Thalamic NMDA receptors and nociceptive sensory synaptic transmission

1990 ◽  
Vol 110 (3) ◽  
pp. 297-302 ◽  
Author(s):  
S.A. Eaton ◽  
T.E. Salt
2012 ◽  
Vol 107 (6) ◽  
pp. 1571-1575 ◽  
Author(s):  
Andrew J. Delaney ◽  
John M. Power ◽  
Pankaj Sah

Ifenprodil is a selective blocker of NMDA receptors that are heterodimers composed of GluN1/GluN2B subunits. This pharmacological profile has been extensively used to test the role of GluN2B-containing NMDA receptors in learning and memory formation. However, ifenprodil has also been reported to have actions at a number of other receptors, including high voltage-activated calcium channels. Here we show that, in the basolateral amygdala, ifenprodil dose dependently blocks excitatory transmission to principal neurons by a presynaptic mechanism. This action of ifenprodil has an IC50 of ∼10 μM and is fully occluded by the P/Q type calcium channel blocker ω-agatoxin. We conclude that ifenprodil reduces synaptic transmission in the basolateral amygdala by partially blocking P-type voltage-dependent calcium channels.


Hippocampus ◽  
2009 ◽  
Vol 19 (9) ◽  
pp. 779-789 ◽  
Author(s):  
Kai Yang ◽  
Catherine H. Trepanier ◽  
Hongbin Li ◽  
Michael A. Beazely ◽  
Ethan A. Lerner ◽  
...  

1997 ◽  
Vol 322 (2-3) ◽  
pp. 173-178 ◽  
Author(s):  
Nicholas A Breakwell ◽  
LingQian Huang ◽  
Michael J Rowan ◽  
Roger Anwyl

2008 ◽  
Vol 12 (6) ◽  
pp. 293 ◽  
Author(s):  
Hyeong Seok Cho ◽  
Hyun Ho Lee ◽  
Se Joon Choi ◽  
Ki Jung Kim ◽  
Seung Hyun Jeun ◽  
...  

2021 ◽  
Vol 22 (4) ◽  
pp. 1536
Author(s):  
Pietro Micheli ◽  
Rui Ribeiro ◽  
Alejandro Giorgetti

Inside hippocampal circuits, neuroplasticity events that individual cells may undergo during synaptic transmissions occur in the form of Long-Term Potentiation (LTP) and Long-Term Depression (LTD). The high density of NMDA receptors expressed on the surface of the dendritic CA1 spines confers to hippocampal CA3-CA1 synapses the ability to easily undergo NMDA-mediated LTP and LTD, which is essential for some forms of explicit learning in mammals. Providing a comprehensive kinetic model that can be used for running computer simulations of the synaptic transmission process is currently a major challenge. Here, we propose a compartmentalized kinetic model for CA3-CA1 synaptic transmission. Our major goal was to tune our model in order to predict the functional impact caused by disease associated variants of NMDA receptors related to severe cognitive impairment. Indeed, for variants Glu413Gly and Cys461Phe, our model predicts negative shifts in the glutamate affinity and changes in the kinetic behavior, consistent with experimental data. These results point to the predictive power of this multiscale viewpoint, which aims to integrate the quantitative kinetic description of large interaction networks typical of system biology approaches with a focus on the quality of a few, key, molecular interactions typical of structural biology ones.


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