Sign learning as a factor in extinction.

Seward, John P.; Levy, Nissim

doi:10.1037/h0060914

Cited by 64 publications

(43 citation statements)

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“…In contrast to typical extinction training that involves performance of a previously reinforced response, during latent extinction training no overt response is made. For example, a food-rewarded approach response in a straight-alley maze can be extinguished by placing the animal in the goal box in the absence of reward (Seward and Levy 1949). Consistent with the hypothesis that multiple memory systems play a role in the learning that occurs during extinction, we observed that the learning underlying response and latent extinction of runway behavior is neuroanatomically dissociable.…”

supporting

confidence: 70%

“…Specifically, neural inactivation of the hippocampus prevented latent extinction of maze runway behavior, but did not block response extinction of the same behavior (Gabriele and Packard 2006). Latent extinction is conducive to a cognitive learning process in which an expectancy (Tolman 1932) of food reward can be altered without performance of the previously acquired response (Seward and Levy 1949). According to the multiple memory systems hypothesis, the hippocampus is selectively involved in cognitive learning and memory (e.g., Hirsh 1974; Mishkin and Petri 1984), and the impairment of latent extinction produced by hippocampal inactivation is consistent with this view.…”

mentioning

confidence: 99%

“…Whereas some extinction therapies used in clinical settings involve training in the presence of overt behavioral responses, other approaches are based on developing cognitive control over maladaptive behaviors, and this latter form of learning may not require overt responding during extinction training. To the extent that latent extinction in lower animals selectively involves cognitive learning and memory (Seward and Levy 1949;Gabriele and Packard 2006), elucidation of the neurochemical bases of this form of extinction learning may potentially inform therapeutic strategies used in the treatment of various psychopathologies. Therefore, the present studies examined whether postextinction training injections of DCS are effective in enhancing memory consolidation underlying hippocampus-dependent latent extinction.…”

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confidence: 99%

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D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

Gabriele¹,

Packard²

2007

Learn. Mem.

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Adult male Long-Evans rats were trained to run in a straight-alley maze for food reward and subsequently received hippocampus-dependent latent extinction training. Immediately following latent extinction, rats received peripheral injections of the NMDA receptor partial agonist D-cycloserine (DCS, 15 mg/kg), or saline. Twenty-four hours later, rats received four extinction "probe" trials. Relative to saline controls, latencies to reach the goal box on probe trials were significantly higher in rats that had received DCS. These findings indicate that memory consolidation underlying hippocampus-dependent latent extinction, a cognitive form of learning in which the previously rewarded response is not made during extinction training, can be enhanced by NMDA-receptor agonism.Behavioral extinction is operationalized as a reduction of a previously acquired response, and this process can involve new learning (for review, see Bouton 2004). The initial acquisition of learned behavior involves multiple memory systems (for review, see Packard 2001) and we have recently expanded this view to the study of the new learning underlying behavioral extinction (Gabriele and Packard 2006). We used a task in which extinction of the same overt behavior could be achieved using either a "response" or "latent" extinction training procedure. In contrast to typical extinction training that involves performance of a previously reinforced response, during latent extinction training no overt response is made. For example, a food-rewarded approach response in a straight-alley maze can be extinguished by placing the animal in the goal box in the absence of reward (Seward and Levy 1949). Consistent with the hypothesis that multiple memory systems play a role in the learning that occurs during extinction, we observed that the learning underlying response and latent extinction of runway behavior is neuroanatomically dissociable. Specifically, neural inactivation of the hippocampus prevented latent extinction of maze runway behavior, but did not block response extinction of the same behavior (Gabriele and Packard 2006). Latent extinction is conducive to a cognitive learning process in which an expectancy (Tolman 1932) of food reward can be altered without performance of the previously acquired response (Seward and Levy 1949). According to the multiple memory systems hypothesis, the hippocampus is selectively involved in cognitive learning and memory (e.g., Hirsh 1974;Mishkin and Petri 1984), and the impairment of latent extinction produced by hippocampal inactivation is consistent with this view.Although our previous study using a reversible lesion technique implicates the hippocampus in latent extinction, the findings do not provide any information concerning the neurochemical basis of this form of cognitive learning. Various neurotransmitter systems play a role in extinction (for review, see Mason 1983) and several recent studies have focused on the role of glutamatergic neurotransmission (for review, see Davis and Myers 2002). For example, adminis...

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confidence: 70%

mentioning

confidence: 99%

mentioning

confidence: 99%

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D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

Gabriele¹,

Packard²

2007

Learn. Mem.

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“…The phenomenon of latent extinction (eg. Seward and Levy 1949) represents this form of extinction in a relatively pure state. Taxon hypotheses are more persistent, though in the intact animal the existence of the locale system provides for exploration, which plays an important role in the extinction of these hypotheses partly by allowing for the development of competing behaviours.…”

Section: 11(c) Extinction Reconsideredmentioning

confidence: 99%

The Hippocampus as a Cognitive Map

Routtenberg¹,

O’Keefe²,

Nadel³

1980

The American Journal of Psychology

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“…Seward and Levy's (1949) demonstration of "latent extinction" is just one case in point. That the influence of the reminder treatments on control trials was statistically unreliable in Gordon and Feldman's (1978;Feldman & Gordon, 1979) studies and marginally reliable in Grant and Marshal's (1985) studies is not sufficient to dismiss consideration of the tendency because, as Grant and Marshal argue, the reminder effect on forgetting trials may represent the summative effects of weak memory of the initial forced run and weak new learning from the goal-ann placement.…”

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confidence: 99%

Enhancement of short-term retention by appetitive-reinforcer reminder treatment

Kasprow

1987

Animal Learning & Behavior

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Choice accuracy by rats in a delayed-alternation paradigm was shown to decrease over a 120-sec retention interval. The decrement in choice accuracy was reversed by presentation of the appetitive reinforcer outside ofthe apparatus during the retention interval. This suggests that the reinforcer served to reactivate the target spatial memory and that the short-term retention deficit in the absence of such memory reactivation was not due to a loss of information. The results are discussed with respect to recent criticisms of memory-reactivation treatments in short-term retention tasks.In principle, associative deficits can be caused by failure of information storage at the time of acquisition, irreversible decay of information during the retention interval, or failure of information retrieval at the time of retention testing. Although it is clear that processes that occur in temporal proximity to the learning event and during the retention interval are important for later retention (e.g., McGaugh, 1966), several memory theorists have emphasized the importance of retrieval processes (e. g., Lewis, 1979;Miller, Kasprow, & Schachtman, 1986;Spear, 1971Spear, , 1973Spear, , 1978.A critical observation in support of retrieval-based models of memory has been the reversal of a variety of associative performance deficits through memory reactivation, that is, "reminder" treatments. A reminder treatment re-presents, prior to testing, some subset of the stimuli present during the original learning episode. It has been hypothesized that such exposure serves to stimulate further processing of the learning event so that future retrieval is facilitated (Spear, 1978). Most studies that have demonstrated the reversal of associative performance deficits have included conditions to preclude nonassociative interpretations of reminder-induced behavioral change (see Miller et al., 1986, for a recent review).The vast majority of successful restorations of associative performance by reminder treatments have used longterm retention tasks. Few studies using animals as subjects have investigated the effect of reminder treatments on short-term retention, but those directed toward the problem have obtained positive results. Feldman and Gordon (1979) alleviated forgetting over a 9O-sec retention interval in aT-maze delayed-alternation preparation using rats. In delayed alternation, an animal is initially forced

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Sign learning as a factor in extinction.

Cited by 64 publications

References 20 publications

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

The Hippocampus as a Cognitive Map

Enhancement of short-term retention by appetitive-reinforcer reminder treatment

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