Interglomerular Center-Surround Inhibition Shapes Odorant-Evoked Input to the Mouse Olfactory Bulb In Vivo

2006 ◽  
Vol 95 (3) ◽  
pp. 1881-1887 ◽  
Author(s):  
Dejan Vučinić ◽  
Lawrence B. Cohen ◽  
Efstratios K. Kosmidis
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Presynaptic Inhibition ◽  
Granule Cells ◽  
Olfactory Receptor Neuron ◽  
Receptor Neuron ◽  
Surround Inhibition ◽  
Neuron Terminals

Mouse olfactory receptor proteins have relatively broad odorant tuning profiles, so single odorants typically activate a substantial subset of glomeruli in the main olfactory bulb, resulting in stereotyped odorant- and concentration-dependent glomerular input maps. One of the functions of the olfactory bulb may be to reduce the extent of this rather widespread activation before transmitting the information to higher olfactory centers. Two circuits have been studied in vitro that could perform center-surround inhibition in the olfactory bulb, one circuit acting between glomeruli, the other through the classical reciprocal synapses between the lateral dendrites of mitral cells and the dendrites of granule cells. One unanswered question from these in vitro measurements was how these circuits would affect the response to odorants in vivo. We made measurements of the odorant-evoked increase in calcium concentration in the olfactory receptor neuron terminals in the anesthetized mouse to evaluate the role of presynaptic inhibition in reshaping the input to the olfactory bulb. We compared the glomerular responses in 2- to 4-wk-old mice before and after suppressing presynaptic inhibition onto the receptor neuron terminals with the GABAB antagonist, CGP46381 . We find that the input maps are modified by an apparent center-surround inhibition: strongly activated glomeruli appear to suppress the release from receptor neurons terminating in surrounding glomeruli. This form of lateral inhibition has the effect of increasing the contrast of the sensory input map.

scholarly journals Dynamics of MASH1 Expression in Vitro and in Vivo Suggest a Non-Stem Cell Site of MASH1 Action in the Olfactory Receptor Neuron Lineage

1995 ◽  
Vol 6 (4) ◽  
pp. 363-379 ◽  
Author(s):  
Melinda K. Gordon ◽  
Jeffrey S. Mumm ◽  
Rachel A. Davis ◽  
J.David Holcomb ◽  
Anne L. Calof
Keyword(s):  
Stem Cell ◽  
Olfactory Receptor ◽  
Olfactory Receptor Neuron ◽  
Receptor Neuron

scholarly journals Combinations of DIPs and Dprs control organization of olfactory receptor neuron terminals in Drosophila

PLoS Genetics ◽  
2018 ◽  
Vol 14 (8) ◽  
pp. e1007560 ◽  
Author(s):  
Scott Barish ◽  
Sarah Nuss ◽  
Ilya Strunilin ◽  
Suyang Bao ◽  
Sayan Mukherjee ◽  
...  
Keyword(s):  
Olfactory Receptor ◽  
Olfactory Receptor Neuron ◽  
Receptor Neuron ◽  
Neuron Terminals

scholarly journals Inhibition of Olfactory Receptor Neuron Input to Olfactory Bulb Glomeruli Mediated by Suppression of Presynaptic Calcium Influx

2005 ◽  
Vol 94 (4) ◽  
pp. 2700-2712 ◽  
Author(s):  
Matt Wachowiak ◽  
John P. McGann ◽  
Philip M. Heyward ◽  
Zuoyi Shao ◽  
Adam C. Puche ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Transmitter Release ◽  
Calcium Influx ◽  
Imaging Techniques ◽  
Olfactory Receptor Neuron ◽  
Olfactory Nerve ◽  
Presynaptic Terminal ◽  
Receptor Neuron ◽  
Paired Pulse

We investigated the cellular mechanism underlying presynaptic regulation of olfactory receptor neuron (ORN) input to the mouse olfactory bulb using optical-imaging techniques that selectively report activity in the ORN presynaptic terminal. First, we loaded ORNs with calcium-sensitive dye and imaged stimulus-evoked calcium influx in a slice preparation. Single olfactory nerve shocks evoked rapid fluorescence increases that were largely blocked by the N-type calcium channel blocker ω-conotoxin GVIA. Paired shocks revealed a long-lasting suppression of calcium influx with ∼40% suppression at 400-ms interstimulus intervals and a recovery time constant of ∼450 ms. Blocking activation of postsynaptic olfactory bulb neurons with APV/CNQX reduced this suppression. The GABAB receptor agonist baclofen inhibited calcium influx, whereas GABAB antagonists reduced paired-pulse suppression without affecting the response to the conditioning pulse. We also imaged transmitter release directly using a mouse line that expresses synaptopHluorin selectively in ORNs. We found that the relationship between calcium influx and transmitter release was superlinear and that paired-pulse suppression of transmitter release was reduced, but not eliminated, by APV/CNQX and GABAB antagonists. These results demonstrate that primary olfactory input to the CNS can be presynaptically regulated by GABAergic interneurons and show that one major intracellular pathway for this regulation is via the suppression of calcium influx through N-type calcium channels in the presynaptic terminal. This mechanism is unique among primary sensory afferents.

Sonic hedgehog-dependent emergence of oligodendrocytes in the telencephalon: evidence for a source of oligodendrocytes in the olfactory bulb that is independent of PDGFRα signaling

Development ◽  
2001 ◽  
Vol 128 (24) ◽  
pp. 4993-5004
Author(s):  
Nathalie Spassky ◽  
Katharina Heydon ◽  
Arnaud Mangatal ◽  
Alexandar Jankovski ◽  
Christelle Olivier ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Olfactory Bulb ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Molecular Mechanisms ◽  
Cell Contact ◽  
Sonic Hedgehog Signaling ◽  
Oligodendrocyte Progenitors

Most studies on the origin of oligodendrocyte lineage have been performed in the spinal cord. By contrast, molecular mechanisms that regulate the appearance of the oligodendroglial lineage in the brain have not yet attracted much attention. We provide evidence for three distinct sources of oligodendrocytes in the mouse telencephalon. In addition to two subpallial ventricular foci, the anterior entopeduncular area and the medial ganglionic eminence, the rostral telencephalon also gives rise to oligodendrocytes. We show that oligodendrocytes in the olfactory bulb are generated within the rostral pallium from ventricular progenitors characterized by the expression of Plp. We provide evidence that these Plp oligodendrocyte progenitors do not depend on signal transduction mediated by platelet-derived growth factor receptors (PDGFRs), and therefore propose that they belong to a different lineage than the PDGFRα-expressing progenitors. Moreover, induction of oligodendrocytes in the telencephalon is dependent on sonic hedgehog signaling, as in the spinal cord. In all these telencephalic ventricular territories, oligodendrocyte progenitors were detected at about the same developmental stage as in the spinal cord. However, both in vivo and in vitro, the differentiation into O4-positive pre-oligodendrocytes was postponed by 4-5 days in the telencephalon in comparison with the spinal cord. This delay between determination and differentiation appears to be intrinsic to telencephalic oligodendrocytes, as it was not shortened by diffusible or cell-cell contact factors present in the spinal cord.

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