High-frequency stimulation of the temporoammonic pathway induces input-specific long-term potentiation in subicular bursting cells

2012 ◽  
Vol 1430 ◽  
pp. 1-7 ◽  
Author(s):  
Pawel Fidzinski ◽  
Matthias Wawra ◽  
Julia Bartsch ◽  
Uwe Heinemann ◽  
Joachim Behr
Keyword(s):  
High Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Term Potentiation ◽  
Frequency Stimulation ◽  
Stimulation Of

Electrical high-frequency stimulation of the human thoracolumbar fascia evokes long-term potentiation-like pain amplification

Pain ◽  
2016 ◽  
Vol 157 (10) ◽  
pp. 2309-2317 ◽  
Author(s):  
Andreas Schilder ◽  
Walter Magerl ◽  
Ulrich Hoheisel ◽  
Thomas Klein ◽  
Rolf-Detlef Treede
Keyword(s):  
High Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Thoracolumbar Fascia ◽  
Term Potentiation ◽  
Frequency Stimulation ◽  
Stimulation Of

scholarly journals Cholecystokinin release triggered by NMDA receptors produces LTP and sound–sound associative memory

2019 ◽  
Vol 116 (13) ◽  
pp. 6397-6406 ◽  
Author(s):  
Xi Chen ◽  
Xiao Li ◽  
Yin Ting Wong ◽  
Xuejiao Zheng ◽  
Haitao Wang ◽  
...  
Keyword(s):  
Associative Learning ◽  
Associative Memory ◽  
High Frequency ◽  
Low Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Low Frequency Stimulation ◽  
Term Potentiation ◽  
Frequency Stimulation

Memory is stored in neural networks via changes in synaptic strength mediated in part by NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). Here we show that a cholecystokinin (CCK)-B receptor (CCKBR) antagonist blocks high-frequency stimulation-induced neocortical LTP, whereas local infusion of CCK induces LTP. CCK−/−mice lacked neocortical LTP and showed deficits in a cue–cue associative learning paradigm; and administration of CCK rescued associative learning deficits. High-frequency stimulation-induced neocortical LTP was completely blocked by either the NMDAR antagonist or the CCKBR antagonist, while application of either NMDA or CCK induced LTP after low-frequency stimulation. In the presence of CCK, LTP was still induced even after blockade of NMDARs. Local application of NMDA induced the release of CCK in the neocortex. These findings suggest that NMDARs control the release of CCK, which enables neocortical LTP and the formation of cue–cue associative memory.

Sign in / Sign up

Export Citation Format

Share Document