Preconceptions and prerequisites: Understanding the function of synaptic plasticity will also depend on a better systems-level understanding of the multiple types of memory

1997 ◽  
Vol 20 (4) ◽  
pp. 624-625 ◽  
Author(s):  
Richard G. M. Morris
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Function ◽  
Nmda Receptor ◽  
Receptor Function ◽  
Relevant Evidence ◽  
Learning Hypothesis ◽  
Nmda Receptor Function

Although it is not their fault, Shors & Matzel's attempt to review the LTP and learning hypothesis suffers from there being no clear published statement of the idea. Their summary of relevant evidence is not without error, however, and it oversimplifies fundamental issues relating to NMDA receptor function. Their attentional hypothesis is intriguing but requires a better systems-level understanding of how attention contributes to cognitive function.

scholarly journals Enhancing NMDA Receptor Function: Recent Progress on Allosteric Modulators

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Lulu Yao ◽  
Qiang Zhou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Nmda Receptor ◽  
Recent Progress ◽  
Brain Diseases ◽  
Allosteric Modulators ◽  
Receptor Function ◽  
Nmda Receptor Function ◽  
Excitatory Neurotransmission

The N-methyl-D-aspartate receptors (NMDARs) are subtype glutamate receptors that play important roles in excitatory neurotransmission and synaptic plasticity. Their hypo- or hyperactivation are proposed to contribute to the genesis or progression of various brain diseases, including stroke, schizophrenia, depression, and Alzheimer’s disease. Past efforts in targeting NMDARs for therapeutic intervention have largely been on inhibitors of NMDARs. In light of the discovery of NMDAR hypofunction in psychiatric disorders and perhaps Alzheimer’s disease, efforts in boosting NMDAR activity/functions have surged in recent years. In this review, we will focus on enhancing NMDAR functions, especially on the recent progress in the generation of subunit-selective, allosteric positive modulators (PAMs) of NMDARs. We shall also discuss the usefulness of these newly developed NMDAR-PAMs.

scholarly journals Protein kinase A-dependent enhanced NMDA receptor function in pain-related synaptic plasticity in rat amygdala neurones

2005 ◽  
Vol 564 (3) ◽  
pp. 907-921 ◽  
Author(s):  
Gary C. Bird ◽  
L. Leanne Lash ◽  
Jeong S. Han ◽  
Xiaoju Zou ◽  
William D. Willis ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Nmda Receptor ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Receptor Function ◽  
Nmda Receptor Function ◽  
Kinase A

Effect of transgenic overexpression of NR2B on NMDA receptor function and synaptic plasticity in visual cortex

2001 ◽  
Vol 41 (6) ◽  
pp. 762-770 ◽  
Author(s):  
Benjamin D. Philpot ◽  
Michael P. Weisberg ◽  
Margarita S. Ramos ◽  
Nathaniel B. Sawtell ◽  
Ya-Ping Tang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Nmda Receptor ◽  
Receptor Function ◽  
Nmda Receptor Function

scholarly journals GPI-1046 Increases Presenilin-1 Expression and Restores NMDA Channel Activity

2010 ◽  
Vol 37 (4) ◽  
pp. 457-467 ◽  
Author(s):  
Joseph P. Steiner ◽  
Kathryn B. Payne ◽  
Christopher Drummond Main ◽  
Sabrina D'Alfonso ◽  
Kirsten X. Jacobsen ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Synaptic Transmission ◽  
Brain Slices ◽  
Synaptic Activity ◽  
Presenilin 1 ◽  
Receptor Function ◽  
Channel Function ◽  
Nmda Channel ◽  
Nmda Receptor Function ◽  
6 Hydroxydopamine

Background:Previously we showed that 6-hydroxydopamine lesions of the substantia nigra eliminate corticostriatal LTP and that the neuroimmunolophilin ligand (NIL), GPI-1046, restores LTP.Methods:We used cDNA microarrays to determine what mRNAs may be over- or under-expressed in response to lesioning and/or GPI-1046 treatment. Patch clamp recordings were performed to investigate changes in NMDA channel function before and after treatments.Results:We found that 51 gene products were differentially expressed. Among these we found that GPI-1046 treatment up-regulated presenilin-1 (PS-1) mRNA abundance. This finding was confirmed using QPCR. PS-1 protein was also shown to be over-expressed in the striatum of lesioned/GPI-1046-treated rats. As PS-1 has been implicated in controlling NMDA-receptor function and LTP is reduced by lesioning we assayed NMDA mediated synaptic activity in striatal brain slices. The lesion-induced reduction of dopaminergic innervation was accompanied by the near complete loss of NDMA receptor-mediated synaptic transmission between the cortex and striatum. GPI-1046 treatment of the lesioned rats restored NMDA-mediated synaptic transmission but not the dopaminergic innervation. Restoration of NDMA channel function was apparently specific as the sodium channel current density was also reduced due to lesioning but GPI-1046 did not reverse this effect. We also found that restoration of NMDA receptor function was also not associated with either an increase in NMDA receptor mRNA or protein expression.Conclusion:As it has been previously shown that PS-1 is critical for normal NMDA receptor function, our data suggest that the improvement of excitatory neurotransmission occurs through the GPI-1046-induced up-regulation of PS-1.

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