Long-term exposure to environmental enrichment since youth prevents recognition memory decline and increases synaptic plasticity markers in aging

2008 ◽  
Vol 90 (3) ◽  
pp. 511-518 ◽  
Author(s):  
Perla Leal-Galicia ◽  
María Castañeda-Bueno ◽  
Ricardo Quiroz-Baez ◽  
Clorinda Arias
Keyword(s):  
Synaptic Plasticity ◽  
Recognition Memory ◽  
Environmental Enrichment ◽  
Memory Decline

scholarly journals Synergy between vesicular and non-vesicular gliotransmission regulates synaptic plasticity and working memory

2021 ◽  
Author(s):  
Ulyana Lalo ◽  
Seyed Rasooli-Nejad ◽  
Alexander Bogdanov ◽  
Lorenzo More ◽  
Wuhyun Koh ◽  
...  
Keyword(s):  
Working Memory ◽  
Synaptic Plasticity ◽  
Small Molecule ◽  
Environmental Enrichment ◽  
Pyramidal Neurons ◽  
Active Element ◽  
Spatial Working Memory ◽  
Phasic Response ◽  
Cortical Astrocytes

Astrocytes are an active element of brain signalling, capable of release of small molecule gliotransmitters by vesicular and channel-mediated mechanisms. However, specific physiological roles of astroglial exocytosis of glutamate and D-Serine remain controversial. Our data demonstrate that cortical astrocytes can release glutamate and D-Serine by combination of SNARE-dependent exocytosis and non-vesicular mechanisms dependent on TREK-1 and Best1 channels. Astrocyte-derived glutamate and D-serine elicited complex multicomponent phasic response in neocortical pyramidal neurons, which is mediated by extra-synaptic GluN2B receptors. Impairment of either pathway of gliotransmission (in the TREK1 KO, Best-1 KO or dnSNARE mice) strongly affected the NMDAR-dependent long-term synaptic plasticity in the hippocampus and neocortex. Moreover, impairment of astroglial exocytosis in dnSNARE mice led to the deficit in the spatial working memory which was rescued by environmental enrichment. We conclude that synergism between vesicular and non-vesicular gliotransmission is crucial for astrocyte-neuron communication and astroglia-driven regulation of synaptic plasticity and memory.

scholarly journals Visual recognition memory, manifested as long-term habituation, requires synaptic plasticity in V1

2015 ◽  
Vol 18 (2) ◽  
pp. 262-271 ◽  
Author(s):  
Sam F Cooke ◽  
Robert W Komorowski ◽  
Eitan S Kaplan ◽  
Jeffrey P Gavornik ◽  
Mark F Bear
Keyword(s):  
Synaptic Plasticity ◽  
Recognition Memory ◽  
Visual Recognition ◽  
Visual Recognition Memory

scholarly journals Erratum: Visual recognition memory, manifested as long-term habituation, requires synaptic plasticity in V1

2015 ◽  
Vol 18 (6) ◽  
pp. 926-926 ◽  
Author(s):  
Sam F Cooke ◽  
Robert W Komorowski ◽  
Eitan S Kaplan ◽  
Jeffrey P Gavornik ◽  
Mark F Bear
Keyword(s):  
Synaptic Plasticity ◽  
Recognition Memory ◽  
Visual Recognition ◽  
Visual Recognition Memory

scholarly journals Astroglia-Derived BDNF and MSK-1 Mediate Experience- and Diet-Dependent Synaptic Plasticity

2020 ◽  
Vol 10 (7) ◽  
pp. 462
Author(s):  
Ulyana Lalo ◽  
Alexander Bogdanov ◽  
Guy W. Moss ◽  
Yuriy Pankratov
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Environmental Enrichment ◽  
Aging Brain ◽  
Excitatory Synapses ◽  
Calcium Dependent ◽  
Beneficial Effects ◽  
Cortical Synapses ◽  
The Impact

Experience- and diet-dependent regulation of synaptic plasticity can underlie beneficial effects of active lifestyle on the aging brain. Our previous results demonstrate a key role for brain-derived neurotrophic factor (BDNF) and MSK1 kinase in experience-related homeostatic synaptic scaling. Astroglia has been recently shown to release BDNF via a calcium-dependent mechanism. To elucidate a role for astroglia-derived BDNF in homeostatic synaptic plasticity in the aging brain, we explored the experience- and diet-related alterations of synaptic transmission and plasticity in transgenic mice with impairment of the BDNF/MSK1 pathway (MSK1 kinase dead knock-in mice, MSK1 KD) and impairment of glial exocytosis (dnSNARE mice). We found that prolonged tonic activation of astrocytes caused BDNF-dependent increase in the efficacy of excitatory synapses accompanied by enlargement of synaptic boutons. We also observed that exposure to environmental enrichment (EE) and caloric restriction (CR) enhanced the Ca2+ signalling in cortical astrocytes and strongly up-regulated the excitatory and down-regulated inhibitory synaptic currents in old wild-type mice, thus counterbalancing the impact of ageing on astroglial and synaptic signalling. The EE- and CR-induced up-scaling of excitatory synaptic transmission in neocortex was accompanied by the enhancement of long-term synaptic potentiation. Importantly, effects of EE and CR on synaptic transmission and plasticity was significantly reduced in the MSK1 KD and dnSNARE mice. Combined, our results suggest that astroglial release of BDNF is important for the homeostatic regulation of cortical synapses and beneficial effects of EE and CR on synaptic transmission and plasticity in aging brain.

Environmental enrichment improves long-term memory impairment and aberrant synaptic plasticity by BDNF/TrkB signaling in nerve-injured mice

2019 ◽  
Vol 694 ◽  
pp. 93-98 ◽  
Author(s):  
Xing-Ming Wang ◽  
Wei Pan ◽  
Ning Xu ◽  
Zhi-Qiang Zhou ◽  
Guang-Fen Zhang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Memory Impairment ◽  
Environmental Enrichment ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Long-term potentiation and the ageing brain

2003 ◽  
Vol 358 (1432) ◽  
pp. 765-772 ◽  
Author(s):  
C. A. Barnes
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Therapeutic Approaches ◽  
Memory Decline ◽  
Memory Impairments ◽  
Age Related ◽  
Term Potentiation ◽  
Normal Ageing ◽  
Ageing Brain

Ageing is associated with learning and memory impairments. Data are reviewed that suggest that age-related impairments of hippocampal-dependent forms of memory, may be caused, in part, by altered synaptic plasticity mechanisms in the hippocampus, including long-term potentiation (LTP). To the extent that the mechanisms responsible for LTP can be understood, it may be possible to develop therapeutic approaches to alleviate memory decline in normal ageing.

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