Cranial Nerves I and II

2021 ◽  
pp. 115-119
Author(s):  
Kelly D. Flemming ◽  
Eduardo E. Benarroch
Keyword(s):  
Optic Nerve ◽  
Sensory Neurons ◽  
Chloride Channels ◽  
Calcium Influx ◽  
Cranial Nerves ◽  
Sensory Information ◽  
Olfactory Receptors ◽  
Olfactory Nerve ◽  
Afferent Nerve ◽  
Gated Channel

Cranial nerves I (olfactory nerve) and II (optic nerve) are supratentorial, paired cranial nerves. This chapter provides an overview of their anatomy. Cranial nerve I is a special visceral afferent nerve carrying sensory information about odors. Olfactory receptors lie in the nasal cavity. Odorants activate receptors within the cilia of olfactory sensory neurons and trigger the opening of a cyclic nucleotide–gated channel. This channel allows a calcium influx and the opening of calcium-activated chloride channels. Depolarization then occurs.

scholarly journals Widespread inhibition, antagonism, and synergy in mouse olfactory sensory neurons in vivo

2019 ◽  
Author(s):  
Shigenori Inagaki ◽  
Ryo Iwata ◽  
Masakazu Iwamoto ◽  
Takeshi Imai
Keyword(s):  
Sensory Neurons ◽  
Calcium Imaging ◽  
Odorant Receptor ◽  
Sensory Information ◽  
Olfactory Sensory Neurons ◽  
Axon Terminals ◽  
Two Photon ◽  
Odor Mixtures ◽  
The Brain

SUMMARYSensory information is selectively or non-selectively inhibited and enhanced in the brain, but it remains unclear whether this occurs commonly at the peripheral stage. Here, we performed two-photon calcium imaging of mouse olfactory sensory neurons (OSNs) in vivo and found that odors produce not only excitatory but also inhibitory responses at their axon terminals. The inhibitory responses remained in mutant mice, in which all possible sources of presynaptic lateral inhibition were eliminated. Direct imaging of the olfactory epithelium revealed widespread inhibitory responses at OSN somata. The inhibition was in part due to inverse agonism toward the odorant receptor. We also found that responses to odor mixtures are often suppressed or enhanced in OSNs: Antagonism was dominant at higher odor concentrations, whereas synergy was more prominent at lower odor concentrations. Thus, odor responses are extensively tuned by inhibition, antagonism, and synergy, at the early peripheral stage, contributing to robust odor representations.

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.

Disorders of cranial nerves

2010 ◽  
pp. 5033-5038
Author(s):  
R.D.M. Hadden ◽  
P.K. Thomas ◽  
R.A.C. Hughes
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Optic Nerve ◽  
Older Patients ◽  
Cranial Nerves ◽  
The Third ◽  
Intracavernous Aneurysm ◽  
System Tract ◽  
Third Nerve ◽  
Sixth Nerve

The 12 cranial nerves are peripheral nerves except for the optic nerve which is a central nervous system tract. Disorders of particular note include the following: Olfactory (I) nerve—anosmia is most commonly encountered as a sequel to head injury. Third, fourth, and sixth cranial nerves—complete lesions lead to the following deficits (1) third nerve—a dilated and unreactive pupil, complete ptosis, and loss of upward, downward and medial movement of the eye; (2) fourth nerve—extorsion of the eye when the patient looks outwards, with diplopia when gaze is directed downwards and medially; (3) sixth nerve—convergent strabismus, with inability to abduct the affected eye and diplopia maximal on lateral gaze to the affected side. The third, fourth, and sixth nerves may be affected singly or in combination: in older patients the commonest cause is vascular disease of the nerves themselves or their nuclei in the brainstem. Other causes of lesions include (1) false localizing signs—third or sixth nerve palsies related to displacement of the brainstem produced by supratentorial space-occupying lesions; (2) intracavernous aneurysm of the internal carotid artery—third, fourth, and sixth nerve lesions. Lesions of these nerves can be mimicked by myasthenia gravis....

scholarly journals Identification of Chloride Channels CLCN3 and CLCN5 Mediating the Excitatory Cl− Currents Activated by Sphingosine-1-Phosphate in Sensory Neurons

2018 ◽  
Vol 11 ◽  
Author(s):  
Yanmei Qi ◽  
Norbert Mair ◽  
Kai K. Kummer ◽  
Michael G. Leitner ◽  
María Camprubí-Robles ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Chloride Channels ◽  
Sphingosine 1 Phosphate

scholarly journals Calmodulin Contributes to Gating Control in Olfactory Calcium-activated Chloride Channels

2006 ◽  
Vol 127 (6) ◽  
pp. 737-748 ◽  
Author(s):  
Hiroshi Kaneko ◽  
Frank Möhrlen ◽  
Stephan Frings
Keyword(s):  
Sensory Neurons ◽  
Signal Amplification ◽  
Single Channel ◽  
Feedback Inhibition ◽  
Ion Selectivity ◽  
Sensory Information ◽  
Activation Mechanism ◽  
Ca Channels ◽  
Cl Channels ◽  
Ca Sensitivity

In sensory neurons of the peripheral nervous system, receptor potentials can be amplified by depolarizing Cl currents. In mammalian olfactory sensory neurons (OSNs), this anion-based signal amplification results from the sequential activation of two distinct types of transduction channels: cAMP-gated Ca channels and Ca-activated Cl channels. The Cl current increases the initial receptor current about 10-fold and leads to the excitation of the neuron. Here we examine the activation mechanism of the Ca-dependent Cl channel. We focus on calmodulin, which is known to mediate Ca effects on various ion channels. We show that the cell line Odora, which is derived from OSN precursor cells in the rat olfactory epithelium, expresses Ca-activated Cl channels. Single-channel conductance, ion selectivity, voltage dependence, sensitivity to niflumic acid, and Ca sensitivity match between Odora channels and OSN channels. Transfection of Odora cells with CaM mutants reduces the Ca sensitivity of the Cl channels. This result points to the participation of calmodulin in the gating process of Ca-ativated Cl channels, and helps to understand how signal amplification works in the olfactory sensory cilia. Calmodulin was previously shown to mediate feedback inhibition of cAMP-synthesis and of the cAMP-gated Ca channels in OSNs. Our results suggest that calmodulin may also be instrumental in the generation of the excitatory Cl current. It appears to play a pivotal role in the peripheral signal processing of olfactory sensory information. Moreover, recent results from other peripheral neurons, as well as from smooth muscle cells, indicate that the calmodulin-controlled, anion-based signal amplification operates in various cell types where it converts Ca signals into membrane depolarization.

Coupling of Calcium Homeostasis to Axonal Sodium in Axons of Mouse Optic Nerve

2002 ◽  
Vol 88 (2) ◽  
pp. 802-816 ◽  
Author(s):  
Yakov Verbny ◽  
Chuan-Li Zhang ◽  
Shing Yan Chiu
Keyword(s):  
Optic Nerve ◽  
Calcium Homeostasis ◽  
Action Potentials ◽  
Calcium Influx ◽  
Repetitive Nerve Stimulation ◽  
Strongly Coupled ◽  
Sodium Load ◽  
Calcium Clearance ◽  
Calcium Dyes ◽  
Ionophore Monensin

Axonal populations in neonatal and mature optic nerves were selectively stained with calcium dyes for analysis of calcium homeostasis and its possible coupling to axonal Na. Repetitive nerve stimulation causes a rise in axonal [Ca2+]i the posttetanus recovery of which is impeded by increasing the number of action potentials in the tetanus. This effect is augmented in 4-aminopyridine (4-AP; 1 mM), which dramatically increases the calcium and presumably sodium load during the tetanus. Increasing axonal [Na]i with the Na-ionophore monensin (4–50 μM) and ouabain (30 μM) retards posttetanus calcium decline, suggesting that efficient calcium clearance depends on a low level of axonal [Na]i. Posttetanus calcium clearance is not affected by K-mediated depolarization. To further examine coupling between axonal [Na]i and [Ca2+]i, the resting axonal [Ca2+]i was monitored as axonal [Na+]i was elevated with ouabain, veratridine, and monensin. In all cases, elevation of axonal [Na+]i evokes a calcium influx into axons. This influx is unrelated to activation of calcium channels but is consistent with calcium influx via reversal of the Na/Ca exchanger expected as a consequence of axonal [Na+]i elevation. In conclusion, this study demonstrates that calcium homeostasis in the axons of the optic nerve is strongly coupled to axonal [Na+]i in a manner consistent with the Na/Ca exchanger playing a major role in extruding calcium following nerve activity.

Antidromic Modulation of a Proprioceptor Sensory Discharge in Crayfish

1997 ◽  
Vol 78 (2) ◽  
pp. 1180-1183 ◽  
Author(s):  
Michelle Bévengut ◽  
François Clarac ◽  
Daniel Cattaert
Keyword(s):  
Nervous System ◽  
Sensory Neurons ◽  
Sensory Information ◽  
Primary Afferents ◽  
Fictive Locomotion ◽  
Current Pulses ◽  
Cell Somata

Bévengut, Michelle, François Clarac, and Daniel Cattaert. Antidromic modulation of a proprioceptor sensory discharge in crayfish. J. Neurophysiol. 78: 1180–1183, 1997. In the proprioceptive neurons of the coxo-basal chortotonal organ, orthodromic spikes convey the sensory information from the cell somata (located peripherally) to the central output terminals. During fictive locomotion, presynaptic depolarizations of these central terminals elicit bursts of antidromic spikes that travel back to the periphery. To determine whether the antidromic spikes modified the orthodromic activity of the sensory neurons, single identified primary afferents of the proprioceptor were recorded intracellularly and stimulated in in vitro preparations of crayfish nervous system. Depolarizing current pulses were delivered in trains whose frequency and duration were controlled to reproduce bursts of antidromic spikes similar to those elicited during fictive locomotion. According to their frequencies, these antidromic bursts reduce or suppress the orthodromic discharges in both position- and movement-sensitive neurons. They induce both a long-lasting silence and a gradual recovery after their occurrences. Neither the collision between the afferent and the efferent messages nor the release of serotonin by the sensory neurons can explain these results. We therefore conclude that antidromic bursts produce a peripheral modulation of the orthodromic activity of the sensory neurons, modifying their sensitivity by mechanisms yet unknown.

Microsurgical Resection of Recurrent Cavernous Sinus Hemangioma by Superior and Lateral Approach: 2-Dimensional Operative Video

2019 ◽  
Vol 19 (2) ◽  
pp. E165-E166
Author(s):  
Qazi Zeeshan ◽  
Juan P Carrasco Hernandez ◽  
Michael K Moore ◽  
Laligam N Sekhar
Keyword(s):  
Optic Nerve ◽  
Carotid Artery ◽  
Cavernous Sinus ◽  
Tumor Resection ◽  
Cranial Nerves ◽  
Brain Magnetic Resonance Imaging ◽  
Mass Effect ◽  
Lateral Approach ◽  
Microsurgical Resection ◽  
The Right

Abstract This video shows the technical nuances of microsurgical resection of recurrent cavernous sinus (CS) hemangioma by superior and lateral approach.  A 77-yr-old woman presented with headache and difficulty in vision in right eye for 6 mo. She had previously undergone attempted resection of a right CS tumor in another hospital with partial removal, and the tumor had grown significantly. Neurological examination revealed proptosis, cranial nerve 3 palsy, and loss of vision in right eye (20/200). Left side visual acuity was 20/20.  Brain magnetic resonance imaging (MRI) demonstrated a large CS mass with homogeneous enhancement, measuring 3.3 × 3.3 × 2.6 cm, extending into the suprasellar cistern with mass effect on the right optic nerve. It extended anteriorly to the region of the right orbital apex and abuted the basilar artery posteriorly.  She underwent right frontotemporal craniotomy, posterolateral orbitotomy and anterior clinoidectomy as well as optic nerve decompression, and the CS tumor was removed by superior and lateral approach. An incision was made into the superior wall of the CS medial to the third nerve. On lateral aspect the tumor had extended outside the CS through the Parkinson's triangle. Posteriorly it extended through the clival dura. Anteriorly tumor encased the carotid artery and it was gradually dissected away. At the end of the operation, all of the cranial nerves were intact.  Postoperative MRI showed near complete tumor resection with preservation of the internal carotid artery. At 6 mo follow-up her modified Rankin Scale was 1 and vision in left eye was normal.  Informed consent was obtained from the patient prior to the surgery that included videotaping of the procedure and its distribution for educational purposes. All relevant patient identifiers have also been removed from the video and accompanying radiology slides.

Temporal Development of Cyclic Nucleotide-Gated and Ca2+-Activated Cl− Currents in Isolated Mouse Olfactory Sensory Neurons

2007 ◽  
Vol 98 (1) ◽  
pp. 153-160 ◽  
Author(s):  
Anna Boccaccio ◽  
Anna Menini
Keyword(s):  
Sensory Neurons ◽  
Flash Photolysis ◽  
Olfactory Receptors ◽  
Cell Voltage ◽  
Equilibrium Potential ◽  
Olfactory Sensory Neurons ◽  
Second Phase ◽  
Current Response ◽  
Intact Mouse ◽  
Secondary Current

A Ca2+-activated Cl− current constitutes a large part of the transduction current in olfactory sensory neurons. The binding of odorants to olfactory receptors in the cilia produces an increase in cAMP concentration; Ca2+ enters into the cilia through CNG channels and activates a Cl− current. In intact mouse olfactory sensory neurons little is known about the kinetics of the Ca2+-activated Cl− current. Here, we directly activated CNG channels by flash photolysis of caged cAMP or 8-Br-cAMP and measured the current response with the whole cell voltage-clamp technique in mouse neurons. We measured multiphasic currents in the rising phase of the response at −50 mV. The current rising phase became monophasic in the absence of extracellular Ca2+, at +50 mV, or when most of the intracellular Cl− was replaced by gluconate to shift the equilibrium potential for Cl− to −50 mV. These results show that the second phase of the current in mouse intact neurons is attributed to a Cl− current activated by Ca2+, similarly to previous results on isolated frog cilia. The percentage of the total saturating current carried by Cl− was estimated in two ways: 1) by measuring the maximum secondary current and 2) by blocking the Cl− channel with niflumic acid. We estimated that in the presence of 1 mM extracellular Ca2+ and in symmetrical Cl− concentrations the Cl− component can constitute up to 90% of the total current response. These data show how to unravel the CNG and Ca2+-activated Cl− component of the current rising phase.

TRPV1 receptors mediate particulate matter-induced apoptosis

2004 ◽  
Vol 286 (3) ◽  
pp. L563-L572 ◽  
Author(s):  
N. Agopyan ◽  
J. Head ◽  
S. Yu ◽  
S. A. Simon
Keyword(s):  
Particulate Matter ◽  
Sensory Neurons ◽  
Calcium Influx ◽  
Airborne Particulate Matter ◽  
Annexin V ◽  
Basic Research ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Trpv1 Receptors ◽  
Induced Apoptosis

Exposure to airborne particulate matter (PM) is a world-wide health problem mainly because it produces adverse cardiovascular and respiratory effects that frequently result in morbidity. Despite many years of epidemiological and basic research, the mechanisms underlying PM toxicity remain largely unknown. To understand some of these mechanisms, we measured PM-induced apoptosis and necrosis in normal human airway epithelial cells and sensory neurons from both wild-type mice and mice lacking TRPV1 receptors using Alexa Fluor 488-conjugated annexin V and propidium iodide labeling, respectively. Exposure of environmental PMs containing residual oil fly ash and ash from Mount St. Helens was found to induce apoptosis, but not necrosis, as a consequence of sustained calcium influx through TRPV1 receptors. Apoptosis was completely prevented by inhibiting TRPV1 receptors with capsazepine or by removing extracellular calcium or in sensory neurons from TRPV1(-/-) mice. Binding of either one of the PMs to the cell membrane induced a capsazepine-sensitive increase in cAMP. PM-induced apoptosis was augmented upon the inhibition of PKA. PKA inhibition on its own also induced apoptosis, thereby suggesting that this pathway may be endogenously protective against apoptosis. In summary, it was found that inhibiting TRPV1 receptors prevents PM-induced apoptosis, thereby providing a potential mechanism to reduce their toxicity.

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