

About