Abstract
Growth factor signal transduction pathways have recently been shown to affect voltage-gated ion channel activity. In this study we report that insulin can modulate the activity of a ligand-gated ion channel, the N-methyl-d-aspartate (NMDA) receptor. In Xenopus oocytes, brief insulin exposure rapidly potentiated NR1a/NR2A and NR1a/NR2B receptor responses 2-3 fold and weakly potentiated NR1a/NR2C and NR1a/NR2D mediated-responses. Insulin potentiation of NR1a/NR2A receptor responses was significantly blocked by staurosporine, suggesting kinase involvement in insulin action. Insulin modulation of native NMDA receptors is suggested by the observation that insulin potentiated the NMDA receptor-mediated synaptic component in hippocampal slices. Regulation of NMDA receptor activity by growth factors may account for previous observations of growth factor modulation of central nervous system excitotoxicity.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 5-8 |
| Number of pages | 4 |
| Journal | Neuroscience Letters |
| Volume | 192 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jun 2 1995 |
Fingerprint
Keywords
- Growth factors
- Hippocampus
- IGF-1
- Insulin
- N-methyl-d-aspartate
- Oocytes
- PKC
- Phorbol ester
- Synaptic transmission
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Insulin potentiates N-methyl-d-aspartate receptor activity in Xenopus oocytes and rat hippocampus. / Liu, Lifei; Brown, James C.; Webster, Wallace W.; Morrisett, Richard A.; Monaghan, Daniel T.
In: Neuroscience Letters, Vol. 192, No. 1, 02.06.1995, p. 5-8.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Insulin potentiates N-methyl-d-aspartate receptor activity in Xenopus oocytes and rat hippocampus
AU - Liu, Lifei
AU - Brown, James C.
AU - Webster, Wallace W.
AU - Morrisett, Richard A.
AU - Monaghan, Daniel T.
PY - 1995/6/2
Y1 - 1995/6/2
N2 - Growth factor signal transduction pathways have recently been shown to affect voltage-gated ion channel activity. In this study we report that insulin can modulate the activity of a ligand-gated ion channel, the N-methyl-d-aspartate (NMDA) receptor. In Xenopus oocytes, brief insulin exposure rapidly potentiated NR1a/NR2A and NR1a/NR2B receptor responses 2-3 fold and weakly potentiated NR1a/NR2C and NR1a/NR2D mediated-responses. Insulin potentiation of NR1a/NR2A receptor responses was significantly blocked by staurosporine, suggesting kinase involvement in insulin action. Insulin modulation of native NMDA receptors is suggested by the observation that insulin potentiated the NMDA receptor-mediated synaptic component in hippocampal slices. Regulation of NMDA receptor activity by growth factors may account for previous observations of growth factor modulation of central nervous system excitotoxicity.
AB - Growth factor signal transduction pathways have recently been shown to affect voltage-gated ion channel activity. In this study we report that insulin can modulate the activity of a ligand-gated ion channel, the N-methyl-d-aspartate (NMDA) receptor. In Xenopus oocytes, brief insulin exposure rapidly potentiated NR1a/NR2A and NR1a/NR2B receptor responses 2-3 fold and weakly potentiated NR1a/NR2C and NR1a/NR2D mediated-responses. Insulin potentiation of NR1a/NR2A receptor responses was significantly blocked by staurosporine, suggesting kinase involvement in insulin action. Insulin modulation of native NMDA receptors is suggested by the observation that insulin potentiated the NMDA receptor-mediated synaptic component in hippocampal slices. Regulation of NMDA receptor activity by growth factors may account for previous observations of growth factor modulation of central nervous system excitotoxicity.
KW - Growth factors
KW - Hippocampus
KW - IGF-1
KW - Insulin
KW - N-methyl-d-aspartate
KW - Oocytes
KW - PKC
KW - Phorbol ester
KW - Synaptic transmission
UR - http://www.scopus.com/inward/record.url?scp=0029000105&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029000105&partnerID=8YFLogxK
U2 - 10.1016/0304-3940(95)11593-L
DO - 10.1016/0304-3940(95)11593-L
M3 - Article
C2 - 7675309
AN - SCOPUS:0029000105
VL - 192
SP - 5
EP - 8
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 1
ER -