scholarly journals Activity-dependent gating of lateral inhibition by correlated mitral cell activity in the mouse main olfactory bulb

2007 ◽  
Vol 8 (S2) ◽  
Author(s):  
Armen C Arevian ◽  
Nathaniel N Urban
Keyword(s):  
Olfactory Bulb ◽  
Lateral Inhibition ◽  
Cell Activity ◽  
Mitral Cell ◽  
Main Olfactory Bulb ◽  
Activity Dependent

scholarly journals Cannabinoid receptor-mediated modulation of inhibitory inputs to mitral cells in the main olfactory bulb

2019 ◽  
Vol 122 (2) ◽  
pp. 749-759 ◽  
Author(s):  
Ze-Jun Wang ◽  
Sherry Shu-Jung Hu ◽  
Heather B. Bradshaw ◽  
Liqin Sun ◽  
Ken Mackie ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Cannabinoid Receptor ◽  
Cell Activity ◽  
Gaba Release ◽  
Mitral Cell ◽  
Mitral Cells ◽  
Main Olfactory Bulb ◽  
Glomerular Layer ◽  
And Behavior

The endocannabinoid (eCB) signaling system has been functionally implicated in many brain regions. Our understanding of the role of cannabinoid receptor type 1 (CB1) in olfactory processing remains limited. Cannabinoid signaling is involved in regulating glomerular activity in the main olfactory bulb (MOB). However, the cannabinoid-related circuitry of inputs to mitral cells in the MOB has not been fully determined. Using anatomical and functional approaches we have explored this question. CB1 was present in periglomerular processes of a GAD65-positive subpopulation of interneurons but not in mitral cells. We detected eCBs in the mouse MOB as well as the expression of CB1 and other genes associated with cannabinoid signaling in the MOB. Patch-clamp electrophysiology demonstrated that CB1 agonists activated mitral cells and evoked an inward current, while CB1 antagonists reduced firing and evoked an outward current. CB1 effects on mitral cells were absent in subglomerular slices in which the olfactory nerve layer and glomerular layer were removed, suggesting the glomerular layer as the site of CB1 action. We previously observed that GABAergic periglomerular cells show the inverse response pattern to CB1 activation compared with mitral cells, suggesting that CB1 indirectly regulates mitral cell activity as a result of cellular activation of glomerular GABAergic processes . This hypothesis was supported by the finding that cannabinoids modulated synaptic transmission to mitral cells. We conclude that CB1 directly regulates GABAergic processes in the glomerular layer to control GABA release and, in turn, regulates mitral cell activity with potential effects on olfactory threshold and behavior. NEW & NOTEWORTHY Cannabinoid signaling with cannabinoid receptor type 1 (CB1) is involved in the regulation of glomerular activity in the main olfactory bulb (MOB). We detected endocannabinoids in the mouse MOB. CB1 was present in periglomerular processes of a GAD65-positive subpopulation of interneurons. CB1 agonists activated mitral cells. CB1 directly regulates GABAergic processes to control GABA release and, in turn, regulates mitral cell activity with potential effects on olfactory threshold and behavior.

Changes in the connections of the main olfactory bulb after mitral cell selective neurodegeneration

2007 ◽  
Vol 85 (11) ◽  
pp. 2407-2421 ◽  
Author(s):  
Javier S. Recio ◽  
Eduardo Weruaga ◽  
Carmela Gómez ◽  
Jorge Valero ◽  
Jesús G. Briñón ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Mitral Cell ◽  
Main Olfactory Bulb

scholarly journals Cell and circuit origins of fast network oscillations in the mammalian main olfactory bulb

2021 ◽  
Author(s):  
Shawn D Burton ◽  
Nathan N Urban
Keyword(s):  
Olfactory Bulb ◽  
Sensory Information ◽  
Cell Types ◽  
Mitral Cell ◽  
Main Olfactory Bulb ◽  
Network Oscillations ◽  
Fast Network ◽  
Synchronous Network ◽  
Gamma Frequencies ◽  
Lateral Excitation

Neural synchrony generates fast network oscillations throughout the brain, including the main olfactory bulb (MOB), the first processing station of the olfactory system. Identifying the mechanisms synchronizing neurons in the MOB will be key to understanding how network oscillations support the coding of a high-dimensional sensory space. Here, using paired recordings and optogenetic activation of glomerular sensory inputs in MOB slices, we uncovered profound differences in principal mitral cell (MC) vs. tufted cell (TC) spike-time synchrony: TCs robustly synchronized across fast- and slow-gamma frequencies, while MC synchrony was weaker and concentrated in slow-gamma frequencies. Synchrony among both cell types was enhanced by shared glomerular input but was independent of intraglomerular lateral excitation. Cell-type differences in synchrony could also not be traced to any difference in the synchronization of synaptic inhibition. Instead, greater TC than MC synchrony paralleled the more periodic firing among resonant TCs than MCs and emerged in patterns consistent with densely synchronous network oscillations. Collectively, our results thus reveal a mechanism for parallel processing of sensory information in the MOB via differential TC vs. MC synchrony, and further contrast mechanisms driving fast network oscillations in the MOB from those driving the sparse synchronization of irregularly-firing principal cells throughout cortex.

scholarly journals Cell and circuit origins of fast network oscillations in the mammalian main olfactory bulb

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Shawn D Burton ◽  
Nathan N Urban
Keyword(s):  
Olfactory Bulb ◽  
Sensory Information ◽  
Cell Types ◽  
Mitral Cell ◽  
Main Olfactory Bulb ◽  
Network Oscillations ◽  
Fast Network ◽  
Synchronous Network ◽  
Gamma Frequencies ◽  
Lateral Excitation

Neural synchrony generates fast network oscillations throughout the brain, including the main olfactory bulb (MOB), the first processing station of the olfactory system. Identifying the mechanisms synchronizing neurons in the MOB will be key to understanding how network oscillations support the coding of a high-dimensional sensory space. Here, using paired recordings and optogenetic activation of glomerular sensory inputs in MOB slices, we uncovered profound differences in principal mitral cell (MC) vs. tufted cell (TC) spike-time synchrony: TCs robustly synchronized across fast- and slow-gamma frequencies, while MC synchrony was weaker and concentrated in slow-gamma frequencies. Synchrony among both cell types was enhanced by shared glomerular input but was independent of intraglomerular lateral excitation. Cell-type differences in synchrony could also not be traced to any difference in the synchronization of synaptic inhibition. Instead, greater TC than MC synchrony paralleled the more periodic firing among resonant TCs than MCs and emerged in patterns consistent with densely synchronous network oscillations. Collectively, our results thus reveal a mechanism for parallel processing of sensory information in the MOB via differential TC vs. MC synchrony, and further contrast mechanisms driving fast network oscillations in the MOB from those driving the sparse synchronization of irregularly-firing principal cells throughout cortex.

scholarly journals BMPR-2 gates activity-dependent stabilization of dendrites during mitral cell remodeling

2020 ◽  
Author(s):  
Shuhei Aihara ◽  
Satoshi Fujimoto ◽  
Richi Sakaguchi ◽  
Takeshi Imai
Keyword(s):  
Olfactory Bulb ◽  
Neuronal Activity ◽  
Mitral Cell ◽  
In Utero ◽  
Mitral Cells ◽  
Selective Stabilization ◽  
Multiple Primary ◽  
Cell Remodeling ◽  
Developing Neurons ◽  
Activity Dependent

SUMMARYDeveloping neurons initially form excessive neurites and then remodel them based on molecular cues and neuronal activity. Developing mitral cells in the olfactory bulb initially extend multiple primary dendrites. They then stabilize single primary dendrites, while eliminating others. However, the mechanisms underlying the selective dendrite remodeling remain elusive. Using CRISPR/Cas9-based knockout screening combined with in utero electroporation, we identified BMPR-2 as a key regulator for the selective dendrite stabilization. Bmpr2 knockout and its rescue experiments show that BMPR-2 inhibits LIMK without ligands and thereby facilitates dendrite destabilization. In contrast, the overexpression of antagonists and agonists indicate that ligand-bound BMPR-2 stabilizes dendrites, most likely by releasing LIMK. Using genetic and FRET imaging experiments, we also demonstrate that free LIMK is activated by NMDARs via Rac1, facilitating dendrite stabilization through F-actin formation. Thus, the selective stabilization of mitral cell dendrites is ensured by concomitant inputs of BMP ligands and neuronal activity.

Effect of vasopressin on rat olfactory bulb mitral cell activity

2009 ◽  
Vol 65 ◽  
pp. S219
Author(s):  
Hirofumi Hashimoto ◽  
Gareth Leng ◽  
Mike Ludwig
Keyword(s):  
Olfactory Bulb ◽  
Cell Activity ◽  
Mitral Cell

scholarly journals Postnatal Developmental Expression of Calbindin, Calretinin and Parvalbumin in Mouse Main Olfactory Bulb

2005 ◽  
Vol 37 (4) ◽  
pp. 276-282 ◽  
Author(s):  
Zhao-Ping Qin ◽  
Shu-Ming Ye ◽  
Ji-Zeng Du ◽  
Gong-Yu Shen
Keyword(s):  
Olfactory Bulb ◽  
Cell Layer ◽  
Plexiform Layer ◽  
Olfactory Nerve ◽  
Mitral Cell ◽  
Granule Cell Layer ◽  
Developmental Expression ◽  
Main Olfactory Bulb ◽  
Glomerular Layer ◽  
Layer 4

Abstract The distribution of calbindin, calretinin and parvalbumin during the development of the mouse main olfactory bulb (MOB) was studied using immunohistochemistry techniques. The results are as follows: (1) calbindin-immunoreactive profiles were mainly located in the glomerular layer, and few large calbindin-immunoreactive cells were found in the subependymal layer of postnatal day 10 (P1 0) to postnatal day 40 (P40) mice; (2) no calbindin was detected in the mitral cell layer at any stage; (3) calretinin-immunoreactive profiles were present in all layers of the main olfactory bulb at all stages, especially in the olfactory nerve layer, glomerular layer and granule cell layer; (4) parvalbumin-immunoreactive profiles were mainly located in the external plexiform layer (except for P10 mice); (5) weakly stained parvalbumin-immunoreactive profiles were present in the glomerular layer at all stages; and (6) no parvalbumin was detected in the mitral cell layer at any stage.

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