Olfactory Nerve Stimulation-Evoked mGluR1 Slow Potentials, Oscillations, and Calcium Signaling in Mouse Olfactory Bulb Mitral Cells

2006 ◽  
Vol 95 (5) ◽  
pp. 3097-3104 ◽  
Author(s):  
Q. Yuan ◽  
T. Knöpfel
Keyword(s):  
Glutamate Receptors ◽  
High Frequency ◽  
Metabotropic Glutamate Receptor ◽  
Olfactory Nerve ◽  
Ionotropic Glutamate Receptors ◽  
Mitral Cells ◽  
Slow Potential ◽  
Metabotropic Glutamate ◽  
Metabotropic Glutamate Receptor 1 ◽  
Intracellular Ca

Fast synaptic transmission between olfactory receptor neurons and mitral cells (MCs) is mediated through AMPA and NMDA ionotropic glutamate receptors. MCs also express high levels of metabotropic glutamate receptor 1 (mGluR1) whose functional significance is less understood. Here we characterized a slow mGluR1-mediated potential that was evoked by high-frequency (100-Hz) olfactory nerve (ON) stimulation in the presence of NBQX and d-APV, blockers of ionotropic glutamate receptors, and that was associated with a local Ca2+ transient in the MC dendritic tuft. High-frequency ON stimulation in the presence of NBQX and d-APV also evoked a slow, nearly 2-Hz oscillation of MC membrane potential that was abolished by the mGluR1 antagonist LY367385 (50 μM). Both mGluR slow potential and slow oscillation persisted in the presence of gabazine (10 μM), a GABAA receptor antagonist, and intracellular QX-314 (10 mM), a Na+ channel blocker. In contrast to a slow mGluR1 potential in cerebellar Purkinje neurons, the MC mGluR1 potential was not depressed by SKF96365 (≤250 μM) and thus is likely not mediated by TRPC1 cation channels, nor was it potentiated by an elevation of intracellular Ca2+ level. Imaging with the Na+ indicator SBFI revealed a Na+ transient in the MC dendrite accompanying the mGluR1 slow potential. We conclude that the MC mGluR1 potential triggered by glutamate released from the ON supports oscillations and synchronizations of MCs associated within one glomerulus.

scholarly journals Olfactory Nerve–Evoked, Metabotropic Glutamate Receptor–Mediated Synaptic Responses in Rat Olfactory Bulb Mitral Cells

2006 ◽  
Vol 95 (4) ◽  
pp. 2233-2241 ◽  
Author(s):  
Matthew Ennis ◽  
Mingyan Zhu ◽  
Thomas Heinbockel ◽  
Abdallah Hayar
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Olfactory Nerve ◽  
Mitral Cell ◽  
Evoked Responses ◽  
Mitral Cells ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Apical Dendrites

The group I metabotropic glutamate receptor (mGluR) subtype, mGluR1, is highly expressed on the apical dendrites of olfactory bulb mitral cells and thus may be activated by glutamate released from olfactory nerve (ON) terminals. Previous studies have shown that mGluR1 agonists directly excite mitral cells. In the present study, we investigated the involvement of mGluR1 in ON-evoked responses in mitral cells in rat olfactory bulb slices using patch-clamp electrophysiology. In voltage-clamp recordings, the average EPSC evoked by single ON shocks or brief trains of ON stimulation (six pulses at 50 Hz) in normal physiological conditions were not significantly affected by the nonselective mGluR antagonist LY341495 (50–100 μΜ) or the mGluR1-specific antagonist LY367385 (100 μM); ON-evoked responses were attenuated, however, in a subset (36%) of cells. In the presence of blockers of ionotropic glutamate and GABA receptors, application of the glutamate uptake inhibitors THA (300 μM) and TBOA (100 μM) revealed large-amplitude, long-duration responses to ON stimulation, whereas responses elicited by antidromic activation of mitral/tufted cells were unaffected. Magnitudes of the ON-evoked responses elicited in the presence of THA–TBOA were dependent on stimulation intensity and frequency, and were maximal during high-frequency (50-Hz) bursts of ON spikes, which occur during odor stimulation. ON-evoked responses elicited in the presence of THA–TBOA were significantly reduced or completely blocked by LY341495 or LY367385 (100 μM). These results demonstrate that glutamate transporters tightly regulate access of synaptically evoked glutamate from ON terminals to postsynaptic mGluR1s on mitral cell apical dendrites. Taken together with other findings, the present results suggest that mGluR1s may not play a major role in phasic responses to ON input, but instead may play an important role in shaping slow oscillatory activity in mitral cells and/or activity-dependent regulation of plasticity at ON–mitral cell synapses.

scholarly journals Parasagittally aligned, mGluR1-dependent patches are evoked at long latencies by parallel fiber stimulation in the mouse cerebellar cortex in vivo

2011 ◽  
Vol 105 (4) ◽  
pp. 1732-1746 ◽  
Author(s):  
Xinming Wang ◽  
Gang Chen ◽  
Wangcai Gao ◽  
Timothy J. Ebner
Keyword(s):  
Glutamate Receptor ◽  
Cerebellar Cortex ◽  
High Frequency ◽  
Metabotropic Glutamate Receptor ◽  
Long Term Potentiation ◽  
Metabotropic Glutamate ◽  
Zebrin Ii ◽  
Long Latency ◽  
Intracellular Ca

The parallel fibers (PFs) in the cerebellar cortex extend several millimeters along a folium in the mediolateral direction. The PFs are orthogonal to and cross several parasagittal zones defined by the olivocerebellar and corticonuclear pathways and the expression of molecular markers on Purkinje cells (PCs). The functions of these two organizations remain unclear, including whether the bands respond similarly or differentially to PF input. By using flavoprotein imaging in the anesthetized mouse in vivo, this study demonstrates that high-frequency PF stimulation, which activates a beamlike response at short latency, also evokes patches of activation at long latencies. These patches consist of increased fluorescence along the beam at latencies of 20–25 s with peak activation at 35 s. The long-latency patches are completely blocked by the type 1 metabotropic glutamate receptor (mGluR1) antagonist LY367385. Conversely, the AMPA and NMDA glutamate receptor antagonists DNQX and APV have little effect. Organized in parasagittal bands, the long-latency patches align with zebrin II-positive PC stripes. Additional Ca2+ imaging demonstrates that the patches reflect increases in intracellular Ca2+. Both the PLCβ inhibitor U73122 and the ryanodine receptor inhibitor ryanodine completely block the long-latency patches, indicating that the patches are due to Ca2+ release from intracellular stores. Robust, mGluR1-dependent long-term potentiation (LTP) of the patches is induced using a high-frequency PF stimulation conditioning paradigm that generates LTP of PF-PC synapses. Therefore, the parasagittal bands, as defined by the molecular compartmentalization of PCs, respond differentially to PF inputs via mGluR1-mediated release of internal Ca2+.

Metabotropic glutamate receptors depress vagal and aortic baroreceptor signal transmission in the NTS

1998 ◽  
Vol 275 (5) ◽  
pp. H1682-H1694 ◽  
Author(s):  
Zhi Liu ◽  
Chao-Yin Chen ◽  
Ann C. Bonham
Keyword(s):  
Glutamate Receptors ◽  
Glutamate Receptor ◽  
High Frequency ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Signal Transmission ◽  
Low Frequency ◽  
Metabotropic Glutamate ◽  
Frequency Stimulation ◽  
Glutamate Receptor Agonist

We sought to determine whether metabotropic glutamate receptors contribute to frequency-dependent depression of vagal and aortic baroreceptor signal transmission in the nucleus of the solitary tract (NTS) in vivo. In α-chloralose-anesthetized rabbits, we determined the number of extracellular action potentials synaptically evoked by low (1 Hz)- or high-frequency vagal (3–20 Hz) or aortic depressor nerve (ADN) (6–80 Hz) stimulation and postsynaptically evoked by the ionotropic glutamate receptor agonist α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). The metabotropic glutamate receptor agonist (2 S,1′ S,2′ S)-2-(carboxycyclopropyl)glycine (L-CCG-I) attenuated NTS responses monosynaptically evoked by 1-Hz vagus stimulation by 34% ( n = 25; P = 0.011), while augmenting AMPA-evoked responses by 64% ( n = 17; P = 0.026). The metabotropic glutamate receptor antagonist α-methyl-4-phosphonophenylglycine (MPPG) did not affect NTS responses to low-frequency vagal stimulation ( n = 11) or AMPA ( n = 10) but augmented responses to high-frequency stimulation by 50% ( n= 25; P = 0.0001). MPPG also augmented NTS responses to high-frequency ADN stimulation by 35% ( n = 9; P = 0.048) but did not affect responses to low-frequency stimulation ( n = 9) or AMPA ( n = 7). The results suggest that metabotropic glutamate receptors, presumably at presynaptic sites, contribute to frequency-dependent depression of vagal and aortic baroreceptor signal transmission in NTS.

Are there ionotropic glutamate receptors on the rod bipolar cell of the mouse retina?

1997 ◽  
Vol 14 (1) ◽  
pp. 103-109 ◽  
Author(s):  
Thomas E. Hughes
Keyword(s):  
Glutamate Receptors ◽  
Glutamate Receptor ◽  
Bipolar Cell ◽  
Metabotropic Glutamate Receptor ◽  
Bipolar Cells ◽  
Ionotropic Glutamate Receptors ◽  
Mouse Retina ◽  
Rod Photoreceptor ◽  
Metabotropic Glutamate ◽  
C Terminus

AbstractThere is some evidence that the mammalian rod bipolar cell expresses ionotropic glutamate receptors. This is surprising in light of the strong evidence that the glutamate released by the rod photoreceptor acts upon a metabotropic glutamate receptor-mGluRo-present in the dendrites of the rod bipolar cell. To reexamine the issue of which glutamate receptor subunits may be present on the rod bipolar cell, an immunohistochemical study of acutely dissociated retinal cells was undertaken. Two monoclonal antibodies provided some evidence that GluR2 and/or GluR4, as well as NMDAR1 subunit, are present on the rod bipolar cell. A monoclonal antibody directed against the N-terminus of GluR2 labeled the rod bipolar cells, but two antisera directed against the C-terminus of the same subunit did not. One possible explanation for this discrepancy could be that the rare splice variant GluR2-long, which is endowed with a different C-terminus, could be expressed by the rod bipolar cell. To explore this possibility, RT-PCR was used to amplify the transcripts encoding GluR2 in the neural retina. This revealed that GluR2-long transcripts, with the flop exon, are present.

Localization of ionotropic glutamate receptors to invaginating dendrites at the cone synapse in primate retina

2005 ◽  
Vol 22 (4) ◽  
pp. 469-477 ◽  
Author(s):  
DAVID J. CALKINS
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Glutamate Release ◽  
Ultrastructural Localization ◽  
Bipolar Cells ◽  
Ionotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Signal Light ◽  
G Protein Coupled ◽  
Microscopic Distribution

The separation of OFF pathways that signal light decrements from ON pathways that signal light increments occurs at the first retinal synapse. The dendrites of OFF bipolar cells abut the cone pedicle at basal positions distal to the site of glutamate release and express ligand-gated or ionotropic glutamate receptors (GluR). The dendrites of ON bipolar cells penetrate narrow invaginations of the cone pedicle proximal to the site of release and express the G-protein-coupled, metabotropic glutamate receptor, mGluR6. However, recent studies demonstrating the expression of GluR subunits in the rodent rod bipolar cell, known to yield an ON response to light, call this basic segregation of receptors into question. The light-microscopic distribution of many glutamate receptors in the primate retina is now well established. We reexamined their ultrastructural localization in the outer retina ofMacaca fascicularisto test systematically whether invaginating dendrites at the cone synapse, presumably from ON bipolar cells, also express one or more ionotropic subunits. Using preembedding immunocytochemistry for electron microscopy, we quantified the distribution of the AMPA-sensitive subunits GluR2/3 and GluR4 and of the kainate-sensitive subunits GluR6/7 across 207 labeled dendrites occupying specific morphological loci at the cone pedicle. We report, in agreement with published investigations, that the majority of labeled processes for GluR2/3 (70%) and GluR4 (67%) either occupy basal positions or arise from horizontal cells. For GluR6/7, we find a significantly lower fraction of labeled processes at these positions (47%). We also find a considerable number of labeled dendrites for GluR2/3 (10%), GluR4 (21%), and GluR6/7 (18%) at invaginating positions. Surprisingly, for each subunit, the remainder of labeled processes corresponds to “fingers” of presynaptic cytoplasm within the cone invagination.

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