Long term potentiation: Attending to levels of organization of learning and memory mechanisms

1997 ◽  
Vol 20 (4) ◽  
pp. 631-632
Author(s):  
Matthew Shapiro ◽  
Eric Hargreaves
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Task Demands ◽  
Memory Storage ◽  
Storage Mechanism ◽  
Levels Of Organization ◽  
Term Potentiation ◽  
Set Up

Shors & Matzel set up a straw man, that LTP is a memory storage mechanism, and knock him down without due consideration of the important relations among different levels of organization and analysis regarding LTP, learning, and memory. Assessing these relationships requires analysis and hypotheses linking specific brain regions, neural circuits, plasticity mechanisms, and task demands. The issue addressed by the authors is important, but their analysis is off target.

Variations in Synaptic Plasticity and Types of Memory in Corticohippocampal Networks

1992 ◽  
Vol 4 (3) ◽  
pp. 189-199 ◽  
Author(s):  
Gary Lynch ◽  
Richard Granger
Keyword(s):  
Synaptic Plasticity ◽  
Assembly Line ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Storage Mechanism ◽  
Behavioral Studies ◽  
Term Potentiation ◽  
Unique Aspect

If Synaptic long-term potentiation (LTP) represents a memory storage mechanism, its induction and expression characteristics may constitute rules governing encoding and read-out of memory in cortical circuitry, The presence of variants of the LTP effect in different anatomical networks provides grounds for predictions about the types of memory operations to which potentiation contributes. Computer modeling studies incorporating the complex rules for LTP induction and the characteristics of expressed potentiation can be used to make such predictions specific. We review ttie types of synaptic plasticity found in the successive stages of the corticohippocampal pathway, and present results indicating that LTP does participate in definably different forms of memory, suggesting a classification of memory types differing somewhat from categories deduced from behavioral studies. Specifically, the results suggest that subtypes of memory operate serially, in an “assembly line” of specialized functions, each of which adds a unique aspect to the processing of memories. The effects of lesions on the encoding versus expression of memory can be interpreted from the perspective of this hypothesis.

Long-term potentiation: Does it deserve attention?

1997 ◽  
Vol 20 (4) ◽  
pp. 625-626
Author(s):  
Shane M. O'Mara ◽  
Sean Commins ◽  
Colin Gemmell ◽  
John Gigg
Keyword(s):  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Storage Mechanism ◽  
Term Potentiation ◽  
Target Article ◽  
Arousal Mechanism

Shors & Matzel's target article is a thought-provoking attempt to reconceptualise long-term potentiation as an attentional or arousal mechanism rather than a memory storage mechanism. This is incompatible with the facts of the neurobiology of attention and of the behavioural neurophysiological properties of hippocampal neurons.

Arousing the LTP and learning debate

1997 ◽  
Vol 20 (4) ◽  
pp. 622-623 ◽  
Author(s):  
Stephen Maren
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Arousal Mechanism

Shors & Matzel provide compelling arguments against a role for hippocampal long-term potentiation (LTP) in mammalian learning and memory. As an alternative, they suggest that LTP is an arousal mechanism. I will argue that this view is not a satisfactory alternative to current conceptions of LTP function.

Dopamine D-1/D-5 Receptor Activation Is Required for Long-Term Potentiation in the Rat Neostriatum In Vitro

2001 ◽  
Vol 85 (1) ◽  
pp. 117-124 ◽  
Author(s):  
J.N.D. Kerr ◽  
J. R. Wickens
Keyword(s):  
Receptor Antagonist ◽  
Learning And Memory ◽  
Sch 23390 ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Striatal Neurons ◽  
Theoretical Understanding ◽  
Endogenous Dopamine ◽  
Term Potentiation

Dopamine and glutamate are key neurotransmitters involved in learning and memory mechanisms of the brain. These two neurotransmitter systems converge on nerve cells in the neostriatum. Dopamine modulation of activity-dependent plasticity at glutamatergic corticostriatal synapses has been proposed as a cellular mechanism for learning in the neostriatum. The present research investigated the role of specific subtypes of dopamine receptors in long-term potentiation (LTP) in the corticostriatal pathway, using intracellular recording from striatal neurons in a corticostriatal slice preparation. In agreement with previous reports, LTP could be induced reliably under Mg2+-free conditions. This Mg2+-free LTP was blocked by dopamine depletion and by the dopamine D-1/D-5 receptor antagonist SCH 23390 but was not blocked by the dopamine D-2 receptor antagonist remoxipride or the GABAA antagonist picrotoxin. In dopamine-depleted slices, the ability to induce LTP could be restored by bath application of the dopamine D-1/D-5 receptor agonist, SKF 38393. These results show that activation of dopamine D-1/D-5 receptors by either endogenous dopamine or exogenous dopamine agonists is a requirement for the induction of LTP in the corticostriatal pathway. These findings have significance for current understanding of learning and memory mechanisms of the neostriatum and for theoretical understanding of the mechanism of action of drugs used in the treatment of psychotic illnesses and Parkinson's disease.

Nicotine-induced impairments of spatial cognition and long-term potentiation in adolescent male rats

2013 ◽  
Vol 33 (2) ◽  
pp. 203-213 ◽  
Author(s):  
G Han ◽  
L An ◽  
B Yang ◽  
L Si ◽  
T Zhang
Keyword(s):  
Young Adult ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Male Rats ◽  
Adolescent Male ◽  
Control Group ◽  
Adult Offspring ◽  
Behavioral Impairment ◽  
Term Potentiation

The aim of the present study was to investigate whether cognitive behavioral impairment, induced by nicotine in offspring rats, was associated with the alteration of hippocampal short-term potentiation (STP) and long-term potentiation (LTP) and to discuss the potential underlying mechanism. Young adult offspring rats were randomly divided into three groups. The groups include: control group (CC), nicotine group 1 (NC), in which their mothers received nicotine from gestational day 3 (GD3) to GD18, and nicotine group 2 (CN), in which young adult offspring rats received nicotine from postnatal day 42 (PD42) to PD56. Morris water maze (MWM) test was performed and then field excitatory postsynaptic potentials elicited by the stimulation of perforant pathway were recorded in the hippocampal dentate gyrus region. The results of the MWM test showed that learning and memory were impaired by either prenatal or postnatal nicotine exposure. In addition, it was found that there was no statistical difference of the MWM data between both nicotine treatments. In the electrophysiological test, LTP and STP were significantly inhibited in both NC and CN groups in comparison with the CC group. Notably, STP in CN group was also lower than that in the NC group. These findings suggested that both prenatal and postnatal exposure to nicotine induced learning and memory deficits, while the potential mechanism might be different from each other due to their dissimilar impairments of synaptic plasticity.

Hippocampal Synaptic Stability and Plasticity

2020 ◽  
pp. 83-95
Author(s):  
Gabriele M. Rune
Keyword(s):  
Embryonic Development ◽  
Learning And Memory ◽  
Brain Region ◽  
Long Term Potentiation ◽  
Synaptic Potentiation ◽  
Term Potentiation ◽  
Synapse Density ◽  
Hippocampal Cultures ◽  
Estradiol Synthesis

Estradiol synthesis depends on the activity of aromatase, the enzyme that specifically and irreversibly converts testosterone to estradiol in steroidogenesis. Aromatase is expressed and is active in the hippocampus, a brain region related to learning and memory. Dynamics of spines and spine synapses, including expression of presynaptic and postsynaptic proteins, are controlled by hippocampus-derived estradiol in female rodents, but not in male rodents. This also holds true for long-term potentiation. Inhibition of aromatase, either pharmacologically or by genetic approaches, results in a decrease in synapse density and synaptic potentiation in female animals and in neonatal hippocampal cultures that originate from females. The consistency of the findings in rodents and in perinatal primary hippocampal cultures points to sex-specific differentiation processes during embryonic development, which underlie sex-dependent differences in neurosteroid action in the hippocampus.

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