TY - JOUR
T1 - GABAA receptor inhibition does not affect mGluR-dependent LTD at hippocampal Schaffer collateral-CA1 synapses
AU - Rohde, Marco
AU - Tokay, Tursonjan
AU - Köhling, Rüdiger
AU - Kirschstein, Timo
N1 - Funding Information:
The authors appreciate Mrs. Katrin Porath, Mrs. Ulrike Mikkat for excellent technical assistance. This study was supported by the Deutsche Forschungsgemeinschaft ( Ki1283/3-1 ) and an intramural grant (FORUN, University of Rostock, Medical Faculty).
PY - 2009/12/18
Y1 - 2009/12/18
N2 - Hippocampal synaptic plasticity between Schaffer collaterals and CA1 pyramidal neurons can be induced by activation of N-methyl-d-aspartate receptors (NMDARs) or of metabotropic glutamate receptors (mGluRs). Inhibitory GABAergic interneurons in this region abundantly terminate on pyramidal neurons and may thus influence synaptic plasticity. Although NMDAR-dependent synaptic plasticity is known to be influenced by inhibitory interneurons, little is known about the role of GABA on mGluR-dependent plasticity. Here, we used field potential recordings of the Schaffer collateral-CA1 synapses in rat hippocampal slices in order to study the effect of GABAA receptor (GABAAR) inhibition on mGluR-dependent long-term depression (LTD). Without GABAAR blockade, mGluR-dependent LTD was induced pharmacologically by the group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG, 100 μM, 10 min) as well as electrically by paired-pulse low-frequency stimulation (PP-LFS, 900 paired pulses at 1 Hz) resulting in a stable depression of the field response lasting at least 80 min after LTD induction. The GABAAR antagonist gabazine (5 μM) itself caused an increase of field responses suggesting an endogenous GABA release inhibiting CA1 field potentials. However, when either DHPG or PP-LFS was applied during GABAAR inhibition, the field responses were significantly reduced. Moreover, normalizing these responses to experiments without GABAAR blockade, there was no significant effect of gabazine on both DHPG- and PP-LFS-induced LTD. Thus, our results show that mGluR-dependent LTD at Schaffer collateral-CA1 synapses is unaffected by GABAAR mediated synaptic transmission.
AB - Hippocampal synaptic plasticity between Schaffer collaterals and CA1 pyramidal neurons can be induced by activation of N-methyl-d-aspartate receptors (NMDARs) or of metabotropic glutamate receptors (mGluRs). Inhibitory GABAergic interneurons in this region abundantly terminate on pyramidal neurons and may thus influence synaptic plasticity. Although NMDAR-dependent synaptic plasticity is known to be influenced by inhibitory interneurons, little is known about the role of GABA on mGluR-dependent plasticity. Here, we used field potential recordings of the Schaffer collateral-CA1 synapses in rat hippocampal slices in order to study the effect of GABAA receptor (GABAAR) inhibition on mGluR-dependent long-term depression (LTD). Without GABAAR blockade, mGluR-dependent LTD was induced pharmacologically by the group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG, 100 μM, 10 min) as well as electrically by paired-pulse low-frequency stimulation (PP-LFS, 900 paired pulses at 1 Hz) resulting in a stable depression of the field response lasting at least 80 min after LTD induction. The GABAAR antagonist gabazine (5 μM) itself caused an increase of field responses suggesting an endogenous GABA release inhibiting CA1 field potentials. However, when either DHPG or PP-LFS was applied during GABAAR inhibition, the field responses were significantly reduced. Moreover, normalizing these responses to experiments without GABAAR blockade, there was no significant effect of gabazine on both DHPG- and PP-LFS-induced LTD. Thus, our results show that mGluR-dependent LTD at Schaffer collateral-CA1 synapses is unaffected by GABAAR mediated synaptic transmission.
KW - DHPG
KW - Gabazine
KW - Interneurons
KW - LTD
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U2 - 10.1016/j.neulet.2009.09.053
DO - 10.1016/j.neulet.2009.09.053
M3 - Article
C2 - 19800390
AN - SCOPUS:70350344420
VL - 467
SP - 20
EP - 25
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 1
ER -