Phospholipase C-Independent Group I Metabotropic Glutamate Receptor-Mediated Inward Current in Mouse Purkinje Cells

1998 ◽  
Vol 251 (3) ◽  
pp. 753-758 ◽  
Author(s):  
Moritoshi Hirono ◽  
Shiro Konishi ◽  
Tohru Yoshioka
Keyword(s):  
Phospholipase C ◽  
Purkinje Cells ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Independent Group ◽  
Inward Current ◽  
Metabotropic Glutamate ◽  
Group I

Metabotropic Glutamate Receptor Agonists Alter Neuronal Excitability and Ca2+ Levels via the Phospholipase C Transduction Pathway in Cultured Purkinje Neurons

1997 ◽  
Vol 78 (1) ◽  
pp. 63-75 ◽  
Author(s):  
Jeffrey G. Netzeband ◽  
Kathy L. Parsons ◽  
Dan D. Sweeney ◽  
Donna L. Gruol
Keyword(s):  
Phospholipase C ◽  
Glutamate Receptor ◽  
Neuronal Excitability ◽  
Metabotropic Glutamate Receptor ◽  
Purkinje Neurons ◽  
Transduction Pathway ◽  
Electrophysiological Response ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Intracellular Ca

Netzeband, Jeffrey G., Kathy L. Parsons, Dan D. Sweeney, and Donna L. Gruol. Metabotropic glutamate receptor agonists alter neuronal excitability and Ca2+ levels via the phospholipase C transduction pathway in cultured Purkinje neurons. J. Neurophysiol. 78: 63–75, 1997. Selective agonists for metabotropic glutamate receptor (mGluR) subtypes were tested on mature, cultured rat cerebellar Purkinje neurons (≥21 days in vitro) to identify functionally relevant mGluRs expressed by these neurons and to investigate the transduction pathways associated with mGluR-mediated changes in membrane excitability. Current-clamp recordings (nystatin/perforated-patch method) were used to measure the membrane response of Purkinje neurons to brief microperfusion pulses (1.5 s) of the group I (mGluR1/mGluR5) agonists (1 S,3 R)-1-aminocyclopentane-1,3-dicarboxylic acid (300 μM), quisqualate (5 μM), and ( R,S)-3,5-dihydroxyphenylglycine (50–500 μM). All group I mGluR agonists elicited biphasic membrane responses and burst activity in the Purkinje neurons. In addition, the group I mGluR agonists produced alterations in the active membrane properties of the Purkinje neurons and depressed the off response after hyperpolarizing current injection. In parallel microscopic Ca2+ imaging experiments, application of the group I mGluR agonists to fura-2-loaded cells elicited increases in intracellular Ca2+ in both the somatic and dendritic regions. The group II (mGluR2/mGluR3) agonist (2 S,3 S,4 S)-α-(carboxycyclopropyl)-glycine (10 μM) and the group III (mGluR4/mGluR6/mGluR7/mGluR8) agonists l(+)-2-amino-4-phosphonobutyric acid (1 mM) and O-phospho-l-serine (200 μM) had no effect on the membrane potential or intracellular Ca2+ levels of the Purkinje neurons. The cultured Purkinje neurons, but not granule neurons or interneurons, showed immunostaining for mGluR1α in both the somatic and dendritic regions. All effects of the group I mGluR agonists were blocked by (+)-α-methyl-4-carboxyphenylglycine (1 mM), an mGluR antagonist. Furthermore, the phospholipase C inhibitor 1-[6-((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]-1H-pyrrole-2,5-dione (2 μM) blocked the group I mGluR agonist-mediated electrophysiological response and greatly attenuated the Ca2+ signal elicited by group I mGluR agonists, particularly in the dendrites. The inactive analogue1-[6-((17β-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl]2,5-pyrrolidine-dione (2 μM) was relatively ineffective against the electrophysiological response and Ca2+ signal. These results indicate that functional group I mGluRs (but not group II or III mGluRs) can be activated on mature Purkinje neurons in culture and result in changes in neuronal excitability and intracellular Ca2+ mediated through phospholipase C. These data obtained from a defined neuronal type, the Purkinje neuron, confirm biochemical and molecular studies on the transduction mechanisms of group I mGluRs and show that this transduction pathway is linked to neuronal excitability and intracellular Ca2+ release in the Purkinje neurons.

Metabotropic Glutamate Receptor Enhancement of Spontaneous IPSCs in Neocortical Interneurons

1997 ◽  
Vol 78 (5) ◽  
pp. 2287-2295 ◽  
Author(s):  
Fu-Ming Zhou ◽  
John J. Hablitz
Keyword(s):  
Glutamate Receptor ◽  
Time Constant ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Slow Component ◽  
Voltage Range ◽  
Inward Current ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Layer I

Zhou, Fu-Ming and John J. Hablitz. Metabotropic glutamate receptor enhancement of spontaneous IPSCs in neocortical interneurons. J. Neurophysiol. 78: 2287–2295, 1997. Using neocortical layer I neurons as a model for GABAergic interneurons, we have studied γ-aminobutyric acid-A (GABAA) receptor-mediated spontaneous inhibitory postsynaptic currents (IPSCs) and modulation by metabotropic glutamate receptors (mGluRs). In the presence of 0.5 μM tetrodotoxin (TTX) and ionotropic glutamate receptor antagonists and under symmetrical Cl− conditions, the mean amplitude of miniature IPSCs (mIPSCs) was ∼50 pA at a holding potential of −70 mV with individual events ranging from 10 to 400 pA. Averaged mIPSCs had a 10–90% rise time of ∼0.6 ms. The decay was double exponential. The fast component had a time constant of ∼4 ms and comprised ∼40% of the total amplitude. The slow component had a time constant of ∼22 ms. The frequency of spontaneous IPSCs (sIPSCs), recorded in the absence of TTX, was increased by bath application of the mGluR agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD; 10–100 μM) or the group I mGluR selective agonist quisqualic acid (Quis; 0.5–1 μM). Under identical conditions, mIPSCs were not affected. The kinetics of sIPSCs and mIPSCs were not altered by ACPD or Quis. Quis (1 μM) induced an inward current of ∼70 pA at a holding potential of −70 mV, whereas ACPD (40–200 μM) induced a smaller inward current. This current was linear over the voltage range −70 to +30 mV and reversed polarity near 0 mV. In current-clamp recordings, both Quis and ACPD induced a depolarization and action potential firing in layer I and deeper layer interneurons. We conclude that neocortical layer I neurons receive GABAA receptor-mediated inhibitory synaptic inputs. Activation of mGluRs, possibly mGluR1 and/or mGluR5, causes an enhancement of inhibitory synaptic transmission by directly depolarizing corticalGABAergic interneurons through the opening of nonselective cation channels.

Group I Metabotropic Glutamate Receptor-mediated Gene Expression in Striatal Neurons

2008 ◽  
Vol 33 (10) ◽  
pp. 1920-1924 ◽  
Author(s):  
Li-Min Mao ◽  
Guo-Chi Zhang ◽  
Xian-Yu Liu ◽  
Eugene E. Fibuch ◽  
John Q. Wang
Keyword(s):  
Gene Expression ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Striatal Neurons ◽  
Metabotropic Glutamate ◽  
Group I

Orai1 is a crucial downstream partner of group I metabotropic glutamate receptor signaling in dorsal horn neurons

Pain ◽  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Jingsheng Xia ◽  
Yannong Dou ◽  
Yixiao Mei ◽  
Frances M. Munoz ◽  
Ruby Gao ◽  
...  
Keyword(s):  
Dorsal Horn ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Receptor Signaling ◽  
Metabotropic Glutamate ◽  
Dorsal Horn Neurons ◽  
Group I
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