scholarly journals Developmental regulation of metabotropic glutamate receptor 1 splice variants in olfactory bulb mitral cells

2009 ◽  
Vol 87 (2) ◽  
pp. 369-379 ◽  
Author(s):  
P. Bovolin ◽  
S. Bovetti ◽  
A. Fasolo ◽  
Z. Katarova ◽  
G. Szabo ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Splice Variants ◽  
Developmental Regulation ◽  
Mitral Cells ◽  
Metabotropic Glutamate ◽  
Metabotropic Glutamate Receptor 1

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 Metabotropic glutamate receptor 1 splice variants mGluR1a and mGluR1b combine in mGluR1a/b dimers in vivo

2014 ◽  
Vol 86 ◽  
pp. 329-336 ◽  
Author(s):  
Šárka Techlovská ◽  
Jayne Nicole Chambers ◽  
Michaela Dvořáková ◽  
Ronald S. Petralia ◽  
Ya-Xian Wang ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Splice Variants ◽  
Metabotropic Glutamate ◽  
Metabotropic Glutamate Receptor 1

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.

scholarly journals Metabotropic glutamate receptor 1 is associated with unfavorable prognosis in ER-negative and triple-negative breast cancer

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Anna E. M. Bastiaansen ◽  
A. Mieke Timmermans ◽  
Marcel Smid ◽  
Carolien H. M. van Deurzen ◽  
Esther S. P. Hulsenboom ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Expression ◽  
Glutamate Receptor ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Metabotropic Glutamate Receptor ◽  
Metabotropic Glutamate ◽  
Metabotropic Glutamate Receptor 1 ◽  
Novel Target ◽  
Cancer Tissues

AbstractNew therapies are an urgent medical need in all breast cancer subgroups. Metabotropic glutamate receptor 1 (mGluR1) is suggested as a potential new molecular target. We examined the prevalence mGluR1 expression in different clinically relevant breast cancer subgroups and determined its association with prognosis. In this retrospective cohort, 394 consecutive primary breast cancer tissues were incorporated into a tissue microarray and immunohistochemically stained for mGluR1. The prevalence of mGluR1 protein expression in different breast cancer subgroups was evaluated and correlated with metastasis-free survival (MFS) and overall survival (OS). In total, 56% (n = 219) breast cancer tissues had mGluR1 expression. In estrogen receptor (ER)-negative tumors, 31% (n = 18/58) had mGluR1 expression that was significantly associated with MFS (HR 5.00, 95% CI 1.03–24.35, p = 0.046) in multivariate analysis, independently from other prognostic factors. Of the 44 triple-negative breast cancer (TNBC), 25% (n = 11) expressed mGluR1. mGluR1 expression in TNBC was significantly associated with shorter MFS (HR 8.60, 95% CI 1.06–20.39, p = 0.044) and with poor OS (HR 16.07, 95% CI 1.16–223.10, p = 0.039). In conclusion, mGluR1 is frequently expressed in breast cancer. In ER-negative breast cancer and in TNBC mGluR1 protein expression is an unfavorable prognostic marker. This study provides rationale to explore mGluR1 as a novel target for breast cancer treatment, especially for the more aggressive TNBC.

scholarly journals Autosomal-Recessive Congenital Cerebellar Ataxia Is Caused by Mutations in Metabotropic Glutamate Receptor 1

2012 ◽  
Vol 91 (3) ◽  
pp. 553-564 ◽  
Author(s):  
Velina Guergueltcheva ◽  
Dimitar N. Azmanov ◽  
Dora Angelicheva ◽  
Katherine R. Smith ◽  
Teodora Chamova ◽  
...  
Keyword(s):  
Cerebellar Ataxia ◽  
Glutamate Receptor ◽  
Autosomal Recessive ◽  
Metabotropic Glutamate Receptor ◽  
Metabotropic Glutamate ◽  
Metabotropic Glutamate Receptor 1
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