scholarly journals The Endocannabinoid System as a Potential Mechanism through which Exercise Influences Episodic Memory Function

2019 ◽  
Vol 9 (5) ◽  
pp. 112 ◽  
Author(s):  
Paul D. Loprinzi ◽  
Liye Zou ◽  
Hong Li

Emerging research demonstrates that exercise, including both acute and chronic exercise, may influence episodic memory function. To date, mechanistic explanations of this effect are often attributed to alterations in long-term potentiation, neurotrophic production, angiogenesis, and neurogenesis. Herein, we discuss a complementary mechanistic model, suggesting that the endocannabinoid system may, in part, influence the effects of exercise on memory function. We discuss the role of the endocannabinoid system on memory function as well as the effects of exercise on endocannabinoid alterations. This is an exciting line of inquiry that should help delineate new insights into the mechanistic role of exercise on memory function.

2019 ◽  
Vol 106 (1) ◽  
pp. 21-28 ◽  
Author(s):  
PD Loprinzi

This review discusses the potential role that glial cells may play in influencing the relationship between exercise and episodic memory function. A narrative review methodology is employed. Herein, the different types of glial cells, their implications in subserving episodic memory function, and how exercise can modulate glial cell activity, particularly astrocyte functionality, are discussed. Although additional experimental work is needed, astrocytes appear to play an important role in the exercise–memory interaction. Exercise may increase astrocytic size, attenuate astrogliodegeneration, improve astrocytic aquaporin-4 expression, and increase astrocytic transporter levels. These effects, in turn, may help to increase the number of synapses that neurons form, increase the number of synaptic structures, and increase presynaptic function and postsynaptic receptor localization. Ultimately, these effects may help influence long-term potentiation and episodic memory function.


Author(s):  
Sujeong Yang ◽  
Sylvain Gigout ◽  
Angelo Molinaro ◽  
Yuko Naito-Matsui ◽  
Sam Hilton ◽  
...  

AbstractPerineuronal nets (PNNs) are chondroitin sulphate proteoglycan-containing structures on the neuronal surface that have been implicated in the control of neuroplasticity and memory. Age-related reduction of chondroitin 6-sulphates (C6S) leads to PNNs becoming more inhibitory. Here, we investigated whether manipulation of the chondroitin sulphate (CS) composition of the PNNs could restore neuroplasticity and alleviate memory deficits in aged mice. We first confirmed that aged mice (20-months) showed memory and plasticity deficits. They were able to retain or regain their cognitive ability when CSs were digested or PNNs were attenuated. We then explored the role of C6S in memory and neuroplasticity. Transgenic deletion of chondroitin 6-sulfotransferase (chst3) led to a reduction of permissive C6S, simulating aged brains. These animals showed very early memory loss at 11 weeks old. Importantly, restoring C6S levels in aged animals rescued the memory deficits and restored cortical long-term potentiation, suggesting a strategy to improve age-related memory impairment.


2017 ◽  
Vol 23 (6) ◽  
pp. 587-604 ◽  
Author(s):  
Julien Gibon ◽  
Philip A. Barker

Neurotrophins have been intensively studied and have multiple roles in the brain. Neurotrophins are first synthetized as proneurotrophins and then cleaved intracellularly and extracellularly. Increasing evidences demonstrate that proneurotrophins and mature neurotrophins exerts opposing role in the central nervous system. In the present review, we explore the role of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4) and their respective proform in cellular processes related to learning and memory. We focused on their roles in synaptic activity and plasticity in the brain with an emphasis on long-term potentiation, long-term depression, and basal synaptic transmission in the hippocampus and the temporal lobe area. We also discuss new findings on the role of the Val66Met polymorphism on the BDNF propeptide on synaptic activity.


1996 ◽  
Vol 3 (1) ◽  
pp. 42-48 ◽  
Author(s):  
D K Selig ◽  
M R Segal ◽  
D Liao ◽  
R C Malenka ◽  
R Malinow ◽  
...  

2000 ◽  
Vol 20 (24) ◽  
pp. 9272-9276 ◽  
Author(s):  
Albert M. Borroni ◽  
Harlan Fichtenholtz ◽  
Brian L. Woodside ◽  
Timothy J. Teyler

2002 ◽  
Vol 22 (13) ◽  
pp. 5432-5441 ◽  
Author(s):  
Kobi Rosenblum ◽  
Marie Futter ◽  
Karen Voss ◽  
Muriel Erent ◽  
Paul A. Skehel ◽  
...  

Physiology ◽  
2006 ◽  
Vol 21 (5) ◽  
pp. 346-351 ◽  
Author(s):  
Stefan Krueger ◽  
Reiko Maki Fitzsimonds

The cellular mechanisms contributing to long-term potentiation and activity-induced formation of glutamatergic synapses have been intensely debated. Recent studies have sparked renewed interest in the role of presynaptic components in these processes. Based on the present evidence, it appears likely that long-term plasticity utilizes both pre- and postsynaptic expression mechanisms.


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