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.

Functional properties of vertebrate olfactory receptor neurons

1986 ◽  
Vol 66 (3) ◽  
pp. 772-818 ◽  
Author(s):  
T. V. Getchell
Keyword(s):  
Olfactory Receptor ◽  
Olfactory Receptor Neuron ◽  
Olfactory Nerve ◽  
Sensory Transduction ◽  
Olfactory Receptor Neurons ◽  
Receptor Neuron ◽  
Olfactory Pathway ◽  
Receptor Neurons ◽  
Molecular Biological Techniques

The interaction of an odorant with the chemosensitive membrane of olfactory receptor neurons initiates a sequence of molecular and membrane events leading to sensory transduction, impulse initiation, and the transmission of sensory information to the brain. The main steps in this sequence are summarized in Figure 6. Several lines of evidence support the hypothesis that the initial molecular events and subsequent stages of transduction are mediated by odorant receptor sites and associated ion channels located in the membrane of the cilia and apical dendritic knob of the olfactory receptor neuron. Similarly, the membrane events associated with impulse initiation and propagation are mediated by voltage-gated channels located in the initial axonal segment and the axolemma. The ionic and electrical events associated with the proposed sequence have been characterized in general using a variety of experimental techniques. The identification, localization, and sequence of membrane events are consistent with the neurophysiological properties observed in specific regions of the bipolar receptor neuron. The influence of other cells in the primary olfactory pathway such as the sustentacular cells in the olfactory epithelium, the Schwann cells in the olfactory nerve, and the astrocytes in the olfactory nerve layer in the olfactory bulb on the physiological activity of the olfactory receptor neuron is an emerging area of research interests. The general principles derived from the experimental results described in this review provide only a framework that is both incomplete and of necessity somewhat speculative. As noted in the Introduction, the multidisciplinary study of the primary olfactory pathway is undergoing a renaissance of research interest. The application of modern biophysical, cell, and molecular biological techniques to the basic issues of odorant recognition and membrane excitability will clarify the speculations and lead to the establishment of new hypotheses. Three broad areas of research will benefit from such studies. First, the application of biophysical techniques will lead to a detailed characterization of the membrane properties and associated ion conductance mechanisms. Second, the isolation and biochemical characterization of intrinsic membrane and cytosolic proteins associated with odorant recognition, sensory transduction, and the subsequent electrical events will result from the utilization of cell and molecular biological techniques.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Effects of Odor Stimulation on Antidromic Spikes in Olfactory Sensory Neurons

2008 ◽  
Vol 100 (6) ◽  
pp. 3074-3085 ◽  
Author(s):  
John W. Scott ◽  
Lisa Sherrill
Keyword(s):  
Electrical Stimulation ◽  
Sensory Neurons ◽  
Olfactory Receptor ◽  
Olfactory Receptor Neuron ◽  
Olfactory Nerve ◽  
Receptor Neuron ◽  
Odor Stimulus ◽  
Olfactory Sensory Neurons ◽  
Strongly Correlated ◽  
Receptor Neurons

Spikes were evoked in rat olfactory sensory neuron (OSN) populations by electrical stimulation of the olfactory bulb nerve layer in pentobarbital anesthetized rats. The latencies and recording positions for these compound spikes showed that they originated in olfactory epithelium. Dual simultaneous recordings indicated conduction velocities in the C-fiber range, around 0.5 m/s. These spikes are concluded to arise from antidromically activated olfactory sensory neurons. Electrical stimulation at 5 Hz was used to track changes in the size and latency of the antidromic compound population spike during the odor response. Strong odorant stimuli suppressed the spike size and prolonged its latency. The latency was prolonged throughout long odor stimuli, indicating continued activation of olfactory receptor neuron axons. The amounts of spike suppression and latency change were strongly correlated with the electroolfactogram (EOG) peak size evoked at the same site across odorants and across stimulus intensities. We conclude that the curve of antidromic spike suppression gives a reasonable representation of spiking activity in olfactory sensory neurons driven by odorants and that the correlation of peak spike suppression with the peak EOG shows the accuracy of the EOG as an estimate of intracellular potential in the population of olfactory sensory neurons. In addition, these results have important implications about traffic in olfactory nerve bundles. We did not observe multiple peaks corresponding to stimulated and unstimulated receptor neurons. This suggests synchronization of spikes in olfactory nerve, perhaps by ephaptic interactions. The long-lasting effect on spike latency shows that action potentials continue in the nerve throughout the duration of an odor stimulus in spite of many reports of depolarization block in olfactory receptor neuron cell bodies. Finally, strong odor stimulation caused almost complete block of antidromic spikes. This indicates that a very large proportion of olfactory axons was activated by single strong odor stimuli.

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.

Disorders of the Cranial Nerves and Brainstem

2021 ◽  
pp. 851-861
Author(s):  
Kelly D. Flemming
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Cranial Nerves ◽  
Olfactory Nerve ◽  
Mitral Cell ◽  
Olfactory Cortex ◽  
Olfactory Receptor Cells ◽  
Receptor Cells ◽  
Clinical Disorders ◽  
Primary Olfactory Cortex

This chapter briefly repeats key anatomic characteristics and then reviews clinical disorders affecting each cranial nerve in addition to the brainstem. More specifically, this chapter covers cranial nerves I, V, VII, and IX through XII plus the brainstem. The olfactory nerve is a special visceral afferent nerve that functions in the sense of smell. The axons of the olfactory receptor cells within the nasal cavity extend through the cribriform plate to the olfactory bulb. These olfactory receptor cell axons synapse with mitral cells in the olfactory bulb. Mitral cell axons project to the primary olfactory cortex and amygdala. The olfactory cortex interconnects with various autonomic and visceral centers.

scholarly journals Olfactory receptor neuron coding in the turbulent realm

2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
Jean-Baptiste Masson ◽  
Christelle Monsempes ◽  
Jean-Pierre Rospars ◽  
Philippe Lucas
Keyword(s):  
Olfactory Receptor ◽  
Olfactory Receptor Neuron ◽  
Receptor Neuron ◽  
Neuron Coding
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