Group I metabotropic glutamate receptor actions in oriens/alveus interneurons of rat hippocampal CA1 region
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Group I metabotropic glutamate receptor actions in oriens/alveus interneurons of rat hippocampal CA1 region. / Gee, Christine E; Lacaille, Jean-Claude.
In: BRAIN RES, Vol. 1000, No. 1-2, 12.03.2004, p. 92-101.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Group I metabotropic glutamate receptor actions in oriens/alveus interneurons of rat hippocampal CA1 region
AU - Gee, Christine E
AU - Lacaille, Jean-Claude
PY - 2004/3/12
Y1 - 2004/3/12
N2 - Group I metabotropic glutamate receptors (mGluRs) are important for hippocampal interneuron function. We used whole-cell recording and confocal imaging to characterize group I mGluR actions in CA1 oriens/alveus interneurons in slices. In tetrodotoxin and ionotropic glutamate receptor antagonists, the group I mGluR specific agonist DHPG increased intradendritic Ca(2+) levels and depolarized interneurons, whereas the group II mGluR specific agonist DCG-IV and the group III mGluR specific agonist L-AP4 did not. DHPG-induced depolarizing and Ca(2+) responses were antagonized by the group I mGluR antagonist 4CPG, but only Ca(2+) responses were significantly inhibited by the mGluR1 antagonist CPCCOEt. DHPG-induced depolarizing responses were not blocked by the inositol-1,4,5-trisphosphate (IP(3)) receptor inhibitor heparin, the protein kinase C (PKC) antagonists GF-109203X, or the inhibitor of phospholipase C (PLC) U73122. Thus, these responses to DHPG may not be transduced by the PLC-->IP(3)/diacylglycerol (DAG) pathway classically linked to group I mGluRs. DHPG-induced depolarizations were not blocked by intracellular GDP beta S or bath-application of N-ethylmaleimide (NEM), suggesting the involvement of a G protein-independent pathway. Our findings indicate that group I mGluRs induce a depolarization of oriens/alveus interneurons via a G protein-independent mechanism different from their classic signalling pathway. Since depolarizations are associated with intracellular Ca(2+) rises, these actions may be important for their synaptic plasticity and vulnerability to excitotoxicity.
AB - Group I metabotropic glutamate receptors (mGluRs) are important for hippocampal interneuron function. We used whole-cell recording and confocal imaging to characterize group I mGluR actions in CA1 oriens/alveus interneurons in slices. In tetrodotoxin and ionotropic glutamate receptor antagonists, the group I mGluR specific agonist DHPG increased intradendritic Ca(2+) levels and depolarized interneurons, whereas the group II mGluR specific agonist DCG-IV and the group III mGluR specific agonist L-AP4 did not. DHPG-induced depolarizing and Ca(2+) responses were antagonized by the group I mGluR antagonist 4CPG, but only Ca(2+) responses were significantly inhibited by the mGluR1 antagonist CPCCOEt. DHPG-induced depolarizing responses were not blocked by the inositol-1,4,5-trisphosphate (IP(3)) receptor inhibitor heparin, the protein kinase C (PKC) antagonists GF-109203X, or the inhibitor of phospholipase C (PLC) U73122. Thus, these responses to DHPG may not be transduced by the PLC-->IP(3)/diacylglycerol (DAG) pathway classically linked to group I mGluRs. DHPG-induced depolarizations were not blocked by intracellular GDP beta S or bath-application of N-ethylmaleimide (NEM), suggesting the involvement of a G protein-independent pathway. Our findings indicate that group I mGluRs induce a depolarization of oriens/alveus interneurons via a G protein-independent mechanism different from their classic signalling pathway. Since depolarizations are associated with intracellular Ca(2+) rises, these actions may be important for their synaptic plasticity and vulnerability to excitotoxicity.
KW - Animals
KW - Excitatory Amino Acid Agonists
KW - Excitatory Amino Acid Antagonists
KW - Hippocampus
KW - Interneurons
KW - Male
KW - Rats
KW - Rats, Sprague-Dawley
KW - Receptors, Metabotropic Glutamate
KW - Synaptic Transmission
U2 - 10.1016/j.brainres.2003.11.046
DO - 10.1016/j.brainres.2003.11.046
M3 - SCORING: Journal article
C2 - 15053957
VL - 1000
SP - 92
EP - 101
JO - BRAIN RES
JF - BRAIN RES
SN - 0006-8993
IS - 1-2
ER -