scholarly journals Brief theta-burst stimulation induces a transcription-dependent late phase of LTP requiring cAMP in area CA1 of the mouse hippocampus.

1997 ◽  
Vol 4 (2) ◽  
pp. 230-243 ◽  
Author(s):  
P V Nguyen ◽  
E R Kandel
2014 ◽  
Vol 112 (8) ◽  
pp. 1916-1924 ◽  
Author(s):  
Guan Cao ◽  
Kristen M. Harris

Hippocampal long-term potentiation (LTP) is a model system for studying cellular mechanisms of learning and memory. Recent interest in mechanisms underlying the advantage of spaced over massed learning has prompted investigation into the effects of distributed episodes of LTP induction. The amount of LTP induced in hippocampal area CA1 by one train (1T) of theta-burst stimulation (TBS) in young Sprague-Dawley rats was further enhanced by additional bouts of 1T given at 1-h intervals. However, in young Long-Evans (LE) rats, 1T did not initially saturate LTP. Instead, a stronger LTP induction paradigm using eight trains of TBS (8T) induced saturated LTP in hippocampal slices from both young and adult LE rats as well as adult mice. The saturated LTP induced by 8T could be augmented by another episode of 8T following an interval of at least 90 min. The success rate across animals and slices in augmenting LTP by an additional episode of 8T increased significantly with longer intervals between the first and last episodes, ranging from 0% at 30- and 60-min intervals to 13–66% at 90- to 180-min intervals to 90–100% at 240-min intervals. Augmentation above initially saturated LTP was blocked by the N-methyl-d-aspartate (NMDA) glutamate receptor antagonist d-2-amino-5-phosphonovaleric acid (d-APV). These findings suggest that the strength of induction and interval between episodes of TBS, as well as the strain and age of the animal, are important components in the augmentation of LTP.


2009 ◽  
Vol 40 (01) ◽  
Author(s):  
AS Sarfeld ◽  
M Ameli ◽  
JT Teo ◽  
S Diekhoff ◽  
G Fink ◽  
...  

2014 ◽  
Vol 7 (2) ◽  
pp. 269-274 ◽  
Author(s):  
Mark F. Jacobs ◽  
Philemon Tsang ◽  
Kevin G.H. Lee ◽  
Michael J. Asmussen ◽  
Christopher M. Zapallow ◽  
...  

2014 ◽  
Vol 7 (2) ◽  
pp. 340-341 ◽  
Author(s):  
Christian Plewnia ◽  
Bastian Zwissler ◽  
Barbara Wasserka ◽  
Andreas J. Fallgatter ◽  
Stefan Klingberg

2021 ◽  
Author(s):  
Angela Sanna ◽  
Paolo Follesa ◽  
Paolo Tacconi ◽  
Mariangela Serra ◽  
Maria Giuseppina Pisu ◽  
...  

AbstractSpinocerebellar ataxia 38 (SCA 38) is an autosomal dominant disorder caused by conventional mutations in the ELOVL5 gene which encodes an enzyme involved in the synthesis of very long fatty acids, with a specific expression in cerebellar Purkinje cells. Three Italian families carrying the mutation, one of which is of Sardinian descent, have been identified and characterized. One session of cerebellar intermittent theta burst stimulation (iTBS) was applied to 6 affected members of the Sardinian family to probe motor cortex excitability measured by motor-evoked potentials (MEPs). Afterwards, patients were exposed to ten sessions of cerebellar real and sham iTBS in a cross-over study and clinical symptoms were evaluated before and after treatment by Modified International Cooperative Ataxia Rating Scale (MICARS). Moreover, serum BDNF levels were evaluated before and after real and sham cerebellar iTBS and the role of BDNF Val66Met polymorphism in influencing iTBS effect was explored. Present data show that one session of cerebellar iTBS was able to increase MEPs in all tested patients, suggesting an enhancement of the cerebello-thalamo-cortical pathway in SCA 38. MICARS scores were reduced after ten sessions of real cerebellar iTBS showing an improvement in clinical symptoms. Finally, although serum BDNF levels were not affected by cerebellar iTBS when considering all samples, segregating for genotype a difference was found between Val66Val and Val66Met carriers. These preliminary data suggest a potential therapeutic use of cerebellar iTBS in improving motor symptoms of SCA38.


Author(s):  
Melanie L. Bozzay ◽  
Sydney Brigido ◽  
Mascha van ’t Wout-Frank ◽  
Emily Aiken ◽  
Robert Swift ◽  
...  

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