scholarly journals Excitatory Actions of Noradrenaline and Metabotropic Glutamate Receptor Activation in Granule Cells of the Accessory Olfactory Bulb

2009 ◽  
Vol 102 (2) ◽  
pp. 1103-1114 ◽  
Author(s):  
Richard S. Smith ◽  
Christopher J. Weitz ◽  
Ricardo C. Araneda
Keyword(s):  
Olfactory Bulb ◽  
Receptor Antagonist ◽  
Glutamate Receptor ◽  
Adrenergic Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Granule Cells ◽  
Mitral Cells ◽  
Accessory Olfactory Bulb ◽  
Metabotropic Glutamate ◽  
Excitatory Action

Modulation of dendrodendritic synapses by the noradrenergic system in the accessory olfactory bulb (AOB) plays a key role in the formation of memory in olfactory-mediated behaviors. We have recently shown that noradrenaline (NA) inhibits mitral cells by increasing γ-aminobutyric acid inhibitory input onto mitral cells in the AOB, suggesting an excitatory action of NA on granule cells (GCs). Here, we show that NA (10 μM) elicits a long-lasting depolarization of GCs. This effect is mediated by activation of α1-adrenergic receptors as the depolarization is mimicked by phenylephrine (PE, 30 μM) and completely blocked by the α1-adrenergic receptor antagonist prazosin (300 nM). In addition to this depolarization, application of NA induced the appearance of a slow afterdepolarization (sADP) following a stimulus-elicited train of action potentials. Similarly, the group I metabotropic glutamate receptor (mGluR1) agonist DHPG (10–30 μM) also produced a depolarization of GCs and the appearance of a stimulus-induced sADP. The ionic and voltage dependence and sensitivity to blockers of the sADP suggest that it is mediated by the nonselective cationic conductance ICAN. Thus the excitatory action resulting from the activation of these receptors could be mediated by a common transduction target. Surprisingly, the excitatory effect of PE on GCs was completely blocked by the mGluR1 antagonist LY367385 (100 μM). Conversely, the effect of DHPG was not antagonized by the α1-adrenergic receptor antagonist prazosin (300 nM). These results suggest that most of the noradrenergic effect on GCs in the AOB is mediated by potentiation of a basal activity of mGluR1s.

Role of a metabotropic glutamate receptor in synaptic modulation in the accessory olfactory bulb

Nature ◽  
1993 ◽  
Vol 366 (6456) ◽  
pp. 687-690 ◽  
Author(s):  
Yasunori Hayashi ◽  
Akiko Momiyama ◽  
Tomoyuki Takahashi ◽  
Hitoshi Ohishi ◽  
Reiko Ogawa-Meguro ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Accessory Olfactory Bulb ◽  
Synaptic Modulation ◽  
Metabotropic Glutamate

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.

315 A role of the mGluR2 metabotropic glutamate receptor in sensory processing of the accessory olfactory bulb

1993 ◽  
Vol 18 ◽  
pp. S42
Author(s):  
Yasunori Hayashi ◽  
Akiko Momiyama ◽  
Tomoyuki Takahashi ◽  
Hitoshi Ohishi ◽  
Reiko Ogawa-Meguro ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptor ◽  
Sensory Processing ◽  
Metabotropic Glutamate Receptor ◽  
Accessory Olfactory Bulb ◽  
Metabotropic Glutamate

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.

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