Long-Term Moderate Exercise Rescues Age-Related Decline in Hippocampal Neuronal Complexity and Memory

Gerontology ◽  
2018 ◽  
Vol 64 (6) ◽  
pp. 551-561 ◽  
Author(s):  
Sheng-Feng Tsai ◽  
Nai-Wen Ku ◽  
Tzu-Feng Wang ◽  
Yan-Hsiang Yang ◽  
Yao-Hsiang Shih ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Function ◽  
Long Term Potentiation ◽  
Treadmill Running ◽  
Moderate Intensity ◽  
Middle Aged ◽  
Ca1 Neurons ◽  
Term Potentiation ◽  
Old Mice

Background: Aging impairs hippocampal neuroplasticity and hippocampus-related learning and memory. In contrast, exercise training is known to improve hippocampal neuronal function. However, whether exercise is capable of restoring memory function in old animals is less clear. Objective: Here, we investigated the effects of exercise on the hippocampal neuroplasticity and memory functions during aging. Methods: Young (3 months), middle-aged (9–12 months), and old (18 months) mice underwent moderate-intensity treadmill running training for 6 weeks, and their hippocampus-related learning and memory, and the plasticity of their CA1 neurons was evaluated. Results: The memory performance (Morris water maze and novel object recognition tests), and dendritic complexity (branch and length) and spine density of their hippocampal CA1 neurons decreased as their age increased. The induction and maintenance of high-frequency stimulation-induced long-term potentiation in the CA1 area and the expressions of neuroplasticity-related proteins were not affected by age. Treadmill running increased CA1 neuron long-term potentiation and dendritic complexity in all three age groups, and it restored the learning and memory ability in middle-aged and old mice. Furthermore, treadmill running upregulated the hippocampal expressions of brain-derived neurotrophic factor and monocarboxylate transporter-4 in middle-aged mice, glutamine synthetase in old mice, and full-length TrkB in middle-aged and old mice. Conclusion: The hippocampus-related memory function declines from middle age, but long-term moderate-intensity running effectively increased hippocampal neuroplasticity and memory in mice of different ages, even when the memory impairment had progressed to an advanced stage. Thus, long-term, moderate intensity exercise training might be a way of delaying and treating aging-related memory decline.

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.

Reversal of long-term potentiation (depotentiation) induced by tetanus stimulation of the input to CA1 neurons of guinea pig hippocampal slices

1991 ◽  
Vol 555 (1) ◽  
pp. 112-122 ◽  
Author(s):  
Satoshi Fujii ◽  
Kazuo Saito ◽  
Hiroyoshi Miyakawa ◽  
Ken-ichi Ito ◽  
Hiroshi Kato
Keyword(s):  
Guinea Pig ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Ca1 Neurons ◽  
Term Potentiation ◽  
Stimulation Of

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.

Exercise decreases aberrant corticostriatal plasticity in an animal model of L-DOPA-induced dyskinesia

2021 ◽  
Author(s):  
Ana E. Speck ◽  
Aderbal S. Aguiar ◽  
Samira G. Ferreira ◽  
Henrique B. Silva ◽  
Angelo R. Tomé ◽  
...  
Keyword(s):  
Animal Model ◽  
Physical Exercise ◽  
Long Term Potentiation ◽  
Moderate Intensity ◽  
Murine Models ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Corticostriatal Plasticity ◽  
6 Hydroxydopamine

Physical exercise attenuates the development of L-DOPA-induced dyskinesia (LID) in 6-hydroxydopamine-induced hemiparkinsonian mice through unknown mechanisms. We now tested if exercise normalizes the aberrant corticostriatal neuroplasticity associated with experimental murine models of LID. C57BL/6 mice received two unilateral intrastriatal injections of 6-hydroxydopamine (12 μg) and were treated after three weeks with L-DOPA/benserazide (25/12.5 mg/kg) for four weeks, with individualized moderate-intensity running (60-70% V̇O2peak) or not (untrained). L-DOPA converted the pattern of plasticity in corticostriatal synapses from a long-term depression (LTD) into a long-term potentiation (LTP). Exercise reduced LID severity and decreased aberrant LTP. These results suggest that exercise attenuates abnormal corticostriatal plasticity to decrease LID.

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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