scholarly journals Hippocampal mossy fiber activity evokes Ca2+ release in CA3 pyramidal neurons via a metabotropic glutamate receptor pathway

Neuroscience ◽  
2001 ◽  
Vol 107 (1) ◽  
pp. 59-69 ◽  
Author(s):  
A Kapur ◽  
M Yeckel ◽  
D Johnston
Keyword(s):  
Glutamate Receptor ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Mossy Fiber ◽  
Metabotropic Glutamate ◽  
Ca3 Pyramidal Neurons

Metabotropic glutamate receptor-mediated suppression of L-type calcium current in acutely isolated neocortical neurons

1992 ◽  
Vol 68 (3) ◽  
pp. 833-842 ◽  
Author(s):  
R. J. Sayer ◽  
P. C. Schwindt ◽  
W. E. Crill
Keyword(s):  
Glutamate Receptor ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
High Threshold ◽  
External Application ◽  
Metabotropic Glutamate ◽  
Neocortical Neurons ◽  
Old Rats ◽  
Low Threshold ◽  
Ca2 Channels

1. The effects of metabotropic glutamate receptor (mGluR) stimulation on whole-cell Ca2+ currents were studied in pyramidal neurons isolated from the dorsal frontoparietal neocortex of rat. The selective mGluR agonist cis-(+/-)-1-aminocyclopentane-1,3-dicarboxylic acid [trans-ACPD (100 microM)] suppressed the peak high-threshold Ca2+ current by 21 +/- 1.7% (mean +/- SE) in 40 of 43 cells from 10- to 21-day-old rats. Consistent with previous findings for mGluR, glutamate, quisqualate, and ibotenate [but not alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)] reduced the Ca2+ currents, and the responses were not blocked by the ionotropic glutamate receptor antagonists 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonovaleric acid (APV). EC50S for Ca2+ current suppression were 29 nM for quisqualate, 2.3 microM for glutamate, and 13 microM for trans-ACPD. 2. The low-threshold Ca2+ current was not modulated by trans-ACPD. The component of the high-threshold CA2+ current suppressed by mGluR was determined by pharmacology; the responses were not affected by omega-conotoxin GVIA but were occluded by the dihydropyridine Ca2+ antagonist nifedipine. Ca2+ tail currents prolonged by the dihydropyridine Ca2+ agonist (+)-SDZ 202-79] were suppressed by mGluR stimulation in parallel with the peak current. These findings strongly suggest that L-type Ca2+ channels are modulated by mGluR. 3. In neurons dialyzed with 100 microM guanosine 5'-(gamma-thio)triphosphate (GTP-gamma-S), Ca2+ current suppression was elicited by the first application of trans-ACPD (in 5 of 6 cells), but not by subsequent applications. Responses in neurons dialyzed with 2 mM guanosine 5'-(beta-thio)diphosphate (GDP-beta-S) were significantly smaller than controls. The results are consistent with mGluR acting via linkage to a G protein. 4. The responses to mGluR agonists were smaller when the external Ca2+ was replaced by Ba2+, indicating that some part of the mechanism underlying the current suppression is Ca2+ dependent. Because mGluR stimulates phosphoinositide turnover and release of Ca2+ from intracellular stores in other types of neurons, the possibility of released Ca2+ mediating inactivation of Ca2+ channels was considered. However, the Ca2+ current suppression was not attenuated by strong intracellular Ca2+ buffering [20 mM bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA)], by dialysis with 100 microM inositol-1,4,5-triphosphate (IP3), or by external application of 1 microM thapsigargin. 5. We conclude that in neocortical neurons, one action of mGluR is to suppress the component of high-threshold Ca2+ current conducted by L-type Ca2+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Experience-Induced Arc/Arg3.1 Primes CA1 Pyramidal Neurons for Metabotropic Glutamate Receptor-Dependent Long-Term Synaptic Depression

Neuron ◽  
2013 ◽  
Vol 80 (1) ◽  
pp. 72-79 ◽  
Author(s):  
Vikram Jakkamsetti ◽  
Nien-Pei Tsai ◽  
Christina Gross ◽  
Gemma Molinaro ◽  
Katie A. Collins ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Synaptic Depression ◽  
Metabotropic Glutamate ◽  
Ca1 Pyramidal Neurons

Properties and ionic mechanisms of a metabotropic glutamate receptor-mediated slow afterdepolarization in neocortical neurons

1994 ◽  
Vol 72 (2) ◽  
pp. 693-704 ◽  
Author(s):  
C. C. Greene ◽  
P. C. Schwindt ◽  
W. E. Crill
Keyword(s):  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptors ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Equilibrium Potential ◽  
Cholinergic Antagonists ◽  
Recording Electrode ◽  
Metabotropic Glutamate ◽  
Ionic Mechanisms ◽  
Layer V

1. Pyramidal neurons from layer V of rat neocortex were recorded intracellularly in a brain slice preparation to study their response to stimulation of metabotropic glutamate receptors (mGluRs) by bath application of the selective mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) and by the nonselective agonists glutamate and quisqualate. 2. The principal postsynaptic effect of mGluR stimulation in the presence of ionotropic glutaminergic and muscarinic cholinergic antagonists was the appearance of a slow afterdepolarization (ADP) after evoked spikes. Only an afterhyperpolarization (AHP) was present in control perfusate. After 20 spikes evoked individually at 100 Hz the ADP peaked at 317 +/- 117 (SD) ms after the spike train, ranged from 1 to 12 mV in peak amplitude, and decayed over 7.4 +/- 4.7 s. This effect was not blocked by L-2-amino-3-phosphono-propionic acid (1 mM). Spikes evoked in the presence of the ionotropic glutamate receptor agonist R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) did not have an ADP. 3. A detectable ADP appeared at concentrations of 0.1 microM quisqualate or 0.5 microM 1S,3R-ACPD. Maximum ADP amplitude was obtained with 5 microM quisqualate or 100 microM 1S,3R-ACPD. The ADP appeared after a single evoked spike in most cells tested and ADP amplitude increased to a maximum as the number of spikes evoked at 100 Hz was increased to between 5 and 20. 4. The ionic mechanisms underlying the ADP were examined by ion substitution and the application of channel-blocking agents. No difference in ADP amplitude was observed when the recording electrode contained CH3SO4. instead of Cl.. The ADP was present after 3 mM extracellular Cs+ were added to block the hyperpolarization-activated cation current or when 100 microM Ba2+ were included to block voltage-gated K+ currents. The ADP was abolished when Mn2+ was substituted for Ca2+ in the perfusate or when the Ca2+ chelator 5,5'-dimethyl-bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid was included in the recording electrode. A large ADP followed Ca2+ spikes evoked in the presence of 1 microM tetrodotoxin with 20 mM tetraethylammonium in the perfusate or with Cs+ substituted for K+ in the recording electrode. The amplitude of the ADP after the Ca2+ spikes was reduced by 49% when extracellular Na+ concentration was reduced from 136 to 26 mM. 5. The voltage dependence of the ADP was examined in relation to K+ equilibrium potential (EK).(ABSTRACT TRUNCATED AT 400 WORDS)

Metabotropic Glutamate Receptor-Mediated Depression of the Slow Afterhyperpolarization Is Gated by Tyrosine Phosphatases in Hippocampal CA1 Pyramidal Neurons

2004 ◽  
Vol 92 (5) ◽  
pp. 2811-2819 ◽  
Author(s):  
David R. Ireland ◽  
Diane Guevremont ◽  
Joanna M. Williams ◽  
Wickliffe C. Abraham
Keyword(s):  
Tyrosine Phosphorylation ◽  
Glutamate Receptor ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Hippocampal Slices ◽  
Specific Inhibitor ◽  
Tyrosine Phosphatases ◽  
Metabotropic Glutamate ◽  
Ca1 Pyramidal Neurons ◽  
Group I

Group I metabotropic glutamate receptor (mGluR) agonists increase the excitability of hippocampal CAl pyramidal neurons via depression of the postspike afterhyperpolarization. In adult rats, this is mediated by both mGluR1 and -5, but the signal transduction processes involved are unknown. In this study, we investigated whether altered levels of tyrosine phosphorylation of proteins are involved in the depression of the slow-duration afterhyperpolarization (sAHP) by the Group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) in CA1 pyramidal neurons of rat hippocampal slices. Preincubation with the tyrosine kinase inhibitors lavendustin A or genistein, or the Src-specific inhibitor 3-(4-chlorophenyl) 1-(1,1-dimethylethyl)-1 H-pyrazolo[3,4-d]pyrimidin-4-amine (PP2), did not inhibit the DHPG-mediated depression of the sAHP. However, preincubation with the tyrosine phosphatase inhibitor orthovanadate reduced the effects of DHPG. This effect of orthovanadate was prevented by simultaneous inhibition of tyrosine kinases with lavendustin A. Selective activation of either mGluR1 or -5 by application of DHPG plus either the mGluR5 antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP) or the mGluR1 antagonist (S)-(+)-α-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385) demonstrated that the effect of inhibiting tyrosine phosphatases is not specific to either subtype of mGluR. These results suggest that the depression of the sAHP induced by activation of mGluR1 and -5 is gated by a balance between tyrosine phosphorylation and dephosphorylation.

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