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.

Organization of primary afferent and local-circuit synapses in the olfactory glomerulus

1994 ◽  
Vol 52 ◽  
pp. 148-149
Author(s):  
Charles A. Greer ◽  
Juan C. Bartolomei ◽  
Jeffrey M. Dembner
Keyword(s):  
Olfactory Receptor ◽  
Room Temperature ◽  
Olfactory Nerve ◽  
Sprague Dawley ◽  
Primary Afferent ◽  
Olfactory Receptor Cells ◽  
Receptor Cells ◽  
Olfactory Glomerulus ◽  
Sprague Dawley Rats ◽  
Confocal And Electron Microscopy

Odorant molecules are transduced by olfactory receptor cells whose axons join to form the olfactory nerve which distributes across the surface of the olfactory bulb (OB). Axons exit the nerve layer to terminate within the glomerular neuropil of the OB. While there appears a gross topography between the epithelium and OB4, it is clear that extensive topographic reorganization of axons occurs within the olfactory nerve. To better understand the mechanisms that may contribute to the establishment of glomerular-specific fascicles and functional domains within the OB, we have investigated axonal organization within the nerve and the intraglomerular distribution of primary afferent synapses using light, confocal and electron microscopy.Sprague-Dawley rats, 30 to 50 days postnatal, were anesthetized, lightly perfused with 0.9% NaCl and the OBs removed. Crystals of the lipophilic dye, Dil, were inserted into the olfactory nerve layer and the tissue placed in 4% paraformaldehyde at room temperature for 10 - 30 days.

scholarly journals The Impact of Ovariectomy on Olfactory Neuron Regeneration in Mice

2020 ◽  
Vol 45 (3) ◽  
pp. 203-209
Author(s):  
Kentaro Yamada ◽  
Hideaki Shiga ◽  
Takuya Noda ◽  
Masayuki Harita ◽  
Tomoko Ishikura ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Receptor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protein Distribution ◽  
Ki 67 ◽  
Olfactory Receptor Cells ◽  
Receptor Cells ◽  
Estrogen Depletion ◽  
The Impact ◽  
Time Point

Abstract Estrogen has been shown to affect differentiation and proliferation as a mitogen in various neural systems. Olfactory receptor cells are unique within the nervous system, and have the ability to regenerate even after an individual has reached maturity. Olfactory receptor cells also regenerate after experimentally induced degeneration. The purpose of this study is to observe the influence of estrogen depletion induced by ovariectomy on olfactory nerve regeneration. Female mice underwent bilateral ovariectomy at 8 weeks of age and received intraperitoneal administration of methimazole 1 week later. At 2, 4, and 6 weeks after methimazole administration, the olfactory mucosa was analyzed histochemically to determine olfactory epithelium (OE) thickness, olfactory marker protein distribution, and Ki-67 immunoreactivity. Furthermore, 2 weeks after ovariectomy, trkA protein distribution in the OE and nerve growth factor (NGF) levels in the olfactory bulb were determined by immunohistochemistry and enzyme-linked immunosorbent assay, respectively. Our results showed that in ovariectomized mice OMP, Ki-67, and trkA-immunopositive cells expression decreased at 2 weeks after methimazole injection, a time point at which regeneration is underway. At this same time point, although NGF production in the olfactory bulb had increased before methimazole administration, no differences were observed between the ovx and control groups. These results suggest that estrogen depletion induces a suppressive effect on regeneration of olfactory neurons, and that estrogen may have a potential use in the treatment of sensorineural olfactory dysfunction.

Regional distribution of rat electroolfactogram

1995 ◽  
Vol 73 (6) ◽  
pp. 2207-2220 ◽  
Author(s):  
P. I. Ezeh ◽  
L. M. Davis ◽  
J. W. Scott
Keyword(s):  
Spatial Distribution ◽  
Olfactory Bulb ◽  
Olfactory Epithelium ◽  
Flow Rate ◽  
Olfactory Receptor ◽  
Action Potentials ◽  
Amyl Acetate ◽  
Flow Rates ◽  
Olfactory Receptor Cells ◽  
Receptor Cells

1. Electroolfactorgram (EOG) recordings were made from different regions of the rat olfactory epithelium to test for spatial distribution of odor responses. 2. The EOG recordings showed spatial distribution of the odor responses in the olfactory epithelium. While some odorants (amyl acetate, anisole, and ethyl butyrate) were more effective in evoking responses in the dorsal recess near the septum, other odorants (including limonene, cineole, cyclooctane, and hexane) were more effective in the lateral recesses among the turbinate bones. These differences were seen as statistically significant odorant-by-position interactions in analysis of variance. 3. Comparisons of recordings along the anteroposterior dimension of the epithelium produced smaller differences between the odor responses. These were not significant for 3-mm distances, but were statistically significant for 5- to 6-mm distances along the dorsomedial epithelium. 4. The latencies were significantly longer in the lateral recesses than in the medial region. This probably reflects a more tortuous air path along the turbinate bones to the lateral recesses. 5. The olfactory receptor cells were activated by antidromic stimulation via the nerve layer of the olfactory bulb. The population spikes evoked from the olfactory receptor cells could be suppressed by prior stimulation with odorants that evoked strong EOG responses. This collision of the antidromic action potentials with the odor-evoked action potentials indicates that the same population of receptor cells was activated in both cases. 6. The flow rate and duration of the artificial sniff were varied systematically in some experiments. The differential distribution of response sizes was present at all flow rates and sniff durations. Some odors (e.g., amyl acetate and anisole) produced increased responses in the epithelium of the lateral recesses when flow rates or sniff durations were high. We suggest that these changes may reflect the sorptive properties of the nasal membranes on these odors. The responses to other odors (e.g., hexane or limonene) were not greatly affected by flow rate or sniff duration. 7. Taken with existing anatomic data, the results indicate that the primary olfactory neurons that project axons to glomeruli in different parts of the olfactory bulb are responsive to different odors. The latency differences between responses at medial and lateral sites are large enough to be physiologically significant in the generation of the patterned responses of olfactory bulb neurons.

Ultrastructural aspects of olfactory signal transduction and its development

1994 ◽  
Vol 52 ◽  
pp. 142-143
Author(s):  
Bert Ph. M. Menco
Keyword(s):  
Signal Transduction ◽  
Olfactory Receptor ◽  
Receptor Cell ◽  
Freeze Substitution ◽  
Luminal Surface ◽  
Tissue Sections ◽  
Olfactory Receptor Cells ◽  
Receptor Cells ◽  
Olfactory Signal ◽  
Odor Molecule

Vertebrate olfactory receptor cells are specialized neurons that have numerous long tapering cilia. The distal parts of these cilia line the interface between the external odorous environment and the luminal surface of the olfactory epithelium. The length and number of these cilia results in a large surface area that presumably increases the chance that an odor molecule will meet a receptor cell. Advanced methods of cryoprepration and immuno-gold labeling were particularly useful to preserve the delicate ultrastructural and immunocytochemical features of olfactory cilia required for localization of molecules involved in olfactory signal-transduction. We subjected olfactory tissues to freeze-substitution in acetone (unfixed tissues) or methanol (fixed tissues) followed by low temperature embedding in Lowicryl K11M for that purpose. Tissue sections were immunoreacted with several antibodies against proteins that are presumably important in olfactory signal-transduction.

Presynaptic Afferent Inhibition of Lobster Olfactory Receptor Cells: Reduced Action-Potential Propagation Into Axon Terminals

1998 ◽  
Vol 80 (2) ◽  
pp. 1011-1015 ◽  
Author(s):  
Matt Wachowiak ◽  
Lawrence B. Cohen
Keyword(s):  
Action Potential ◽  
Olfactory Receptor ◽  
Receptor Cell ◽  
Action Potential Propagation ◽  
Cell Axon ◽  
Axon Terminals ◽  
Olfactory Receptor Cells ◽  
Receptor Cells ◽  
Afferent Inhibition ◽  
Reduced Action

Wachowiak, Matt and Lawrence B. Cohen. Presynaptic afferent inhibition of lobster olfactory receptor cells: reduced action-potential propagation into axon terminals. J. Neurophysiol. 80: 1011–1015, 1998. Action-potential propagation into the axon terminals of olfactory receptor cells was measured with the use of voltage-sensitive dye imaging in the isolated spiny lobster brain. Conditioning shocks to the olfactory nerve, known to cause long-lasting suppression of olfactory lobe neurons, allowed the selective imaging of activity in receptor cell axon terminals. In normal saline the optical signal from axon terminals evoked by a test stimulus was brief (40 ms) and small in amplitude. In the presence of low-Ca2+/high-Mg2+ saline designed to reduce synaptic transmission, the test response was unchanged in time course but increased significantly in amplitude (57 ± 16%, means ± SE). This increase suggests that propagation into receptor cell axon terminals is normally suppressed after a conditioning shock; this suppression is presumably synaptically mediated. Thus our results show that presynaptic inhibition occurs at the first synapse in the olfactory pathway and that the inhibition is mediated, at least in part, via suppression of action-potential propagation into the presynaptic terminal.

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