Interleukin-2 inhibits NMDA receptor-mediated currents directly and may differentially affect subtypes

Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl- d-aspartate (NMDA) receptor-mediated currents ( I NMDA) in rat cultured hippocampal neurons and human embryonic kidney (HEK) 293 cells expressing recombinant NMDA receptors. We found tha...

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Published inBiochemical and biophysical research communications Vol. 351; no. 2; pp. 449 - 454
Main Authors Shen, Yi, Zhu, Li-Jun, Liu, Shuang-Shuang, Zhou, Su-Ya, Luo, Jian-Hong
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 15.12.2006
Subjects
Animals
Cells, Cultured
Cloning, Molecular
Hippocampal neuron
Hippocampus - cytology
Humans
Interleukin-2
Interleukin-2 - pharmacology
Interleukin-2 - physiology
Ion Channel Gating
Neurons - drug effects
Neurons - physiology
NMDA receptors
Patch-Clamp Techniques
Protein Isoforms - genetics
Protein Isoforms - physiology
Rat
Rats
Receptors, N-Methyl-D-Aspartate - genetics
Receptors, N-Methyl-D-Aspartate - physiology
Whole-cell patch clamp
Interleukin-2
Hippocampal neuron
Rat
NMDA receptors
Whole-cell patch clamp
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Abstract Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl- d-aspartate (NMDA) receptor-mediated currents ( I NMDA) in rat cultured hippocampal neurons and human embryonic kidney (HEK) 293 cells expressing recombinant NMDA receptors. We found that IL-2 (0.01–1 ng/ml) immediately and significantly decreased peak I NMDA in cultured neurons. Interestingly, the peak I NMDA induced in HEK 293 cells was also inhibited by IL-2. We also found that IL-2 differentially decreased the peak amplitudes of NR2A- and NR2B-containing NMDA receptor-mediated currents ( I NR2A and I NR2B) by 54 ± 5% and 30 ± 4%, respectively. These results provide new evidence that IL-2 induces rapid inhibition of peak currents of NMDA receptor-mediated responses with possible NR1/NR2A and NR1/NR2B subtype-differentiation, and suggest that the inhibition is mediated by direct interaction between IL-2 and NMDA receptors.
AbstractList Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl-d-aspartate (NMDA) receptor-mediated currents (I(NMDA)) in rat cultured hippocampal neurons and human embryonic kidney (HEK) 293 cells expressing recombinant NMDA receptors. We found that IL-2 (0.01-1ng/ml) immediately and significantly decreased peak I(NMDA) in cultured neurons. Interestingly, the peak I(NMDA) induced in HEK 293 cells was also inhibited by IL-2. We also found that IL-2 differentially decreased the peak amplitudes of NR2A- and NR2B-containing NMDA receptor-mediated currents (I(NR2A) and I(NR2B)) by 54+/-5% and 30+/-4%, respectively. These results provide new evidence that IL-2 induces rapid inhibition of peak currents of NMDA receptor-mediated responses with possible NR1/NR2A and NR1/NR2B subtype-differentiation, and suggest that the inhibition is mediated by direct interaction between IL-2 and NMDA receptors.
Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl- d-aspartate (NMDA) receptor-mediated currents ( I NMDA) in rat cultured hippocampal neurons and human embryonic kidney (HEK) 293 cells expressing recombinant NMDA receptors. We found that IL-2 (0.01–1 ng/ml) immediately and significantly decreased peak I NMDA in cultured neurons. Interestingly, the peak I NMDA induced in HEK 293 cells was also inhibited by IL-2. We also found that IL-2 differentially decreased the peak amplitudes of NR2A- and NR2B-containing NMDA receptor-mediated currents ( I NR2A and I NR2B) by 54 ± 5% and 30 ± 4%, respectively. These results provide new evidence that IL-2 induces rapid inhibition of peak currents of NMDA receptor-mediated responses with possible NR1/NR2A and NR1/NR2B subtype-differentiation, and suggest that the inhibition is mediated by direct interaction between IL-2 and NMDA receptors.
Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl-d-aspartate (NMDA) receptor-mediated currents (I sub(N) sub(M) sub(D) sub(A)) in rat cultured hippocampal neurons and human embryonic kidney (HEK) 293 cells expressing recombinant NMDA receptors. We found that IL-2 (0.01-1ng /ml) immediately and significantly decreased peak I sub(N) sub(M) sub(D) sub(A) in cultured neurons. Interestingly, the peak I sub(N) sub(M) sub(D) sub(A) induced in HEK 293 cells was also inhibited by IL-2. We also found that IL-2 differentially decreased the peak amplitudes of NR2A- and NR2B-containing NMDA receptor-mediated currents (I sub(N) sub(R) sub(2) sub(A) and I sub(N) sub(R) sub(2) sub(B)) by 54+/-5% and 30+/-4%, respectively. These results provide new evidence that IL-2 induces rapid inhibition of peak currents of NMDA receptor-mediated responses with possible NR1/NR2A and NR1/NR2B subtype-differentiation, and suggest that the inhibition is mediated by direct interaction between IL-2 and NMDA receptors.
Author Liu, Shuang-Shuang
Luo, Jian-Hong
Zhu, Li-Jun
Zhou, Su-Ya
Shen, Yi
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Keywords Interleukin-2
Hippocampal neuron
Rat
NMDA receptors
Whole-cell patch clamp
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Snippet Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl- d-aspartate (NMDA) receptor-mediated currents...
Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl-d-aspartate (NMDA) receptor-mediated currents...
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SubjectTerms Animals
Cells, Cultured
Cloning, Molecular
Hippocampal neuron
Hippocampus - cytology
Humans
Interleukin-2
Interleukin-2 - pharmacology
Interleukin-2 - physiology
Ion Channel Gating
Neurons - drug effects
Neurons - physiology
NMDA receptors
Patch-Clamp Techniques
Protein Isoforms - genetics
Protein Isoforms - physiology
Rat
Rats
Receptors, N-Methyl-D-Aspartate - genetics
Receptors, N-Methyl-D-Aspartate - physiology
Whole-cell patch clamp
Title Interleukin-2 inhibits NMDA receptor-mediated currents directly and may differentially affect subtypes
URI https://dx.doi.org/10.1016/j.bbrc.2006.10.047
https://www.ncbi.nlm.nih.gov/pubmed/17069761
https://search.proquest.com/docview/19507490
https://search.proquest.com/docview/68195989
Volume 351
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