The Role of Norepinephrine in Long-Term Potentiation at Mossy-Fiber Synapses in the Hippocampus

1989 ◽  
pp. 307-328 ◽  
Author(s):  
Daniel Johnston ◽  
William F. Hopkins ◽  
Richard Gray
PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0165257 ◽  
Author(s):  
Akira Minami ◽  
Masakazu Saito ◽  
Shou Mamada ◽  
Daisuke Ieno ◽  
Tomoya Hikita ◽  
...  

Neuron ◽  
1994 ◽  
Vol 12 (2) ◽  
pp. 261-269 ◽  
Author(s):  
Pablo E. Castillo ◽  
Marc G. Weisskopf ◽  
Roger A. Nicoll

1995 ◽  
Vol 131 (6) ◽  
pp. 1789-1800 ◽  
Author(s):  
Y Takei ◽  
A Harada ◽  
S Takeda ◽  
K Kobayashi ◽  
S Terada ◽  
...  

Synapsin I is one of the major synaptic vesicle-associated proteins. Previous experiments implicated its crucial role in synaptogenesis and transmitter release. To better define the role of synapsin I in vivo, we used gene targeting to disrupt the murine synapsin I gene. Mutant mice lacking synapsin I appeared to develop normally and did not have gross anatomical abnormalities. However, when we examined the presynaptic structure of the hippocampal CA3 field in detail, we found that the sizes of mossy fiber giant terminals were significantly smaller, the number of synaptic vesicles became reduced, and the presynaptic structures altered, although the mossy fiber long-term potentiation remained intact. These results suggest significant contribution of synapsin I to the formation and maintenance of the presynaptic structure.


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.


Hippocampus ◽  
2013 ◽  
Vol 23 (6) ◽  
pp. 529-543 ◽  
Author(s):  
Grzegorz Wiera ◽  
Grazyna Wozniak ◽  
Malgorzata Bajor ◽  
Leszek Kaczmarek ◽  
Jerzy W. Mozrzymas

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.


Sign in / Sign up

Export Citation Format

Share Document