scholarly journals Long-term potentiation in the hippocampus: discovery, mechanisms and function

Neuroforum ◽  
2018 ◽  
Vol 24 (3) ◽  
pp. A103-A120 ◽  
Author(s):  
Tim V.P. Bliss ◽  
Graham L. Collingridge ◽  
Richard G.M. Morris ◽  
Klaus G. Reymann
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
And Function

Abstract In this review we reflect upon our contributions to the study of the properties and mechanisms of long-term potentiation (LTP) and describe some of the major influences on our work. We then go on to consider whether LTP has fulfilled its early promise of providing a compelling account of the synaptic basis of learning and memory.

scholarly journals Brevican-Deficient Mice Display Impaired Hippocampal CA1 Long-Term Potentiation but Show No Obvious Deficits in Learning and Memory

2002 ◽  
Vol 22 (21) ◽  
pp. 7417-7427 ◽  
Author(s):  
Cord Brakebusch ◽  
Constanze I. Seidenbecher ◽  
Fredrik Asztely ◽  
Uwe Rauch ◽  
Henry Matthies ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Brain Anatomy ◽  
Perineuronal Nets ◽  
Functional Roles ◽  
Term Potentiation ◽  
And Function ◽  
Deficient Mice

ABSTRACT Brevican is a brain-specific proteoglycan which is found in specialized extracellular matrix structures called perineuronal nets. Brevican increases the invasiveness of glioma cells in vivo and has been suggested to play a role in central nervous system fiber tract development. To study the role of brevican in the development and function of the brain, we generated mice lacking a functional brevican gene. These mice are viable and fertile and have a normal life span. Brain anatomy was normal, although alterations in the expression of neurocan were detected. Perineuronal nets formed but appeared to be less prominent in mutant than in wild-type mice. Brevican-deficient mice showed significant deficits in the maintenance of hippocampal long-term potentiation (LTP). However, no obvious impairment of excitatory and inhibitory synaptic transmission was found, suggesting a complex cause for the LTP defect. Detailed behavioral analysis revealed no statistically significant deficits in learning and memory. These data indicate that brevican is not crucial for brain development but has restricted structural and functional roles.

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.

scholarly journals Environmental noise degrades hippocampus-related learning and memory

2020 ◽  
Vol 118 (1) ◽  
pp. e2017841117
Author(s):  
Yifan Zhang ◽  
Min Zhu ◽  
Yutian Sun ◽  
Binliang Tang ◽  
Guimin Zhang ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Sound Pressure ◽  
Noise Exposure ◽  
Long Term Potentiation ◽  
Modern Human ◽  
Pressure Level ◽  
Neural Mechanisms ◽  
Loud Noise ◽  
Term Potentiation

The neural mechanisms underlying the impacts of noise on nonauditory function, particularly learning and memory, remain largely unknown. Here, we demonstrate that rats exposed postnatally (between postnatal days 9 and 56) to structured noise delivered at a sound pressure level of ∼65 dB displayed significantly degraded hippocampus-related learning and memory abilities. Noise exposure also suppressed the induction of hippocampal long-term potentiation (LTP). In parallel, the total or phosphorylated levels of certain LTP-related key signaling molecules in the synapses of the hippocampus were down-regulated. However, no significant changes in stress-related processes were found for the noise-exposed rats. These results in a rodent model indicate that even moderate-level noise with little effect on stress status can substantially impair hippocampus-related learning and memory by altering the plasticity of synaptic transmission. They support the importance of more thoroughly defining the unappreciated hazards of moderately loud noise in modern human environments.

Sign in / Sign up

Export Citation Format

Share Document