Intraoperative sneezing secondary to indirect Olfactory nerve stimulation

2022 ◽  
Author(s):  
Miljyot Singh Sangha ◽  
Kapil Mohan Rajwani ◽  
Ana Mirallave Pescador ◽  
Keyoumars Ashkan ◽  
Francesco Vergani ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Olfactory Nerve

Evidence for glutamate as the olfactory receptor cell neurotransmitter

1994 ◽  
Vol 71 (6) ◽  
pp. 2557-2561 ◽  
Author(s):  
D. A. Berkowicz ◽  
P. Q. Trombley ◽  
G. M. Shepherd
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Nerve Stimulation ◽  
Olfactory Receptor ◽  
Olfactory Receptor Neuron ◽  
Olfactory Nerve ◽  
Nmda Receptor Antagonist ◽  
Receptor Antagonists ◽  
Cell Recording ◽  
Tufted Cells

1. Synaptic transmission between olfactory receptor neurons and mitral/tufted cells was examined using a whole-cell recording technique in a hemisected preparation of the turtle olfactory bulb. To determine the olfactory receptor neuron transmitter, we isolated components of the synaptic response of mitral/tufted cells to olfactory nerve stimulation using postsynaptic receptor antagonists. 2. Low-intensity stimulation of the olfactory nerve evoked monosynaptic excitatory postsynaptic potentials in mitral/tufted cells that consisted of a rapid and prolonged depolarization with little contribution from other bulb neurons. The exogenous application of glutamate mimicked the response of mitral/tufted cells to olfactory nerve stimulation. 3. Olfactory nerve stimulation evoked in mitral/tufted cells a two component response that was reversibly blocked by glutamate receptor antagonists. The first, a rapid depolarization of short duration, was sensitive to the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX); the second, a depolarization of slower onset but longer duration, was sensitive to the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (AP5). When DNQX and AP5 were both present the postsynaptic response was completely abolished. These results strongly support the notion that glutamate is the neurotransmitter at the olfactory nerve to mitral/tufted cell synapse.

Olfactory nerve stimulation activates rat mitral cells via NMDA and non-NMDA receptors in vitro

Neuroreport ◽  
1996 ◽  
Vol 7 (5) ◽  
pp. 989-992 ◽  
Author(s):  
Matthew Ennis ◽  
Lee A. Zimmer ◽  
Michael T. Shipley
Keyword(s):  
Nmda Receptors ◽  
Nerve Stimulation ◽  
Olfactory Nerve ◽  
Mitral Cells

scholarly journals Top-down acetylcholine signaling via olfactory bulb vasopressin cells contributes to social discrimination in rats

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Hajime Suyama ◽  
Veronica Egger ◽  
Michael Lukas
Keyword(s):  
Social Interaction ◽  
Olfactory Bulb ◽  
Nerve Stimulation ◽  
Action Potentials ◽  
Muscarinic Acetylcholine Receptor ◽  
Olfactory Nerve ◽  
Olfactory Cues ◽  
Social Discrimination ◽  
Top Down

AbstractSocial discrimination in rats requires activation of the intrinsic bulbar vasopressin system, but it is unclear how this system comes into operation, as olfactory nerve stimulation primarily inhibits bulbar vasopressin cells (VPCs). Here we show that stimulation with a conspecific can activate bulbar VPCs, indicating that VPC activation depends on more than olfactory cues during social interaction. A series of in vitro electrophysiology, pharmacology and immunohistochemistry experiments implies that acetylcholine, probably originating from centrifugal projections, can enable olfactory nerve-evoked action potentials in VPCs. Finally, cholinergic activation of the vasopressin system contributes to vasopressin-dependent social discrimination, since recognition of a known rat was blocked by bulbar infusion of the muscarinic acetylcholine receptor antagonist atropine and rescued by additional bulbar application of vasopressin. Thus, our results implicate that top-down cholinergic modulation of bulbar VPC activity is involved in social discrimination in rats.

Effect of Transcutaneous Vagus Nerve Stimulation in Dysphagia After Lateral Medullary Infarction: A Case Report

2019 ◽  
Vol 28 (4) ◽  
pp. 1381-1387
Author(s):  
Ying Yuan ◽  
Jie Wang ◽  
Dongyu Wu ◽  
Dahua Zhang ◽  
Weiqun Song
Keyword(s):  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Rating Scale ◽  
Tube Feeding ◽  
Nasogastric Feeding ◽  
Lateral Medullary Infarction ◽  
Severe Dysphagia ◽  
Transcutaneous Vagus Nerve Stimulation ◽  
Medullary Infarction

Purpose Severe dysphagia with weak pharyngeal peristalsis after dorsal lateral medullary infarction (LMI) requires long-term tube feeding. However, no study is currently available on therapeutic effectiveness in severe dysphagia caused by nuclear damage of vagus nerve after dorsal LMI. The purpose of the present investigation was to explore the potential of transcutaneous vagus nerve stimulation (tVNS) to improve severe dysphagia with weak pharyngeal peristalsis after dorsal LMI. Method We assessed the efficacy of 6-week tVNS in a 28-year-old woman presented with persisting severe dysphagia after dorsal LMI who had been on nasogastric feeding for 6 months. tVNS was applied for 20 min twice a day, 5 days a week, for 6 weeks. The outcome measures included saliva spitted, Swallow Function Scoring System, Functional Oral Intake Scale, Clinical Assessment of Dysphagia With Wallenberg Syndrome, Yale Pharyngeal Residue Severity Rating Scale, and upper esophagus X-ray examination. Results After tVNS, the patient was advanced to a full oral diet without head rotation or spitting. No saliva residue was found in the valleculae and pyriform sinuses. Contrast medium freely passed through the upper esophageal sphincter. Conclusion Our findings suggest that tVNS might provide a useful means for recovery of severe dysphagia with weak pharyngeal peristalsis after dorsal LMI. Supplemental Material https://doi.org/10.23641/asha.9755438

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