scholarly journals Activation of Group I Metabotropic Glutamate Receptors on Main Olfactory Bulb Granule Cells and Periglomerular Cells Enhances Synaptic Inhibition of Mitral Cells

2007 ◽  
Vol 27 (21) ◽  
pp. 5654-5663 ◽  
Author(s):  
H.-W. Dong ◽  
A. Hayar ◽  
M. Ennis
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Granule Cells ◽  
Synaptic Inhibition ◽  
Mitral Cells ◽  
Main Olfactory Bulb ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Periglomerular Cells

Group I Metabotropic Glutamate Receptors Are Differentially Expressed by Two Populations of Olfactory Bulb Granule Cells

2007 ◽  
Vol 97 (4) ◽  
pp. 3136-3141 ◽  
Author(s):  
Thomas Heinbockel ◽  
Kathryn A. Hamilton ◽  
Matthew Ennis
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Granule Cells ◽  
Mitral Cell ◽  
Mitral Cells ◽  
Patch Clamp Recording ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Bath Application

In the main olfactory bulb, several populations of granule cells (GCs) can be distinguished based on the soma location either superficially, interspersed with mitral cells within the mitral cell layer (MCL), or deeper, within the GC layer (GCL). Little is known about the physiological properties of superficial GCs (sGCs) versus deep GCs (dGCs). Here, we used patch-clamp recording methods to explore the role of Group I metabotropic glutamate receptors (mGluRs) in regulating the activity of GCs in slices from wildtype and mGluR−/− mutant mice. In wildtype mice, bath application of the selective Group I mGluR agonist DHPG depolarized and increased the firing rate of both GC subtypes. In the presence of blockers of fast synaptic transmission (APV, CNQX, gabazine), DHPG directly depolarized both GC subtypes, although the two GC subtypes responded differentially to DHPG in mGluR1−/− and mGluR5−/− mice. DHPG depolarized sGCs in slices from mGluR5−/− mice, although it had no effect on sGCs in slices from mGluR1−/− mice. By contrast, DHPG depolarized dGCs in slices from mGluR1−/− mice but had no effect on dGCs in slices from mGluR5−/− mice. Previous studies showed that mitral cells express mGluR1 but not mGluR5. The present results therefore suggest that sGCs are more similar to mitral cells than dGCs in terms of mGluR expression.

Modulation of mEPSCs in Olfactory Bulb Mitral Cells by Metabotropic Glutamate Receptors

1997 ◽  
Vol 78 (3) ◽  
pp. 1468-1475 ◽  
Author(s):  
N. E. Schoppa ◽  
G. L. Westbrook
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Mitral Cells ◽  
Group Iii ◽  
Metabotropic Glutamate ◽  
Selective Agonist ◽  
Group I ◽  
Mepsc Frequency ◽  
Group Ii

Schoppa, N. E. and G. L. Westbrook. Modulation of mEPSCs in olfactory bulb mitral cells by metabotropic glutamate receptors. J. Neurophysiol. 78: 1468–1475, 1997. Olfactory bulb mitral cells express group I (mGluR1), group II (mGluR2), and group III (mGluR7 and mGluR8) metabotropic glutamate receptors. We examined the role of these mGluRs on excitatory synaptic transmission in cultured mitral cells with the use of whole cell patch-clamp recordings. The effects of group-selective mGluR agonists and antagonists were tested on α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor-mediated miniature excitatory postsynaptic currents (mEPSCs). (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylate (ACPD) or the group-I-selective agonist 3,5-dihydroxyphenylglycine evoked an inward current accompanied by a decrease in membrane conductance, consistent with the previously described closure of potassium channels by group I agonists. The increased cellular excitability was accompanied by an increase in mEPSC frequency in some cells. When calcium entry was blocked by cadmium, ACPD or the group-II-selective agonist 2-(2,3-dicarboxycyclopropyl)-glycine reduced the mEPSC frequency. l-2-amino-4-phosphonobutyric acid (l-AP4), a group-III-selective agonist, caused a similar decrease. The concentration-dependence ofl-AP4-mediated inhibition was most consistent with activation of mGluR8. We investigated two possible effector mechanisms for the group III presynaptic receptor. Bath application of forskolin or 3-isobutyl-1-methylxantine had no effect on mEPSC frequency. Increasing calcium influx by raising extracellular K+ caused a large increase in the mEPSC frequency but did not enhance l-AP4-mediated inhibition. Thus inhibition of mEPSCs involves a mechanism downstream of calcium entry and appears to be independent of adenosine 3′,5′-cyclic monophosphate. Our results indicate that both group II and III receptors can inhibit glutamate release at mitral cell terminals. Although group II/III receptors had a similar effect on mEPSCs, differences in location on nerve terminals and in glutamate sensitivity suggest that each mGluR may have discrete actions on mitral cell activity.

scholarly journals Metabotropic Glutamate Receptors and Dendrodendritic Synapses in the Main Olfactory Bulb

2009 ◽  
Vol 1170 (1) ◽  
pp. 224-238 ◽  
Author(s):  
Hong-Wei Dong ◽  
Thomas Heinbockel ◽  
Kathryn A. Hamilton ◽  
Abdallah Hayar ◽  
Matthew Ennis
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Main Olfactory Bulb ◽  
Metabotropic Glutamate ◽  
Dendrodendritic Synapses

scholarly journals Metabotropic Glutamate Receptors in the Main Olfactory Bulb Drive Granule Cell-Mediated Inhibition

2007 ◽  
Vol 97 (1) ◽  
pp. 858-870 ◽  
Author(s):  
Thomas Heinbockel ◽  
Nora Laaris ◽  
Matthew Ennis
Keyword(s):  
Olfactory Bulb ◽  
Metabotropic Glutamate Receptor ◽  
Feedback Inhibition ◽  
Mitral Cell ◽  
Equilibrium Potential ◽  
Mitral Cells ◽  
Main Olfactory Bulb ◽  
Inward Current ◽  
Metabotropic Glutamate ◽  
Group I

Main olfactory bulb (MOB) granule cells (GCs) express high levels of the group I metabotropic glutamate receptor (mGluR), mGluR5. We investigated the role of mGluRs in regulating GC activity in rodent MOB slices using whole cell patch-clamp electrophysiology. The group I/II mGluR agonist (±)-1-aminocyclopentane- trans-1,3-dicarboxylic acid (ACPD) or the selective group I agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) depolarized (∼20 mV) and increased the firing rate of GCs. In the presence of ionotropic glutamate and GABA receptor antagonists, DHPG evoked a more modest depolarization (∼8 mV). In voltage clamp, DHPG, but not group II [(2S,2′R,3)-2-(2′,3′-dicarboxycyclopropyl)glycine, DCG-IV] or group III [L(+)-2-amino-4-phosphonobutyric acid, L-AP4] mGluR agonists, induced an inward current. The inward current reversed polarity near the potassium equilibrium potential, suggesting mediation by closure of potassium channels. The DHPG-evoked inward current was unaffected by the mGluR1 antagonist ( S)-(+)-α-amino-4-carboxy-2-methylbenzeneacetic acid (LY367385), was blocked by the group I/II mGluR antagonist (α S)-α-amino-α-[(1 S,2 S)-2-carboxycyclopropyl]-9H-xanthine-9-propanoic acid (LY341495), and was absent in GCs from mGluR5 knockout mice. LY341495 also attenuated mitral cell-evoked voltage-sensitive dye signals in the external plexiform layer and mitral cell-evoked spikes in GCs. These results suggest that activation of mGluR5 increases GC excitability, an effect that should increase GC-mediated GABAergic inhibition of mitral cells. In support of this: DHPG increased the frequency of spontaneous GABAergic inhibitory postsynaptic currents in mitral cells and LY341495 attenuated the feedback GABAergic postsynaptic potential elicited by intracellular depolarization of mitral cells. Our results suggest that activation of mGluR5 participates in feedforward and/or feedback inhibition at mitral cell to GC dendrodendritic synapses, possibly to modulate lateral inhibition and contrast in the MOB.

scholarly journals Activation of group I metabotropic glutamate receptors enhances persistent sodium current and rhythmic bursting in main olfactory bulb external tufted cells

2014 ◽  
Vol 111 (3) ◽  
pp. 641-647 ◽  
Author(s):  
Hong-Wei Dong ◽  
Matthew Ennis
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Sodium Current ◽  
Network Activity ◽  
Burst Frequency ◽  
Metabotropic Glutamate ◽  
Calcium Dependent ◽  
State Dependent ◽  
Group I

Rhythmically bursting olfactory bulb external tufted (ET) cells are thought to play a key role in synchronizing glomerular network activity to respiratory-driven sensory input. Whereas spontaneous bursting in these cells is intrinsically generated by interplay of several voltage-dependent currents, bursting strength and frequency can be modified by local intrinsic and centrifugal synaptic input. Activation of metabotropic glutamate receptors (mGluRs) engages a calcium-dependent cation current ( ICAN) that increases rhythmic bursting, but mGluRs may also modulate intrinsic mechanisms involved in bursting. Here, we used patch-clamp electrophysiology in rat olfactory bulb slices to investigate whether mGluRs modulate two key intrinsic currents involved in ET cell burst initiation: persistent sodium ( INaP) and hyperpolarization-activated cation ( Ih) currents. Using a BAPTA-based internal solution to block ICAN, we found that the mGluR1/5 agonist DHPG enhanced INaP but did not alter Ih. INaP enhancement consisted of increased current at membrane potentials between −60 and −50 mV and a hyperpolarizing shift in activation threshold. Both effects would be predicted to shorten the interburst interval. In agreement, DHPG modestly depolarized (∼3.5 mV) ET cells and increased burst frequency without effect on other major burst parameters. This increase was inversely proportional to the basal burst rate such that slower ET cells exhibited the largest increases. This may enable ET cells with slow intrinsic burst rates to pace with faster sniff rates. Taken with other findings, these results indicate that multiple neurotransmitter mechanisms are engaged to fine-tune rhythmic ET cell bursting to context- and state-dependent changes in sniffing frequency.

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