scholarly journals MPTP modulates hippocampal synaptic transmission and activity-dependent synaptic plasticity via dopamine receptors

2012 ◽  
Vol 122 (3) ◽  
pp. 582-593 ◽  
Author(s):  
GuoQi Zhu ◽  
YuYing Huang ◽  
Ying Chen ◽  
YingHan Zhuang ◽  
Thomas Behnisch
2006 ◽  
Vol 290 (5) ◽  
pp. R1175-R1182 ◽  
Author(s):  
Dionysia T. Theodosis ◽  
Andrei Trailin ◽  
Dominique A. Poulain

Neurons, including their synapses, are generally ensheathed by fine processes of astrocytes, but this glial coverage can be altered under different physiological conditions that modify neuronal activity. Changes in synaptic connectivity accompany astrocytic transformations so that an increased number of synapses are associated with reduced astrocytic coverage of postsynaptic elements, whereas synaptic numbers are reduced on reestablishment of glial coverage. A system that exemplifies activity-dependent structural synaptic plasticity in the adult brain is the hypothalamo-neurohypophysial system, and in particular, its oxytocin component. Under strong, prolonged activation (parturition, lactation, chronic dehydration), extensive portions of somatic and dendritic surfaces of magnocellular oxytocin neurons are freed of intervening astrocytic processes and become directly juxtaposed. Concurrently, they are contacted by an increased number of inhibitory and excitatory synapses. Once stimulation is over, astrocytic processes again cover oxytocinergic surfaces and synaptic numbers return to baseline levels. Such observations indicate that glial ensheathment of neurons is of consequence to neuronal function, not only directly, for example by modifying synaptic transmission, but indirectly as well, by preparing neuronal surfaces for synapse turnover.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Emily Petrus ◽  
Hey-Kyoung Lee

Alzheimer’s disease (AD) is the most common form of age-related dementia, which is thought to result from overproduction and/or reduced clearance of amyloid-beta (Aβ) peptides. Studies over the past few decades suggest that Aβis produced in an activity-dependent manner and has physiological relevance to normal brain functions. Similarly, physiological functions forβ- andγ-secretases, the two key enzymes that produce Aβby sequentially processing the amyloid precursor protein (APP), have been discovered over recent years. In particular, activity-dependent production of Aβhas been suggested to play a role in homeostatic regulation of excitatory synaptic function. There is accumulating evidence that activity-dependent immediate early gene Arc is an activity “sensor,” which acts upstream of Aβproduction and triggers AMPA receptor endocytosis to homeostatically downregulate the strength of excitatory synaptic transmission. We previously reported that Arc is critical for sensory experience-dependent homeostatic reduction of excitatory synaptic transmission in the superficial layers of visual cortex. Here we demonstrate that mice lacking the major neuronalβ-secretase, BACE1, exhibit a similar phenotype: stronger basal excitatory synaptic transmission and failure to adapt to changes in visual experience. Our results indicate that BACE1 plays an essential role in sensory experience-dependent homeostatic synaptic plasticity in the neocortex.


BIOspektrum ◽  
2020 ◽  
Vol 26 (6) ◽  
pp. 600-602
Author(s):  
Marta Zagrebelsky

Abstract Activity-dependent plastic changes at synapses are essential for learning, but maintaining memory traces requires stable neuronal networks. The balance between plasticity and stability of the brain circuitry is tightly regulated. Among the mechanisms involved in regulating neuronal plasticity is the modulation of excitation and inhibition. Nogo-A was recently described for its ability to limit synaptic plasticity and to reciprocally regulate excitatory and inhibitory synaptic transmission.


2011 ◽  
Vol 254 (3) ◽  
pp. 332-341 ◽  
Author(s):  
GuoQi Zhu ◽  
Ying Chen ◽  
YuYing Huang ◽  
QingLin Li ◽  
Thomas Behnisch

2006 ◽  
Vol 573 (3) ◽  
pp. 711-721 ◽  
Author(s):  
Aude Panatier ◽  
Stephen J. Gentles ◽  
Charles W. Bourque ◽  
Stéphane H. R. Oliet

2022 ◽  
Author(s):  
Alberto Lazari ◽  
Piergiorgio Salvan ◽  
Michiel Cottaar ◽  
Daniel Papp ◽  
Matthew FS Rushworth ◽  
...  

Synaptic plasticity is required for learning and follows Hebb's Rule, the computational principle underpinning associative learning. In recent years, a complementary type of brain plasticity has been identified in myelinated axons, which make up the majority of brain's white matter. Like synaptic plasticity, myelin plasticity is required for learning, but it is unclear whether it is Hebbian or whether it follows different rules. Here, we provide evidence that white matter plasticity operates following Hebb's Rule in humans. Across two experiments, we find that co-stimulating cortical areas to induce Hebbian plasticity leads to relative increases in cortical excitability and associated increases in a myelin marker within the stimulated fiber bundle. We conclude that Hebbian plasticity extends beyond synaptic changes, and can be observed in human white matter fibers.


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