Faculty Opinions recommendation of An important role of neural activity-dependent CaMKIV signaling in the consolidation of long-term memory.

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.

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HYPERMNESIA EUPHORIA OR ANY OTHER DESIRABLE FROM THE POINT OF VIEW OF THE CONSUMER, A PSYCHOTROPIC EFFECT - FIRST AND LEADING ELEMENT IN THE OCCURRENCE AND PRESERVATION OF THE BODY’S DEPENDENCE ON PSYCHOACTIVE FACTORS

HERALD of North-Western State Medical University named after I I Mechnikov ◽

10.17816/mechnikov20179340-46 ◽

2017 ◽

Vol 9 (3) ◽

pp. 40-46

Author(s):

D G Baitubayev ◽

M D Baitubayeva

Keyword(s):

Substance Dependence ◽

Point Of View ◽

The Body ◽

Long Term Memory ◽

Vegetative Nervous System ◽

Term Memory ◽

Psychotropic Effect

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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The Role of Originality in Retrieval from Long-Term Memory: Relations Between Fluency, Originality, Working Memory Capacity, and Crystallized Intelligence

Oregon Undergraduate Research Journal ◽

10.5399/uo/ourj.15.1.4 ◽

2019 ◽

Vol 15 (1) ◽

pp. 18-33

Author(s):

Dillon Murphy

Keyword(s):

Working Memory ◽

Working Memory Capacity ◽

Memory Capacity ◽

Long Term Memory ◽

Term Memory ◽

Crystallized Intelligence

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The Role of Histone Acetylation in Long-Term Memory Storage

Research and Perspectives in Neurosciences - Epigenetics, Brain and Behavior ◽

10.1007/978-3-642-27913-3_7 ◽

2012 ◽

pp. 71-80

Author(s):

Shane G. Poplawski ◽

Ted Abel

Keyword(s):

Histone Acetylation ◽

Memory Storage ◽

Long Term Memory ◽

Term Memory

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Role of Gene Transcription in Long-Term Memory Storage

Encyclopedia of Behavioral Neuroscience ◽

10.1016/b978-0-08-045396-5.00030-0 ◽

2010 ◽

pp. 161-179 ◽

Cited By ~ 3

Author(s):

J. Hawk ◽

T. Abel

Keyword(s):

Gene Transcription ◽

Memory Storage ◽

Long Term Memory ◽

Term Memory

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Manifold Visual Working Memory

Working Memory ◽

10.1093/oso/9780198842286.003.0011 ◽

2020 ◽

pp. 311-332

Author(s):

Nicole Hakim ◽

Edward Awh ◽

Edward K. Vogel

Keyword(s):

Working Memory ◽

Visual Working Memory ◽

Neural Activity ◽

Long Term Memory ◽

Term Memory ◽

Memory Representations ◽

Latent Representations ◽

Definition Of ◽

Spatial Locations

Visual working memory allows us to maintain information in mind for use in ongoing cognition. Research on visual working memory often characterizes it within the context of its interaction with long-term memory (LTM). These embedded-processes models describe memory representations as existing in three potential states: inactivated LTM, including all representations stored in LTM; activated LTM, latent representations that can quickly be brought into an active state due to contextual priming or recency; and the focus of attention, an active but sharply limited state in which only a small number of items can be represented simultaneously. This chapter extends the embedded-processes framework of working memory. It proposes that working memory should be defined operationally based on neural activity. By defining working memory in this way, the important theoretical distinction between working memory and LTM is maintained, while still acknowledging that they operate together. It is additionally proposed that active working memory should be further subdivided into at least two subcomponent processes that index item-based storage and currently prioritized spatial locations. This fractionation of working memory is based on recent research that has found that the maintenance of information distinctly relies on item-based representations as well as prioritization of spatial locations. It is hoped that this updated framework of the definition of working memory within the embedded-processes model provides further traction for understanding how we maintain information in mind.

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The amnestic agent anisomycin disrupts intrinsic membrane properties of hippocampal neurons via a loss of cellular energetics

Journal of Neurophysiology ◽

10.1152/jn.00370.2019 ◽

2019 ◽

Vol 122 (3) ◽

pp. 1123-1135 ◽

Cited By ~ 1

Author(s):

C. J. Scavuzzo ◽

M. J. LeBlancq ◽

F. Nargang ◽

H. Lemieux ◽

T. J. Hamilton ◽

...

Keyword(s):

Protein Synthesis ◽

Mitochondrial Function ◽

Neural Activity ◽

Memory Consolidation ◽

Hippocampal Neurons ◽

Membrane Properties ◽

Long Term Memory ◽

Term Memory ◽

Cellular Energetics

The nearly axiomatic idea that de novo protein synthesis is necessary for long-term memory consolidation is based heavily on behavioral studies using translational inhibitors such as anisomycin. Although inhibiting protein synthesis has been shown to disrupt the expression of memory, translational inhibitors also have been found to profoundly disrupt basic neurobiological functions, including the suppression of ongoing neural activity in vivo. In the present study, using transverse hippocampal brain slices, we monitored the passive and active membrane properties of hippocampal CA1 pyramidal neurons using intracellular whole cell recordings during a brief ~30-min exposure to fast-bath-perfused anisomycin. Anisomycin suppressed protein synthesis to 46% of control levels as measured using incorporation of radiolabeled amino acids and autoradiography. During its application, anisomycin caused a significant depolarization of the membrane potential, without any changes in apparent input resistance or membrane time constant. Anisomycin-treated neurons also showed significant decreases in firing frequencies and spike amplitudes, and showed increases in spike width across spike trains, without changes in spike threshold. Because these changes indicated a loss of cellular energetics contributing to maintenance of ionic gradients across the membrane, we confirmed that anisomycin impaired mitochondrial function by reduced staining with 2,3,5-triphenyltetrazolium chloride and also impaired cytochrome c oxidase (complex IV) activity as indicated through high-resolution respirometry. These findings emphasize that anisomycin-induced alterations in neural activity and metabolism are a likely consequence of cell-wide translational inhibition. Critical reevaluation of studies using translational inhibitors to promote the protein synthesis dependent idea of long-term memory is absolutely necessary. NEW & NOTEWORTHY Memory consolidation is thought to be dependent on the synthesis of new proteins because translational inhibitors produce amnesia when administered just after learning. However, these agents also disrupt basic neurobiological functions. We show that blocking protein synthesis disrupts basic membrane properties of hippocampal neurons that correspond to induced disruptions of mitochondrial function. It is likely that translational inhibitors cause amnesia through their disruption of neural activity as a result of dysfunction of intracellular energetics.

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