Perseverative neural processes and consolidation of the memory trace.

Glickman, Stephen E.

doi:10.1037/h0044212

Cited by 304 publications

(170 citation statements)

References 68 publications

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“…In particular, learning and memory are adversely affected. There appear to be at least two types of effect present: (1) a loss of memory for events occurring immediately before a convulsion (Glickman, 1961), and (2) a long-term generalized deterioration of cerebral function which impairs retention of old habits and acquisition of new ones as well as disrupting performance of instinctive activities such as food hoarding or care of the young (Munn, 1950). Furthermore, E.C.T.…”

Section: Discussionmentioning

confidence: 99%

Recovery from large medial thalamic lesions as a result of electroconvulsive therapy.

Vanderwolf¹

1968

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Discussionmentioning

confidence: 99%

Recovery from large medial thalamic lesions as a result of electroconvulsive therapy.

Vanderwolf¹

1968

Journal of Neurology, Neurosurgery & Psychiatry

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“…1Ai) (Ebbinghaus 1885; Müller and Pilzecker 1900;Glickman 1961;McGaugh 1966, Dudai 2004. At the synaptic level of analysis, this process, referred to as synaptic consolidation, is thought to be a universal property of neurons that subserve memory formation.…”

Section: Consolidation: the Dominant Model Of Memory Storagementioning

confidence: 99%

“…Staying strictly within the commonly accepted consolidation framework, and applying only the rationale on which this framework is The critical point is to show that once a memory is in LTM, it is thought to remain fixed or permanent (Glickman 1961;McGaugh 1966). (Aii) A typical demonstration of a consolidation blockade (Schafe and LeDoux 2000)-intact short-term memory (STM) and impaired LTM, a pattern of impairment that defines a consolidation impairment (Dudai 2004;McGaugh 2004).…”

Section: Behavioral Evidence For a Reconsolidation Processmentioning

confidence: 99%

“…There is the learning or encoding phase, in which information is acquired, by stabilization phase, in which specific mechanisms are engaged to stabilize initially unstable new information (referred to as synaptic consolidation) (Glickman 1961;McGaugh 1966), the "storage" or maintenance phase, during which other mechanisms are involved to maintain the memory, and the retrieval phase, in which specific mechanisms permit a memory to be retrieved (Miller and Springer 1973;Spear 1973). For a long time, from a neurobiological perspective, only acquisition and memory stabilization (Martin et al 2000;Kandel 2001;Dudai 2004) were considered to be active phases, in the sense that neurons had to perform certain computations or synthesize new RNA and proteins for these phases of memory processing to be performed successfully.…”

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confidence: 99%

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Reconsolidation and the Dynamic Nature of Memory

Nader

2015

Cold Spring Harb Perspect Biol

148

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Memory reconsolidation is the process in which reactivated long-term memory (LTM) becomes transiently sensitive to amnesic agents that are effective at consolidation. The phenomenon was first described more than 50 years ago but did not fit the dominant paradigm that posited that consolidation takes place only once per LTM item. Research on reconsolidation was revitalized only more than a decade ago with the demonstration of reconsolidation in a well-defined behavioral protocol (auditory fear conditioning in the rat) subserved by an identified brain circuit (basolateral amygdala). Since then, reconsolidation has been shown in many studies over a range of species, tasks, and amnesic agents, and cellular and molecular correlates of reconsolidation have also been identified. In this review, I will first define the evidence on which reconsolidation is based, and proceed to discuss some of the conceptual issues facing the field in determining when reconsolidation does and does not occur. Last, I will refer to the potential clinical implications of reconsolidation.

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“…The PFC is considered the executive center of the brain due to its involvement in a multiplicity of functions. These include goal-directed behaviors, impulsivity and response inhibition, reward expectancy, salience attribution, emotional learning, drive and motivation, decision making, selective attention [88][89][90][91], memory consolidation, which can be defined as the process of stabilizing, storing, and strengthening new memories [92], as well as memory recall, which can be defined as the reactivation and/or retrieval of a previously consolidated memory [93].…”

Section: The Prefrontal Cortex Functional Role and Anatomical Connectmentioning

confidence: 99%

Neuroanatomical Structures Underlying the Extinction of Drug-Seeking Behavior

Cleva¹,

Gass²

2013

TOADDJ

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This review summarizes current knowledge about the neurobiological components underlying the extinction of drug-associated memories and how they may contribute to the treatment of drug addiction. Evidence suggests that extinction learning is not the forgetting, or unlearning, of the associations between external stimuli and drug effects, but that new reinforcer expectancies are necessary for extinction of drug-seeking behavior to take place. Several theories suggest that addiction is a disorder of learning and memory, and recent evidence indicates that the brain circuits, neurotransmitters, and signal transduction mechanisms that underlie drug addiction are similar to those that mediate learning and memory processes. According to these theories, drug addiction results from repeated drug use and the formation of lasting associations between a drug's effects, withdrawal symptoms, and the environmental cues and contexts within which they are experienced. Unfortunately, standard behavioral modification techniques, such as cue exposure therapy, have shown only moderate efficacy in reducing and/or extinguishing the salience of drug-associated cues and contexts. Therefore, a greater understanding of the neurobiological mechanisms involved in the extinction of drug-related memories could provide novel therapeutic interventions for the treatment of drug addiction.

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Perseverative neural processes and consolidation of the memory trace.

Cited by 304 publications

References 68 publications

Recovery from large medial thalamic lesions as a result of electroconvulsive therapy.

Recovery from large medial thalamic lesions as a result of electroconvulsive therapy.

Reconsolidation and the Dynamic Nature of Memory

Neuroanatomical Structures Underlying the Extinction of Drug-Seeking Behavior

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