NLPre "pipeline" example

February 7, 2018 ยท View on GitHub

The source text comes from the abstract of PMID 18974824, "The effects of NR2 subunit-dependent NMDA receptor kinetics on synaptic transmission and CaMKII activation."

FunctionDescription
originalN-Methyl-d-aspartic acid (NMDA) receptors are widely expressed in the brain and are critical for many forms of synaptic plasticity. Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development; in the forebrain, the NR2B receptor is dominant early in development, and later both NR2A and NR2B are expressed. In heterologous expression systems, NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors. However, conflicting data, showing similar open probabilities, exist for receptors expressed in neurons. Similarly, studies of synaptic plasticity have produced divergent results, with some showing that only NR2A-containing receptors can drive long-term potentiation and others showing that either subtype is capable of driving potentiation. In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse, we constructed a Monte Carlo model of glutamate release, diffusion, and binding to NMDA receptors and of receptor opening and closing as well as a model of the activation of calcium-calmodulin kinase II, an enzyme critical for induction of synaptic plasticity, by NMDA receptor-mediated calcium influx. Our results suggest that the conflicting data concerning receptor open probabilities can be resolved, with NR2A- and NR2B-containing receptors having very different opening probabilities. They also support the conclusion that receptors containing either subtype can drive long-term potentiation. We also are able to estimate the number of functional receptors at a synapse from experimental data. Finally, in our models, the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not. These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function.
dedashN-Methyl-d-aspartic acid (NMDA) receptors are widely expressed in the brain and are critical for many forms of synaptic plasticity. Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development; in the forebrain, the NR2B receptor is dominant early in development, and later both NR2A and NR2B are expressed. In heterologous expression systems, NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors. However, conflicting data, showing similar open probabilities, exist for receptors expressed in neurons. Similarly, studies of synaptic plasticity have produced divergent results, with some showing that only NR2A-containing receptors can drive long-term potentiation and others showing that either subtype is capable of driving potentiation. In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse, we constructed a Monte Carlo model of glutamate release, diffusion, and binding to NMDA receptors and of receptor opening and closing as well as a model of the activation of calcium-calmodulin kinase II, an enzyme critical for induction of synaptic plasticity, by NMDA receptor-mediated calcium influx. Our results suggest that the conflicting data concerning receptor open probabilities can be resolved, with NR2A- and NR2B-containing receptors having very different opening probabilities. They also support the conclusion that receptors containing either subtype can drive long-term potentiation. We also are able to estimate the number of functional receptors at a synapse from experimental data. Finally, in our models, the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not. These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function.
titlecapsN-Methyl-d-aspartic acid ( NMDA ) receptors are widely expressed in the brain and are critical for many forms of synaptic plasticity . Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development ; in the forebrain , the NR2B receptor is dominant early in development , and later both NR2A and NR2B are expressed . In heterologous expression systems , NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors . However , conflicting data , showing similar open probabilities , exist for receptors expressed in neurons . Similarly , studies of synaptic plasticity have produced divergent results , with some showing that only NR2A-containing receptors can drive long-term potentiation and others showing that either subtype is capable of driving potentiation . In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse , we constructed a Monte Carlo model of glutamate release , diffusion , and binding to NMDA receptors and of receptor opening and closing as well as a model of the activation of calcium-calmodulin kinase II , an enzyme critical for induction of synaptic plasticity , by NMDA receptor-mediated calcium influx . Our results suggest that the conflicting data concerning receptor open probabilities can be resolved , with NR2A - and NR2B-containing receptors having very different opening probabilities . They also support the conclusion that receptors containing either subtype can drive long-term potentiation . We also are able to estimate the number of functional receptors at a synapse from experimental data . Finally , in our models , the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not . These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function .
replace_acronymsN-Methyl-d-aspartic acid ( NMDA ) receptors are widely expressed in the brain and are critical for many forms of synaptic plasticity .
Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development ; in the forebrain , the NR2B receptor is dominant early in development , and later both NR2A and NR2B are expressed .
In heterologous expression systems , NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors .
However , conflicting data , showing similar open probabilities , exist for receptors expressed in neurons .
Similarly , studies of synaptic plasticity have produced divergent results , with some showing that only NR2A-containing receptors can drive long-term potentiation and others showing that either subtype is capable of driving potentiation .
In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse , we constructed a Monte Carlo model of glutamate release , diffusion , and binding to NMDA receptors and of receptor opening and closing as well as a model of the activation of calcium-calmodulin kinase II , an enzyme critical for induction of synaptic plasticity , by NMDA receptor-mediated calcium influx .
Our results suggest that the conflicting data concerning receptor open probabilities can be resolved , with NR2A - and NR2B-containing receptors having very different opening probabilities .
They also support the conclusion that receptors containing either subtype can drive long-term potentiation .
We also are able to estimate the number of functional receptors at a synapse from experimental data .
Finally , in our models , the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not .
These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function .
separated_parenthesisN-Methyl-d-aspartic acid receptors are widely expressed in the brain and are critical for many forms of synaptic plasticity .
NMDA .
Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development ; in the forebrain , the NR2B receptor is dominant early in development , and later both NR2A and NR2B are expressed .
In heterologous expression systems , NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors .
However , conflicting data , showing similar open probabilities , exist for receptors expressed in neurons .
Similarly , studies of synaptic plasticity have produced divergent results , with some showing that only NR2A-containing receptors can drive long-term potentiation and others showing that either subtype is capable of driving potentiation .
In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse , we constructed a Monte Carlo model of glutamate release , diffusion , and binding to NMDA receptors and of receptor opening and closing as well as a model of the activation of calcium-calmodulin kinase II , an enzyme critical for induction of synaptic plasticity , by NMDA receptor-mediated calcium influx .
Our results suggest that the conflicting data concerning receptor open probabilities can be resolved , with NR2A - and NR2B-containing receptors having very different opening probabilities .
They also support the conclusion that receptors containing either subtype can drive long-term potentiation .
We also are able to estimate the number of functional receptors at a synapse from experimental data .
Finally , in our models , the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not .
These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function .
replace_from_dictionaryMeSH_N-Methylaspartate receptors are widely expressed in the brain and are critical for many forms of MeSH_Neuronal_Plasticity .
NMDA .
Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development ; in the forebrain , the NR2B receptor is dominant early in development , and later both NR2A and NR2B are expressed .
In heterologous expression systems , NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors .
However , conflicting data , showing similar open probabilities , exist for receptors expressed in neurons .
Similarly , studies of MeSH_Neuronal_Plasticity have produced divergent results , with some showing that only NR2A-containing receptors can drive MeSH_Long-Term_Potentiation and others showing that either subtype is capable of driving potentiation .
In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse , we constructed a Monte Carlo model of glutamate release , diffusion , and binding to MeSH_Receptors_N-Methyl-D-Aspartate and of receptor opening and closing as well as a model of the activation of calcium-MeSH_Calcium-Calmodulin-Dependent_Protein_Kinases II , an enzyme critical for induction of MeSH_Neuronal_Plasticity , by NMDA receptor-mediated calcium influx .
Our results suggest that the conflicting data concerning receptor open probabilities can be resolved , with NR2A - and NR2B-containing receptors having very different opening probabilities .
They also support the conclusion that receptors containing either subtype can drive MeSH_Long-Term_Potentiation .
We also are able to estimate the number of functional receptors at a synapse from experimental data .
Finally , in our models , the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not .
These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function .
token_replacementMeSH_N-Methylaspartate receptors are widely expressed in the brain and are critical for many forms of MeSH_Neuronal_Plasticity .
NMDA .
Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development ; in the forebrain , the NR2B receptor is dominant early in development , and later both NR2A and NR2B are expressed .
In heterologous expression systems , NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors .
However , conflicting data , showing similar open probabilities , exist for receptors expressed in neurons .
Similarly , studies of MeSH_Neuronal_Plasticity have produced divergent results , with some showing that only NR2A-containing receptors can drive MeSH_Long-Term_Potentiation and others showing that either subtype is capable of driving potentiation .
In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse , we constructed a Monte Carlo model of glutamate release , diffusion , and binding to MeSH_Receptors_N-Methyl-D-Aspartate and of receptor opening and closing as well as a model of the activation of calcium-MeSH_Calcium-Calmodulin-Dependent_Protein_Kinases II , an enzyme critical for induction of MeSH_Neuronal_Plasticity , by NMDA receptor-mediated calcium influx .
Our results suggest that the conflicting data concerning receptor open probabilities can be resolved , with NR2A - and NR2B-containing receptors having very different opening probabilities .
They also support the conclusion that receptors containing either subtype can drive MeSH_Long-Term_Potentiation .
We also are able to estimate the number of functional receptors at a synapse from experimental data .
Finally , in our models , the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not .
These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function .
decaps_textMeSH_N-Methylaspartate receptors are widely expressed in the brain and are critical for many forms of MeSH_Neuronal_Plasticity .
NMDA .
Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development ; in the forebrain , the NR2B receptor is dominant early in development , and later both NR2A and NR2B are expressed .
In heterologous expression systems , NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors .
However , conflicting data , showing similar open probabilities , exist for receptors expressed in neurons .
Similarly , studies of MeSH_Neuronal_Plasticity have produced divergent results , with some showing that only NR2A-containing receptors can drive MeSH_Long-Term_Potentiation and others showing that either subtype is capable of driving potentiation .
In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse , we constructed a Monte Carlo model of glutamate release , diffusion , and binding to MeSH_Receptors_N-Methyl-D-Aspartate and of receptor opening and closing as well as a model of the activation of calcium-MeSH_Calcium-Calmodulin-Dependent_Protein_Kinases II , an enzyme critical for induction of MeSH_Neuronal_Plasticity , by NMDA receptor-mediated calcium influx .
Our results suggest that the conflicting data concerning receptor open probabilities can be resolved , with NR2A - and NR2B-containing receptors having very different opening probabilities .
They also support the conclusion that receptors containing either subtype can drive MeSH_Long-Term_Potentiation .
We also are able to estimate the number of functional receptors at a synapse from experimental data .
Finally , in our models , the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not .
These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function .
pos_tokenizerMeSH_N-Methylaspartate receptor brain critical many form MeSH_Neuronal_Plasticity
NMDA
subtype NMDA receptor NR2 subunit development forebrain NR2B receptor dominant development NR2A NR2B
heterologou expression system receptor faster open kinetic NR2B-containing receptor
datum similar open probability receptor neuron
study MeSH_Neuronal_Plasticity divergent result show NR2A-containing receptor MeSH_Long-Term_Potentiation other subtype capable potentiation
order result open question number location functional receptor synapse monte carlo model glutamate release diffusion bound MeSH_Receptors_N-Methyl-D-Aspartate receptor open close model activation calcium-MeSH_Calcium-Calmodulin-Dependent_Protein_Kinases Ius enzyme critical induction MeSH_Neuronal_Plasticity NMDA receptor-mediated calcium influx
result datum receptor open probability NR2A NR2B-containing receptor different open probability
conclusion receptor subtype MeSH_Long-Term_Potentiation
able number functional receptor synapse experimental datum
model open NR2B-containing receptor dependent location receptor relative site glutamate release open NR2A-containing receptor
result previou find future experiment open question NMDA receptor function