Differential expression of molecular markers of synaptic plasticity in the hippocampus, prefrontal cortex, and amygdala in response to spatial learning, predator exposure, and stress-induced amnesia

Hippocampus ◽  
2011 ◽  
Vol 22 (3) ◽  
pp. 577-589 ◽  
Author(s):  
Phillip R. Zoladz ◽  
Collin R. Park ◽  
Joshua D. Halonen ◽  
Samina Salim ◽  
Karem H. Alzoubi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Molecular Markers ◽  
Synaptic Plasticity ◽  
Differential Expression ◽  
Spatial Learning

scholarly journals Treadmill Exercise Prevents Decline in Spatial Learning and Memory in 3×Tg-AD Mice through Enhancement of Structural Synaptic Plasticity of the Hippocampus and Prefrontal Cortex

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 244
Author(s):  
Lianwei Mu ◽  
Jiajia Cai ◽  
Boya Gu ◽  
Laikang Yu ◽  
Cui Li ◽  
...  
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Treadmill Exercise ◽  
Spatial Working Memory ◽  
Spatial Learning And Memory ◽  
Pathological Feature ◽  
Dendritic Complexity

Alzheimer’s disease (AD) is characterized by deficits in learning and memory. A pathological feature of AD is the alterations in the number and size of synapses, axon length, dendritic complexity, and dendritic spine numbers in the hippocampus and prefrontal cortex. Treadmill exercise can enhance synaptic plasticity in mouse or rat models of stroke, ischemia, and dementia. The aim of this study was to examine the effects of treadmill exercise on learning and memory, and structural synaptic plasticity in 3×Tg-AD mice, a mouse model of AD. Here, we show that 12 weeks treadmill exercise beginning in three-month-old mice improves spatial working memory in six-month-old 3×Tg-AD mice, while non-exercise six-month-old 3×Tg-AD mice exhibited impaired spatial working memory. To investigate potential mechanisms for the treadmill exercise-induced improvement of spatial learning and memory, we examined structural synaptic plasticity in the hippocampus and prefrontal cortex of six-month-old 3×Tg-AD mice that had undergone 12 weeks of treadmill exercise. We found that treadmill exercise led to increases in synapse numbers, synaptic structural parameters, the expression of synaptophysin (Syn, a presynaptic marker), the axon length, dendritic complexity, and the number of dendritic spines in 3×Tg-AD mice and restored these parameters to similar levels of non-Tg control mice without treadmill exercise. In addition, treadmill exercise also improved these parameters in non-Tg control mice. Strengthening structural synaptic plasticity may represent a potential mechanism by which treadmill exercise prevents decline in spatial learning and memory and synapse loss in 3×Tg-AD mice.

scholarly journals BAI1 regulates spatial learning and synaptic plasticity in the hippocampus

2015 ◽  
Vol 125 (4) ◽  
pp. 1497-1508 ◽  
Author(s):  
Dan Zhu ◽  
Chenchen Li ◽  
Andrew M. Swanson ◽  
Rosa M. Villalba ◽  
Jidong Guo ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Learning

Interleukin-18 regulates motor activity, anxiety and spatial learning without affecting synaptic plasticity

2010 ◽  
Vol 206 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Takahiro Yaguchi ◽  
Tetsu Nagata ◽  
Dongqin Yang ◽  
Tomoyuki Nishizaki
Keyword(s):  
Synaptic Plasticity ◽  
Motor Activity ◽  
Spatial Learning ◽  
Interleukin 18

scholarly journals Synapse Plasticity in Motor, Sensory, and Limbo-Prefrontal Cortex Areas as Measured by Degrading Axon Terminals in an Environment Model of Gerbils (Meriones unguiculatus)

2009 ◽  
Vol 2009 ◽  
pp. 1-14 ◽  
Author(s):  
Janina Neufeld ◽  
Gertraud Teuchert-Noodt ◽  
Keren Grafen ◽  
York Winter ◽  
A. Veronica Witte
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Meriones Unguiculatus ◽  
Secondary Lysosome ◽  
Axon Terminals ◽  
Environment Model ◽  
Naturally Occurring ◽  
Synapse Plasticity ◽  
Map Adaptation ◽  
Cortical Map

Still little is known about naturally occurring synaptogenesis in the adult neocortex and related impacts of epigenetic influences. We therefore investigated (pre)synaptic plasticity in various cortices of adult rodents, visualized by secondary lysosome accumulations (LA) in remodeling axon terminals. Twenty-two male gerbils from either enriched (ER) or impoverished rearing (IR) were used for quantification of silver-stained LA. ER-animals showed rather low LA densities in most primary fields, whereas barrel and secondary/associative cortices exhibited higher densities and layer-specific differences. In IR-animals, these differences were evened out or even inverted. Basic plastic capacities might be linked with remodeling of local intrinsic circuits in the context of cortical map adaptation in both IR- and ER-animals. Frequently described disturbances due to IR in multiple corticocortical and extracortical afferent systems, including the mesocortical dopamine projection, might have led to maladaptations in the plastic capacities of prefronto-limbic areas, as indicated by different LA densities in IR- compared with ER-animals.

scholarly journals Tripchlorolide May Improve Spatial Cognition Dysfunction and Synaptic Plasticity after Chronic Cerebral Hypoperfusion

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Zhao-Hui Yao ◽  
Xiao-li Yao ◽  
Shao-feng Zhang ◽  
Ji-chang Hu ◽  
Yong Zhang
Keyword(s):  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Long Term Potentiation ◽  
Chronic Cerebral Hypoperfusion ◽  
Synaptic Proteins ◽  
Cerebral Hypoperfusion ◽  
Spatial Learning And Memory ◽  
Pathophysiological Mechanism

Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism that underlies cognitive decline and degenerative processes in dementia and other neurodegenerative diseases. Low cerebral blood flow (CBF) during CCH leads to disturbances in the homeostasis of hemodynamics and energy metabolism, which in turn results in oxidative stress, astroglia overactivation, and synaptic protein downregulation. These events contribute to synaptic plasticity and cognitive dysfunction after CCH. Tripchlorolide (TRC) is an herbal compound with potent neuroprotective effects. The potential of TRC to improve CCH-induced cognitive impairment has not yet been determined. In the current study, we employed behavioral techniques, electrophysiology, Western blotting, immunofluorescence, and Golgi staining to investigate the effect of TRC on spatial learning and memory impairment and on synaptic plasticity changes in rats after CCH. Our findings showed that TRC could rescue CCH-induced spatial learning and memory dysfunction and improve long-term potentiation (LTP) disorders. We also found that TRC could prevent CCH-induced reductions in N-methyl-D-aspartic acid receptor 2B, synapsin I, and postsynaptic density protein 95 levels. Moreover, TRC upregulated cAMP-response element binding protein, which is an important transcription factor for synaptic proteins. TRC also prevented the reduction in dendritic spine density that is caused by CCH. However, sham rats treated with TRC did not show any improvement in cognition. Because CCH causes disturbances in brain energy homeostasis, TRC therapy may resolve this instability by correcting a variety of cognitive-related signaling pathways. However, for the normal brain, TRC treatment led to neither disturbance nor improvement in neural plasticity. Additionally, this treatment neither impaired nor further improved cognition. In conclusion, we found that TRC can improve spatial learning and memory, enhance synaptic plasticity, upregulate the expression of some synaptic proteins, and increase the density of dendritic spines. Our findings suggest that TRC may be beneficial in the treatment of cognitive impairment induced by CCH.

Interleukin 6 Dependent Synaptic Plasticity in a Social Defeat-Susceptible Prefrontal Cortex Circuit

Neuroscience ◽  
2019 ◽  
Vol 414 ◽  
pp. 280-296
Author(s):  
Eric Esquivel-Rendón ◽  
Jorge Vargas-Mireles ◽  
Roberto Cuevas-Olguín ◽  
Marcela Miranda-Morales ◽  
Palmira Acosta-Mares ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Interleukin 6 ◽  
Social Defeat
Sign in / Sign up

Export Citation Format

Share Document