The effect of NMDA-NR2B receptor subunit over-expression on olfactory memory task performance in the mouse

2004 ◽  
Vol 1021 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Theresa L. White ◽  
Steven L. Youngentob
2004 ◽  
Vol 371 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Ruth O’Donnell ◽  
Sylvain Molon-Noblot ◽  
Philippe Laroque ◽  
Michael Rigby ◽  
David Smith

2003 ◽  
Vol 89 (2) ◽  
pp. 822-832 ◽  
Author(s):  
Erik Harvey-Girard ◽  
Robert J. Dunn

The amino acid sequence of the N-methyl-d-aspartate (NMDA) receptor subunit NR2B from the brown ghost knife fish Apteronotus leptorhynchus has been determined and compared with the sequence of the murine NR2B. This comparison revealed high levels of sequence conservation throughout the ligand binding and membrane spanning segments. The functional properties of the NR1 and NR2B receptor complex were examined by coexpression in HEK cells. The recombinant AptNR1/NR2B receptors produced robust currents after stimulation with glutamate or NMDA in the presence of glycine. Measurements of the concentration dependencies for these agonists indicated that the agonist binding sites on the apteronotid receptor are highly conserved, with nearly identical agonist affinities to those of the murine NR1/NR2B receptor. The kinetic responses of the fish receptor were also highly conserved, with deactivation rates for the AptNR2B receptor matching those of the murine NR2B containing receptor. Evidently, most of the unique functional properties that reside in the NR2B receptor subunit have been well conserved in teleost NMDA receptors. On the other hand, the apteronitid receptor displayed a lowered sensitivity to voltage-dependent Mg2+ block and a reduced affinity for the NR2B-specific noncompetitive antagonist ifenprodil. We conclude that the functional properties that result from the incorporation of the NR2B receptor in the NMDA receptor complex have been maintained since the evolutionary divergence of teleost and mammalian organisms.


2006 ◽  
Vol 399 (1-2) ◽  
pp. 157-161 ◽  
Author(s):  
Paula I. Fuller ◽  
Courtney Reddrop ◽  
Jennifer Rodger ◽  
Mark C. Bellingham ◽  
Jacqueline K. Phillips

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Mukta Chakraborty ◽  
Liang-Fu Chen ◽  
Emma E. Fridel ◽  
Marguerita E. Klein ◽  
Rebecca A. Senft ◽  
...  

Author(s):  
Maryam Daniali ◽  
Dario D. Salvucci ◽  
Maria T. Schultheis

Concussions are common cognitive impairments, but their effects on task performance in general, and on driving in particular, are not well understood. To better understand the effects of concussion on driving, we investigated previously gathered data on twenty-two people with a concussion, driving in a virtual-reality driving simulator (VRDS), and twenty-two non-concussed matched drivers. Participants were asked to per-form a behavioral task (either coin sorting or a verbal memory task) while driving. In this study, we chose a few common metrics from the VRDS and tracked their changes through time for each participant. Our pro-posed method—namely, the use of convolutional neural networks for classification and analysis—can accu-rately classify concussed driving and extract local features on driving sequences that translate to behavioral driving signatures. Overall, our method improves identification and understanding of clinically relevant driv-ing behaviors for concussed individuals and should generalize well to other types of impairments.


2021 ◽  
Vol 11 (7) ◽  
pp. 935
Author(s):  
Ying Xing Feng ◽  
Masashi Kiguchi ◽  
Wei Chun Ung ◽  
Sarat Chandra Dass ◽  
Ahmad Fadzil Mohd Hani ◽  
...  

The effect of stress on task performance is complex, too much or too little stress negatively affects performance and there exists an optimal level of stress to drive optimal performance. Task difficulty and external affective factors are distinct stressors that impact cognitive performance. Neuroimaging studies showed that mood affects working memory performance and the correlates are changes in haemodynamic activity in the prefrontal cortex (PFC). We investigate the interactive effects of affective states and working memory load (WML) on working memory task performance and haemodynamic activity using functional near-infrared spectroscopy (fNIRS) neuroimaging on the PFC of healthy participants. We seek to understand if haemodynamic responses could tell apart workload-related stress from situational stress arising from external affective distraction. We found that the haemodynamic changes towards affective stressor- and workload-related stress were more dominant in the medial and lateral PFC, respectively. Our study reveals distinct affective state-dependent modulations of haemodynamic activity with increasing WML in n-back tasks, which correlate with decreasing performance. The influence of a negative effect on performance is greater at higher WML, and haemodynamic activity showed evident changes in temporal, and both spatial and strength of activation differently with WML.


2004 ◽  
Vol 92 (4) ◽  
pp. 2610-2614 ◽  
Author(s):  
Leonardo Coutinho Faria ◽  
Istvan Mody

In the brain, spreading depression (SD) is characterized by a large extracellular DC shift, a massive failure of ion homeostasis and a transient cessation of neuronal function. Clinically, SD is believed to be involved in various neurological disorders including migraine and cerebrovascular diseases. The propagation of cortical SD requires the release of glutamate, and N-methyl-d-aspartate (NMDA) receptors play a crucial role in this process. Here, we have isolated the NMDA receptor-mediated component of extracellularly recorded field excitatory postsynaptic potentials (fEPSPs) in layers 2–3 of the entorhinal cortex of murine brain slices. In the absence of GABAA and AMPA receptor-mediated synaptic transmission, stimulation of layer 6 afferents every 15–90 s elicited spontaneous SD on average within 18.5 min after the start of the stimulation. In the presence of ifenprodil, an NR2B receptor subunit-selective NMDA receptor antagonist, the occurrence of SD was nearly abolished. Our results are consistent with an important role of NR2B subunits in triggering SD in the entorhinal cortex.


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