GABAB receptor-mediated inhibition of tetrodotoxin-resistant GABA release in rodent hippocampal CA1 pyramidal cells
Tight-seal whole-cell recordings from CA1 pyramidal cells of rodent hippocampus were performed to study GABAB receptor-mediated inhibition of tetrodotoxin (TTX)-resistant IPSCs. IPSCs were recorded in the presence of TTX and glutamate receptor antagonists. (R)-(−)-baclofen reduced the frequency of T...
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| Main Authors: | , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
1 February 1997
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| In: |
The journal of neuroscience
Year: 1997, Volume: 17, Issue: 3, Pages: 1025-1032 |
| ISSN: | 1529-2401 |
| DOI: | 10.1523/JNEUROSCI.17-03-01025.1997 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1523/JNEUROSCI.17-03-01025.1997 Verlag, lizenzpflichtig, Volltext: https://www.jneurosci.org/content/17/3/1025 
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| Author Notes: | Wolfgang Jarolimek and Ulrich Misgeld |
MARC
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| 245 | 1 | 0 | |a GABAB receptor-mediated inhibition of tetrodotoxin-resistant GABA release in rodent hippocampal CA1 pyramidal cells |c Wolfgang Jarolimek and Ulrich Misgeld |
| 246 | 3 | 3 | |a GABA B receptor-mediated inhibition of tetrodotoxin-resistant GABA release in rodent hippocampal CA1 pyramidal cells |
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| 520 | |a Tight-seal whole-cell recordings from CA1 pyramidal cells of rodent hippocampus were performed to study GABAB receptor-mediated inhibition of tetrodotoxin (TTX)-resistant IPSCs. IPSCs were recorded in the presence of TTX and glutamate receptor antagonists. (R)-(−)-baclofen reduced the frequency of TTX-resistant IPSCs by a presynaptic action. The inhibition by (R)-(−)-baclofen was concentration-dependent, was not mimicked by the less effective enantiomer (S)-(+)-baclofen, and was blocked by the GABAB receptor antagonist CGP 55845A, suggesting a specific effect on GABAB receptors. The inhibition persisted in the presence of the Ca2+ channel blocker Cd2+. There was no requirement for an activation of K+conductances by (R)-(−)-baclofen, because the inhibition of TTX-resistant IPSCs persisted in Ba2+ and Cd2+. Because the time courses of TTX-resistant IPSCs were not changed by (R)-(−)-baclofen, there was no evidence for a selective inhibition of quantal release from a subgroup of GABAergic terminals. (R)-(−)-baclofen reduced the frequency of TTX-resistant IPSCs in guinea pigs and Wistar rats, whereas the inhibition was much smaller in Sprague Dawley rats. In Cd2+ and Ba2+, β-phorbol-12,13-dibutyrate and forskolin enhanced the frequency of TTX-resistant IPSCs. Only β-phorbol-12,13-dibutyrate reduced the inhibition by (R)-(−)-baclofen. We conclude that GABABreceptors inhibit TTX-resistant GABA release through a mechanism independent from the well known effects on Ca2+ or K+ channels. The inhibition of quantal GABA release can be reduced by an activator of protein kinase C. | ||
| 650 | 4 | |a adenylate cyclase | |
| 650 | 4 | |a baclofen | |
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| 650 | 4 | |a presynaptic | |
| 650 | 4 | |a protein kinase C | |
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