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

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

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.

The role of metabotropic glutamate receptor 5 in developmental lead neurotoxicity

2009 ◽  
Vol 191 (2-3) ◽  
pp. 223-230 ◽  
Author(s):  
Jian Xu ◽  
Chong-huai Yan ◽  
Bo Yang ◽  
Han-fang Xie ◽  
Xiang-yu Zou ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Metabotropic Glutamate Receptor 5 ◽  
Metabotropic Glutamate

The inhibiting role of periaqueductal gray metabotropic glutamate receptor subtype 8 in a rat model of central neuropathic pain

2020 ◽  
Vol 42 (6) ◽  
pp. 515-521 ◽  
Author(s):  
Marjan Hosseini ◽  
Mohsen Parviz ◽  
Alireza P. Shabanzadeh ◽  
Elham Zamani ◽  
Parvaneh Mohseni-Moghaddam ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Glutamate Receptor ◽  
Rat Model ◽  
Metabotropic Glutamate Receptor ◽  
Periaqueductal Gray ◽  
Receptor Subtype ◽  
Central Neuropathic Pain ◽  
Metabotropic Glutamate

Suppression of the glutamate receptor delta 2 subunit produces a specific impairment in cerebellar long-term depression

1996 ◽  
Vol 76 (5) ◽  
pp. 3578-3583 ◽  
Author(s):  
A. Jeromin ◽  
R. L. Huganir ◽  
D. J. Linden
Keyword(s):  
Glutamate Receptor ◽  
Antisense Oligonucleotide ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Calcium Influx ◽  
Long Term Depression ◽  
Metabotropic Glutamate ◽  
Flow Through

1. The role of the glutamate receptor subunit delta 2 in the induction of cerebellar long-term depression (LTD) was investigated by application of antisense oligonucleotides. The delta 2 subunit is selectively localized to Purkinje cells (PCs), with the highest levels being in the PC dendritic spines, where parallel fibers are received and where cerebellar LTD is expressed. 2. Immunocytochemical analysis of calbindin-positive PCs revealed that both the dendritic and somatic expression of delta 2 was reduced in antisense-but not in sense-treated cultures. An antisense oligonucleotide directed against the related subunit delta 1 did not affect the expression of delta 2 in PCs. 3. Cerebellar LTD may be reliably induced in a preparation of cultured embryonic cerebellar neurons from the mouse when parallel and climbing fiber stimulation are replaced by brief glutamate pulses and strong, direct depolarization of the PC, respectively. Application of an antisense oligonucleotide directed against delta 2 completely blocked the induction of LTD produced by glutamate/ depolarization conjunctive stimulation. A delta 2 sense oligonucleotide or an antisense oligonucleotide directed against the related delta 1 subunit had no effect. 4. The effect of the delta 2 antisense oligonucleotide was not related to attenuation of calcium influx via voltage-gated channels or calcium mobilization via metabotropic glutamate receptors, as assessed with fura-2 microfluorimetry. Current flow through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-receptor-associated ion channels also appeared unaltered. All three of these processes have previously been shown to be required for cerebellar LTD induction. The observation that delta 2 is involved in a metabotropic-glutamate-receptor-independent signaling pathway that is required for LTD induction supports the view that delta 2 participates in the formation of a novel postsynaptic receptor complex.

Sign in / Sign up

Export Citation Format

Share Document