Release from proactive interference in long-term memory: The role of retrieval

2010 ◽  
Author(s):  
Bridgid Finn ◽  
Kathleen B. McDermott ◽  
Nate Kornell
1966 ◽  
Vol 18 (3) ◽  
pp. 266-269 ◽  
Author(s):  
R. Conrad ◽  
A. J. Hull

It has been proposed that a single set of operations based on classical interference theory is adequate to describe the phenomena of both short- and long-term memory. An article by Keppel and Underwood (1962) argues that short-term forgetting is due to proactive interference and, by implication, not a result of trace decay. An experiment which varied retention interval and the nature of the interpolated task, gave results which indicate that when the amount forgotten and the nature of errors are considered, a decay model is supported, the proactive interference suggestion being untenable.


2014 ◽  
Vol 40 (4) ◽  
pp. 1039-1048 ◽  
Author(s):  
Yana Weinstein ◽  
Adrian W. Gilmore ◽  
Karl K. Szpunar ◽  
Kathleen B. McDermott

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Hamish Patel ◽  
Reza Zamani

Abstract Long-term memories are thought to be stored in neurones and synapses that undergo physical changes, such as long-term potentiation (LTP), and these changes can be maintained for long periods of time. A candidate enzyme for the maintenance of LTP is protein kinase M zeta (PKMζ), a constitutively active protein kinase C isoform that is elevated during LTP and long-term memory maintenance. This paper reviews the evidence and controversies surrounding the role of PKMζ in the maintenance of long-term memory. PKMζ maintains synaptic potentiation by preventing AMPA receptor endocytosis and promoting stabilisation of dendritic spine growth. Inhibition of PKMζ, with zeta-inhibitory peptide (ZIP), can reverse LTP and impair established long-term memories. However, a deficit of memory retrieval cannot be ruled out. Furthermore, ZIP, and in high enough doses the control peptide scrambled ZIP, was recently shown to be neurotoxic, which may explain some of the effects of ZIP on memory impairment. PKMζ knockout mice show normal learning and memory. However, this is likely due to compensation by protein-kinase C iota/lambda (PKCι/λ), which is normally responsible for induction of LTP. It is not clear how, or if, this compensatory mechanism is activated under normal conditions. Future research should utilise inducible PKMζ knockdown in adult rodents to investigate whether PKMζ maintains memory in specific parts of the brain, or if it represents a global memory maintenance molecule. These insights may inform future therapeutic targets for disorders of memory loss.


Author(s):  
D G Baitubayev ◽  
M D Baitubayeva

The work shows the role of the vegetative nervous system (VNS) in the functioning of long-term memory, identity mechanisms of long-term memory in the human evolutionary adaptation and substance dependence. It is shown that, depending on the substance of the body are states like pro- gressive adaptation, that the bodycondition, depending on the chemical and psychogenic psychoactive- factors state of the same circle. It proposed the creation of a branch of medicine that combines study of the dependence of the organism, both on the chemical and psychoactive psychogenic factors. Given the classification of psychoactive factors.Onomastics formulated definitions of terminology changes and additions to be used in a new branch of medicine. Proposed allocation of the International Classifica- tion of diseases separate chapter for the classification of states like progressive adaptation of the body depending on psychoactive factors.


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