Abstract
The β1 and γ2L subunits of the γ-aminobutyric acid type A receptor (GABAR) contain phosphorylation sites for PKC. To determine the effect of PKC on GABAR function, whole-cell recordings were obtained from mouse fibroblasts expressing recombinant α1β1γ2L receptors, and catalytically active PKC (PKM) was applied via the recording pipette. The first experiment was a population study. Intracellular application of PKM increased GABAR currents, and the enhancement was antagonized by coapplication of the PKC inhibitory peptide. No acceleration or deceleration of GABAR desensitization was observed. The second experiment was a reimpalement study in which paired recordings were made successively from individual cells. Enhancement of GABAR currents by PKM was again obtained. PKM increased GABAR currents at high (>10 μM) but not at low (<10 μM) GABA concentrations, resulting in increases in both EC50 and maximal GABAR current. Thus, PKC phosphorylation enhanced recombinant α1β1γ2L GABAR current by increasing maximal current without increasing the affinity of GABA for the GABAAs.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1421-1431 |
| Number of pages | 11 |
| Journal | Neuron |
| Volume | 13 |
| Issue number | 6 |
| DOIs | |
| State | Published - 1994 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Protein kinase C enhances recombinant bovine α1β1γ2L GABAA receptor whole-cell currents expressed in L929 fibroblasts. / Lin, Yu-Fung; Browning, Michael D.; Dudek, Ellen M.; Macdonald, Robert L.
In: Neuron, Vol. 13, No. 6, 1994, p. 1421-1431.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Protein kinase C enhances recombinant bovine α1β1γ2L GABAA receptor whole-cell currents expressed in L929 fibroblasts
AU - Lin, Yu-Fung
AU - Browning, Michael D.
AU - Dudek, Ellen M.
AU - Macdonald, Robert L.
PY - 1994
Y1 - 1994
N2 - The β1 and γ2L subunits of the γ-aminobutyric acid type A receptor (GABAR) contain phosphorylation sites for PKC. To determine the effect of PKC on GABAR function, whole-cell recordings were obtained from mouse fibroblasts expressing recombinant α1β1γ2L receptors, and catalytically active PKC (PKM) was applied via the recording pipette. The first experiment was a population study. Intracellular application of PKM increased GABAR currents, and the enhancement was antagonized by coapplication of the PKC inhibitory peptide. No acceleration or deceleration of GABAR desensitization was observed. The second experiment was a reimpalement study in which paired recordings were made successively from individual cells. Enhancement of GABAR currents by PKM was again obtained. PKM increased GABAR currents at high (>10 μM) but not at low (<10 μM) GABA concentrations, resulting in increases in both EC50 and maximal GABAR current. Thus, PKC phosphorylation enhanced recombinant α1β1γ2L GABAR current by increasing maximal current without increasing the affinity of GABA for the GABAAs.
AB - The β1 and γ2L subunits of the γ-aminobutyric acid type A receptor (GABAR) contain phosphorylation sites for PKC. To determine the effect of PKC on GABAR function, whole-cell recordings were obtained from mouse fibroblasts expressing recombinant α1β1γ2L receptors, and catalytically active PKC (PKM) was applied via the recording pipette. The first experiment was a population study. Intracellular application of PKM increased GABAR currents, and the enhancement was antagonized by coapplication of the PKC inhibitory peptide. No acceleration or deceleration of GABAR desensitization was observed. The second experiment was a reimpalement study in which paired recordings were made successively from individual cells. Enhancement of GABAR currents by PKM was again obtained. PKM increased GABAR currents at high (>10 μM) but not at low (<10 μM) GABA concentrations, resulting in increases in both EC50 and maximal GABAR current. Thus, PKC phosphorylation enhanced recombinant α1β1γ2L GABAR current by increasing maximal current without increasing the affinity of GABA for the GABAAs.
UR - http://www.scopus.com/inward/record.url?scp=0028569777&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028569777&partnerID=8YFLogxK
U2 - 10.1016/0896-6273(94)90427-8
DO - 10.1016/0896-6273(94)90427-8
M3 - Article
C2 - 7993633
AN - SCOPUS:0028569777
VL - 13
SP - 1421
EP - 1431
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 6
ER -